Archives of Indian Psychiatry April 2007

Archives of Indian Psychiatry 9(1), April 2007

Honorary Editor

G.K.Vankar Professor and Head Dept. of Psychiatry B.J.Medical College and Civil Hospital Ahmedabad 380016 Cell : 099041 60338

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Editorial Board

R.Srinivasa Murthy E.Mohandas Vikram Patel Nimesh Desai K.S.Jacob Nilesh Shah Chittaranjan Andrade Bharat Panchal Shekhar Sheshadri Ashok Nagpal

Board of directors

Laxman Dutt I.R.Rajkumar V.G.Vatwe S.M.Amin R.CManiar Mukesh Jagiwala Rajendra Hegde K.S.Ayyar Hemangee Dhavle Govind Bang Shubhangi Parkar Kaushik Gupte

Corresponding Members

Dinesh Bhugra Stuart Montgomary Sushrut Jadhav Afzal Javed Joseph Johar Prakash Masand Andre Joubert Manoj Shah

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Rashmin Cholera Parag Shah Ritambhara Mehta Khyati Mehtalia Charles Pinto Yusuf Matcheswala Rajesh Dhume D.M.Dhavle Shivarathnamma Vivek Kirpekar A,S.Kadri

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CONTENTSIn this issue Parag Shah 4Editorial : Polypharmacy in Psychiatry E.Mohandas 5 Depression, chronic medical disease and perceived health Chittaranjan Andrade 8Dr.L.P.Shah Oration Chronic Pain Syndrome Manilal Gada 10Review Article Metabolic Syndrome: A Psychiatric Perspective E.Mohandas V.Rajmohan 22Dr.A.V.Shah Best Paper Award PTSD and Depression in Children and Adolescents G.K.Vankar, Girish Banwari, 29 Four years after communal violence Viral Parikh,Hemang Shah Original Research Paper Patterns of prescription in private psychiatry: A comparison with public sector Navneet Kumar Johri, Trupti Sharma 36Original Research Paper Depression in Diabetes Mellitus G.K.Vankar ,Viral Parikh, 41 Girish Banwari, Minakshi Parikh Brief Research Communication AClinical Study in Childhood onset Trichotillomania Avinash De Souza 46Brief Research Communication Verbal learning difficulty in schizophrenia and epilepsy : implications for retraining Shweta Kadaba and Anuradha Sovani 49Brief Research Communication Aripiprazole in autism Hemang Shah, G.K.Vankar 53Case Reports Schizotypal Personality Disorder : Bimal Tamakuwala, Parag Shah, 57 A Diagnosis Often Missed Kamlesh Dave, Ritambhara Mehta Tardive Dystonia : Two Cases Sachin Sinha, Ramesh Parmar, 59 Mukesh SamaniLetter to editor ECT is effective not only when it is administered Nilesh Shah 61 but also when merely recommended ! Being cautious about using spirituality as Minakshi Parikh 61 a psychiatric treatment toolQuiz T.Asokan 62 Poetry Freedom Parag Shah 63Obituary Dr. N.S.Vahia J. S.Apte 64

Offical Publication of The Indian Psychiatric Society,

Western Zonal BranchVolume 9, No. 1, April



Chronic pain – role of a psychiatristWith pharmacological and psychological treatment proven effective, psychiatrists should take active role as medical specialists in the management of chronic pain disorder. In Dr. L P Shah Oration for 2006 (page 10), Gada talks about concept of pain with reference to chronic pain disorder, its assessment, management and correlation with psychiatric disorders.

Depression and Chronic Medical DiseasesA 60 nation, cross-sectional, WHO World Health Survey shows that depression is more likely to arise in the context of a chronic medical condition than by itself and has a greater negative impact on the perceived health. Andrade discusses details of the study and its outcome in his editorial on page 8.A study of 225 subjects attending a Diabetes Clinic by Vankar et al. (page 41) found depression in 11.5% of them and positively correlated with female gender, illiteracy, duration as well as complications arising out of it.

Metabolic disorder a psychiatric perspective E.Mohandas reviews ( page 22 )atypical antipsychotic associated metabolic syndrome.With increasing use of atypical antipsy-chotic drugs,this rticle is of immense practical use for any psychiatrist.The article summarizes knowledge regarding etiopathol-ogy, patient evaluation and management.

PTSD and Major Depression in Children and AdolescentsChildren and adolescents suffer from PTSD and major depression even after four years of exposure to extreme stressors. Vankar et al. studied a group of 225 subjects who had lost their parents during communal violence before four years. PTSD was found among 17.2% and major depression among 10.5% of children and adolescents. Vankar et al. bring about more of phenomeno-logical and demographic characteristic on page 29.

Prescription Patterns in PsychiatryMohandas reviews Polypharmacy in his editorial (page 5) on types, factors causing polypharmacy and principles of rationale polypharmacy. Current evidence for rationale polypharmacy in various psychiatric disorders is discussed.“Its time to review our knowledge and audit our practising trends by developing therapeutic guidelines, or else be prepared for legal litigations” report Johri and Sharma on page 36. A study of case records of 100 patients visiting general hospital setting reveals startling facts, ranging from absence of rationale documentation, polypharmacy, erratic drug combinations and more.

Verbal Learning in Schizophrenia & EpilepsyKadaba and Sovani studied verbal learning deficits in a group matched comparison design for patients diagnosed for Schizo-phrenia and Temporal lobe epilepsy. The study highlights implications for rehabilitation of both the groups, especially with reference to verbal retraining on page 49..

Childhood onset TrichotillomaniaDe Souza reports a study of 26 children and adolescents with childhood onset trichotillomania, assessing demographics, phe-nomenology, comorbidity and treatment history for a span of 3 years (page 46). Adding to the few Indian reports available, it stresses the need for larger studies across diverse population.

Parag ShahAssistant.Professor of Psychiatry, Medical College , Vadodara

Correspondence : A-404, Jeevandham Towers,Nr. Bimanagar, Satellite Road, Ahmedabad – 380 015Cell : 094261 38318 E-mail: [email protected]

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In this issue


Editorial Polypharmacy in Psychiatry E. Mohandas

“The true polypharmacy is the skillful combination of remedies” Sir William Osler

The word polypharmacy first appeared in medical literature in 1959 in the New England Journal of Medicine and in the psychiatric literature in 1969 (Cuevas and Sanz, 2004). The emergence of evidence-based psychiatry and the demand for the rational therapy have cast the limelight on polypharmacy (Ananth et al, 2004). Many terms like polytherapy, polypharmacotherapy, cotherapy, copharmacy, combination therapy and combination treatment have been tried to differentiate a skillful or rational approach to combining medications from the presumably more haphazard approach implied by the term polypharmacy. Multifarious definitions exist to explain polypharmacy. One of the few definitions given in the psychiatric literature states that polypharmacy occurs when a patient receives two or more psychoactive drugs for the management of behavioral symptoms (Merlis et al, 1970). Experts have recently defined polypharmacy in psychiatry as a state of multiple drug treatment that occurs when two psychotropic agents are used to treat the same psychiatric condition (e.g., bipolar disorder) or two commonly associated conditions (e.g., bipolar disorder and panic disorder). The term also applies to any combination of three or more medications for whatever purpose. It is argued that in reality polypharmacy is sometimes skillful and sometimes unskillful, sometimes thought through and sometimes haphazard, and logical and illogical at the same time in different degrees (Ghaemi, 2001). The ever increasing incidence of polypharmacy necessitates the need for a closer examination of the causes and ramifications of this practice. The factors causing polypharmacy include drug-related, system-related, disease-related, society-based and pharmaceutical industry based factors (Ananth et al, 2004). The drug related factors include fear and laziness to change the drug, sloppy diagnoses, botched drug titrations, and withdrawal or rebound exacerbation leading to drug increase. The systems related factors include pressure from families, pressure from insurance companies and managed care short hospital stays. The disease related factors encompass comorbidity and lack of cure for the condition. The societal factors involve economics, low doctor-to-patient ratio, and fear of litigation. The pharmaceutical industry has contributed to polypharmacy by advertising and exuberant promises they make (Ghaemi, 2002). Polypharmacy in clinical practice can be categorized as: 1. Drug targeting the available known pathogenetic

mechanism with a drug to treat additional symptoms (e.g. Antidepressants to treat depression and benzodiazepines for sedation)

2. Drug targeting the available known pathogenetic mechanism with a drug to treat a co-morbid psychiatric condition [e.g. Antipsychotics to treat schizophrenia and selective serotonin reuptake inhibitors (SSRI) for obsessive

compulsive disorder (OCD)]

3. Drug targeting the available known pathogenetic mechanism with a drug to control side effects (e.g. Antipsychotics to treat schizophrenia and antiparkinsonian agent to control extrapyramidal symptoms)

4. Drug targeting the available known pathogenetic mechanism with a drug augmenting the first agent (e.g. Antidepressants to treat depression and lithium or thyroxine to augment the agent)

5. Drug targeting the available known pathogenetic mechanism with a drug to provide acute amelioration while awaiting the delayed effect of the primary medication (e.g., using lorazepam in acute mania while waiting for the antimanic effects of lithium)

6. Drug targeting the available known pathogenetic mechanism with a drug to treat intervening phases of an illness (e.g., adding an antidepressant to a mood stabilizer when a bipolar patient develops a depressive episode)

7. Drug targeting the available known pathogenetic mechanism with a drug augmenting the first agent with additional drug used as desperate remedy (e.g. Antidepressants to treat depression, lithium or thyroxine to augment the agent and other mood stabilizer, atypical antipsychotics, or novel therapies)

8. Drug targeting the available known pathogenetic mechanism with a drug to treat a co morbid medical illness (e.g., Antipsychotics to treat schizophrenia and antidiabetic agent to control diabetes).

The need for rational basis is primal in this era of polypharmacy. Criteria for rational polypharmacy have been put forth by many groups. The factors to be considered while instituting polypharmacy include

1. The combination must have a positive effect on the pathophysiology or pathoetiology of the disorder

2. There must be convincing evidence that the combination is more effective, including more cost-effective, than monodrug therapy

3. The combination should not pose a significantly greater safety or tolerability risks than monotherapy

4. Drugs should not interact both pharmacokinetically and pharmacodynamically

5. Drugs should have mechanisms of action that are likely to interact in a way that augments response

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6. Drugs should not have the same mechanism or opposing mechanisms of action

7. Each drug should have simple metabolism with an intermediate half-life and linear pharmacokinetics. (Preskorn and Lacey, 2007)

The use of three or more medications in managing bipolar disorder increased from 3.3% in the 1970s to 9.3% in the early 1980s, 34.9% in the late 1980s, and 43.8% in the early 1990s. Evidence based on eight RCTs with 1124 participants’ shows that co-therapy with an antipsychotic and a mood stabilizer is more efficacious than a mood stabilizer alone. Response rate was more than 50% higher in those receiving co-therapy (Smith et al, 2007). Polypharmacy was associated with higher discharge rates from hospital and a 78% moderate to marked improvement rate overall. Polypharmacy in bipolar disorder is generally necessary because standard mood stabilizers are mostly ineffective in monotherapy. The current evidence suggests polypharmacy the rule rather than the exception in the treatment of bipolar disorder. Guidelines for bipolar disorder recommend using a standard mood stabilizer and an atypical neuroleptic agent together from the start. In less severe manic, mixed, and rapid-cycling states, one can begin with a standard mood stabilizer alone. Evidence based psychiatry does not recommend frequent polypharmacy with antidepressants in the treatment of bipolar disorder. However antidepressant use maybe warranted for acute, severe, non–rapid-cycling bipolar depression with severe suicidal ideation. Antidepressants are also recommended in the hospitalized bipolar depressed patient with economic limitations on length of stay. This is best done when the antidepressant can be tapered post discharge on an outpatient basis. The use of antidepressants in bipolar I depression may induce a switch. However, in bipolar II depression there may be a significant role for antidepressant use. The evidence for such a conclusion needs further study. The evidence shows that polypharmacy is a double-edged sword in the treatment of bipolar disorder: it can lead to improvement, but it usually is practiced ineffectively (Ghaemi and Ko, 2001).

Treating depression is complex and often requires polypharmacy as 45% of patients treated with an antidepressant medication do not achieve remission. Polypharmacy is defined as the use of two or more agents specifically for the treatment of depression. Some experts do not define a treatment to be polypharmacy if only one agent is used primarily for depression and another agent used for short-term treatment of depression-related symptoms, such as insomnia or anxiety. However, if three or more medications are used for whatever purpose, then the term polypharmacy would seem appropriate. A double-blind study did not show any difference between monotherapy and fluoxetine–desipramine combination. Two double-blind placebo-controlled trials have shown that adjunctive mianserin augments response to SSRIs in resistant major depression. Another large study found no advantage of sertraline plus mianserin over sertraline monotherapy. The largest summation of the data is a meta-analysis which found that combination antidepressant treatment produced a 62% response rate when

monotherapy had failed. (Keks et al, 2007). These trials reveal that the evidence supporting antidepressant polypharmacy is largely inconclusive.

Treatment guidelines for depression recommend the initiation of pharmacotherapy with a single antidepressant and switching to another antidepressant of a different class in case of no response. If the second agent also is ineffective, then it seems appropriate to engage in polypharmacy with two antidepressants or the addition of other augmenting agents like lithium or thyroid hormone. In partial responders to the first antidepressant, the tendency is to lean towards augmentation with relatively benign agents like thyroid hormone or buspirone. For psychotic unipolar depression, combined treatment with an atypical antipsychotic agent and an antidepressant is recommended. However, some recommend that one might consider monotherapy with an atypical antipsychotic agent initially in psychotic major depression, followed by the addition of an antidepressant in the case of non response (Ghaemi and Appleton, 2001). The unfortunate scenario is the recommendations in treatment resistant depression. Treatment resistance is typically observed in bipolar depression rather than unipolar depression. There is considerable overlap of pseudounipolar depression (in effect, bipolar depression) in the basket of treatment resistant depression. The recommendation of augmentation in treatment resistant unipolar depression becomes diluted when we consider bipolar depression. So, the field is still fertile for further research.Psychotic disorders are a heterogeneous group sharing some descriptive features, but without clearly identified etiological or pathogenetic commonalities. Studies show that 40 - 50 % of schizophrenic inpatients and up to 90% schizophrenic outpatients receive antipsychotic combination therapies (Oepen, 2001).Studies have revealed that patients on olanzapine/ risperidone monotherapy, when switched to the combination of both, experienced additional improvement of 30% on the total BPRS scores. Sulpiride augmentation in patients on clozapine and risperidone augmentation to existing antipsychotic regimen including clozapine have been found beneficial in chronic refractory cases of schizophrenia. A review of all the available data on antipsychotic polypharmacy concluded that there was insufficient data to properly evaluate polypharmacy; instead provided guidelines for the use of polypharmacy (Ananth et al, 2004). Recently official guidelines such as the Texas Medication Algorithm Project have recommended the combination of antipsychotics if monotherapy fails to achieve satisfactory results (Oepen, 2001). The sad part of the story is that the preachers of monotherapy often practice polypharmacy, probably rational.

Anxiety disorders, substance use disorders and even the dementing syndromes do not escape from the use of multiple drugs. Clinicians usually combine medications to give utmost symptom relief to their clients. It would be prudent to start with single drug, but rational addition of drugs may be attempted taking into account the pharmacokinetic and pharmacodynamic

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considerations.

The use of polypharmacy occurs when treatment is targeted against symptoms rather than syndromes. Psychiatric syndromes are notorious for overlap of symptoms breaching boundaries of syndromal classification. The neurobiological underpinnings also have considerable overlap. Instead of prophesizing monotherapy for good tolerability, data on rational polypharmacy have to emerge targeting efficacy.

REFERENCES1. Cuevas C De las , Sanz EJ. (2004) Polypharmacy in

psychiatric practice in the Canary Islands.BMC Psychiatry. 5; 4:18.

2. Ananth J, Parameswaran S, Gunatilake S. (2004) Antipsychotic polypharmacy. Curr Pharm Des.; 10:2231-8.

3. Merlis S, Sheppard C, Collins L, Fiorentino D. (1970) Polypharmacy in psychiatry: patterns of differential treatment. Am J Psychiatry 126:1647–51.

4. Ghaemi SN. (2001) ‘‘All the Worse for the Fishes’’: Conceptual and Historical Background of Polypharmacy

in Psychiatry. In: Polypharmacy in Psychiatry. Ed: Ghaemi SN. Marcel Dekker, Inc: 1-35.

5. Ghaemi SN and Appleton A. (2001) Polypharmacy in Depression. In: Polypharmacy in Psychiatry. Ed: Ghaemi SN. Marcel Dekker, Inc: 79-101

6. Keks NA, Burrows GD, Copolov DL, et al. (2007) Beyond the evidence: is there a place for antidepressant combinations in the pharmacotherapy of depression? Med J Aust.; 186(3):142-4.

7. Preskorn SH and Lacey RL. (2007) Polypharmacy:When Is It Rational?.Journal of Psychiatric Practice Vol. 13: 97-105.

8. Smith LA, Cornelius V, Warnock A, et al. (2007) Acute bipolar mania: a systematic review and meta-analysis of co-therapy vs. monotherapy. Acta Psychiatr Scand.; 115(1):12-20.

9. Ghaemi SN and Ko JY (2001) Polypharmacy of Bipolar Disorder. In: Polypharmacy in Psychiatry. Ed: Ghaemi SN. Marcel Dekker, Inc: 35-79.

10. Oepen G. (2001) Polypharmacy in Schizophrenia. In: Polypharmacy in Psychiatry. Ed: Ghaemi SN. Marcel Dekker, Inc: 101-133

Source of support : None Conflict of interest: None Dr.E.Mohandas Senior Consultant Psychiatrist,

Elite Mission Hospital, Koorkencherry, Thrissur, Kerala-680007 E-mail: [email protected] Phone: 0487-3011400

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Editorial

Depression, Chronic Medical Disease, and Perceived Health Chittaranjan Andrade

asthma. However, among the subjects who had two or more chronic physical conditions, depression was comorbid in nearly a quarter (23%). Strikingly, depression comorbid with a chronic physical disease was significantly more likely than depression alone.

On a scale of 0-100 where 100 represented the best health score, the mean health score was 91 for subjects with neither depression nor any chronic medical condition; it was 79-80 for subjects with one chronic medical condition; it was 73 for subjects with depression alone, and 72 for subjects with two chronic medical conditions; it was 59-67 for subjects with depression and one chronic medical condition (lowest score for depression with diabetes); and it was as low as 56 for depression with two or more chronic medical conditions. In a multivariate model which sought to identify variables which predicted health burden, all of the following were associated with poorer health scores: being older, being female, being less educated, being unemployed, being separated, widowed, or divorced, having a lower income, having a chronic medical condition, and having depression. Having depression had a greater effect than each of the other variables, including the presence of two or more chronic medical conditions. Having depression along with a chronic medical condition had the greatest adverse impact of all; and the worst perceived health was experienced by subjects with depression and diabetes.Across countries and across different demographic characteristics, subjects with depression along with one or more chronic diseases consistently had the worst health scores of all the disease states. Importantly, the findings remained much the same even when the analyses focused on health items which were relatively different from the symptom domains of depression.IN SUMMARY

In summary, data from the 60-nation, cross-sectional, WHO World Health Survey show that an ICD-10 depressive episode is more likely to arise in the context of a chronic medical condition (angina, arthritis, asthma, or diabetes) than by itself. Depression has a greater negative impact on perceived health than these chronic medical conditions. The negative effect of depression alone is similar to that of two chronic medical conditions combined. Depression comorbid with these diseases has the greatest adverse impact on health.

POINTS TO POINDER

1. The health scores described in this study were self-rated, descriptive measures. Therefore, cognitive distortions associated with depression could have resulted in an

In the World Health Organization (WHO) Global Burden of Disease 2000 study, Ustun et al (2004) found that depression was the fourth leading cause of disease burden, accounting for 4.4% of the total disability-adjusted life-years during the year 2000. Furthermore, depression was responsible for the largest non-fatal burden, accounting for almost 12% of all total years lived with disability worldwide.

After heart disease, depression is expected to become the second leading cause of disease burden by the year 2020. Depression is well known to arise in the context of different chronic medical conditions. How does depression impact upon health status in comparison with such chronic medical conditions? And, how is health status perceived when depression coexists with such conditions? The answers to these questions have important implications for public health, and were the subject of a large study from the World Health Organzation. The results were reported in the Lancet by Moussavi et al (2007).

The data for the study were drawn from the cross-sectional WHO World Health Surveys of 245,404 adults in 60 countries across the world. There were 26 countries from Europe, 15 from Africa, 6 from the Americas, 4 from the eastern Mediterranean region, 5 from southeast Asia, and 4 from the western Pacific. India was also part of the study. To qualify for inclusion in the analysis, the sample had to be nationally representative and probabilistically selected; and sampling weights information had to be available.

The data were based on self-reports obtained during face-to-face interviews in all but 2 countries (telephone interviews were conducted in Israel and Luxembourg). The response rates ranged from a low of 63% in Israel to a high of 99% in the Philippines. Health status was assessed using an 18-item questionnaire; responses were recorded on a 5-point scale ranging from ‘no difficulty or problem’ to ‘extreme difficulty/inability’. Depression was diagnosed using ICD-10. Four chronic medical conditions were chosen for study along with depression; these conditions were ischemic heart disease, arthritis, asthma, and diabetes.

WHAT THE STUDY FOUND

The epidemiological data were in line with expectations. The 1-year prevalence was 3.2% (95% CI, 3.0-3.5%) for an ICD-10 depressive episode alone; 4.5% for angina; 4.1% for arthritis; 3.3% for asthma; and 2.0% for diabetes.

How often did depression coexist with these chronic medical conditions? Across the world, depression was comorbid in about 9-18% of the subjects who had a chronic medical condition; this figure was lowest for diabetes and highest for 5


exaggeration of disability. Subjectivity notwithstanding, self-reported ill-health is an important measure, especially when objective measures are unavailable.

2. The findings were generally consistent across countries, suggesting that the negative impact of depression on health is similar across cultures.

3. This study examined only four chronic medical conditions in addition to depression. It is possible, and indeed likely, that depression may coexist with other chronic medical conditions, and is associated with similar findings therein as described in this study.

4. In assigning importance to the findings of this study, it must be remembered that depression increases disability and distress and worsens outcomes for many chronic medical conditions, including those examined in this study.

5. Demyttenaere et al (2004) examined the World Mental Health Surveys data of 60,463 community-dwelling adults in 6 developing and 8 developed countries. They found that greater disorder severity was associated with a greater likelihood of treatment in almost all countries. Nevertheless, 36-50% of serious cases in developed countries and

76-85% of serious cases developing countries received no treatment during the 12 months before the study. In this context, we do not know the extent to which the findings of Moussavi et al (2007) were moderated by effective treatment of depression. In any case, the findings emphasize that the prevention of depression, and its early diagnosis and treatment, are both important public health priorities.

REFERENCES

1. Ustun TB, Ayusob-Mateos JL, Chatterji, Mathers C., Murray CJ. Global burden of depressive disorders in the year 2000.Br. J.Psychiatry 2004;184:386-392

2. Moussavi S, Chatterji S, Verdes E, Tandon A, Patel V, Ustun B. Depression, chronic diseases, and decrements in health: results from the World Health Surveys. Lancet 2007; 370: 851-858.

3. Demyttenaere K, Bruffaerts R, Posada-Villa J, Gasquet I, Kovess V, Lepine JP et al for the WHO World Mental Health Survey Consortium. Prevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health Surveys. JAMA 2004; 291: 2581-2590.

Source of support: None Conflict of interest: None Chittaranjan Andrade MD Professor and Head, Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore 560 029, India

e- mail:[email protected]; [email protected]

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adverse consequences of Under-treated pains are considerable. Under-treated chronic pain can impair an individual’s ability to carry out daily activities and diminish quality of life (American Pain Society 2001). In addition to disability, under-treated pain causes significant suffering. Individuals with poorly controlled pain may experience anxiety, fear, anger, or depression. (Becker 1997),

Pain is also a major cause of work absenteeism, underemployment, and unemployment.

Mounting health care costs and disability compensation reflect, in part, poor care for pain related conditions. (Butler et al 1997). Thus, under-treated pain has significant physical, psychological, and financial consequences.

The neurological and psychological mechanisms that underlie pain are complex, and knowledge of mechanisms is limited. The discussion of pathophysiology in this review emphasizes practical knowledge that will facilitate diagnosis and/or the selection of appropriate interventions. A host of factors, including the setting, characteristics of the pain, and patient factors (e.g., age, medical condition, language and cognitive abilities) influence pain assessment.

What Is Pain?

In 1968, McCaffery defined pain as “whatever the experiencing person says it is, existing whenever s/he says it does”. (McCaffery 1968) This definition emphasizes that pain is a subjective experience with no objective measures. It also stresses that the patient, not clinician, is the authority on the pain and that his or her self-report is the most reliable indicator of pain.

In 1979, the International Association for the Study of Pain (IASP) introduced the most widely used definition of pain. The IASP defined pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.’’( Merskey & Bugduk 1994). This definition emphasizes that pain is a complex experience that includes multiple dimensions.

How Does Injury Lead to Pain?

Nociception refers to the process by which information about tissue damage is conveyed to the central nervous system (CNS). Exactly how this information is ultimately perceived as painful is unclear. In addition, there can be pain without nociception (e.g., phantom limb pain) and nociception without pain. But classic descriptions of pain typically include four processes: ( Fields 1987, Besson & Chaouch 1987).

Transduction: the conversion of the energy from a noxious thermal, mechanical, or chemical stimulus into electrical energy (nerve impulses) by sensory receptors called nociceptors

I am thankful to Indian Psychiatric Society Western Zonal Branch and members of Award Committee for bestowing on I am thankful to Indian Psychiatric Society Western Zonal Branch and its members of Awards Committee for bestowing on me me prestigious “Dr. L. P. Shah Oration” for 2006.

Dr. L. P. Shah needs no introduction. He has been pioneer in taking Indian psychiatry to where it is today. He has not only been my teacher but a true friend, philosopher and guide- a mentor in true sense. He was always approachable and helpful to one and all. He has a special place in the hearts of all psychiatrist of Mumbai. He recognized almost all people just by their voices after he had lost his vision. I take this opportunity to pay my utmost respect and tribute to him. It is my proud privilege that I have been honored with an oration in his name.

There are a couple of things which are making me more proud. First, I am Dr. L.P. Shah’s first student to have received the honour. Second, the fact that this honour has been bestowed on a Kutchhi in a conference organized by Saurashtra Kutchh Branch of Indian Psychiatric Society is very pleasing.

INTRODUCTION :

The word pain is derived from the Latin word “poena” meaning “penalty” or “punishment”. In the past pain was viewed as a punishment inflicted by God for the sins committed by the sufferer.

Pain is common. About 9 in 10 Americans regularly suffer from pain, (Gallup survey 1999) and pain is the most common reason individuals seek health care.( Fox et al, 2000) Each year, an estimated 25 million Americans experience acute pain due to injury or surgery and another 50 million suffer chronic pain. (National Pain Survey1999, American Pain Foundation 2001). Chronic pain is the most common cause of long-term disability and almost one third of all Americans will experience severe chronic pain at some point in their lives. (Brookoff D.2001). As the population ages, the number of people who will need treatment is expected to rise. (Brookoff D.2001).

Pain is often under-treated. Improved understanding of pain mechanisms has advanced treatment for pain. The recent studies, reports, and a position statement (American Pain Society Quality of Care Committee 1980; Field & Cassel 1997) suggest that many types of pain (e.g., postoperative pain, cancer pain, chronic non-cancer pain) and patient populations (e.g., elderly patients, children, minorities, substance abusers) (Carr & Goudas 1999) are under-treated. Data from a 1999 survey suggest that only 1 in 4 individuals with pain receive appropriate therapy. (Chronic Pain in America Survey 1999).

Inadequate pain management has adverse consequences. The 7

Dr. L. P. Shah Oration

Chronic Pain Disorder Manilal Gada


Transmission: the transmission of these neural signals from the site of transduction (periphery) to the spinal cord and brain

Perception: the appreciation of signals arriving in higher structures as pain

Modulation: descending inhibitory and facilitory input from the brain that influences (modulates) nociceptive transmission at the level of the spinal cord.

What Is Perception?

The perception of pain is an uncomfortable awareness of some part of the body, characterized by a distinctly unpleasant sensation and negative emotion best described as threat. Both cortical and limbic system structures are involved. (Chapman 2001). Nociceptive information from dorsal horn (DH) projection neurons travels via the thalamus to the contra lateral somatosensory cortex (Terman & Bonica 2001), where input is somatotopically mapped to preserve information about the location, intensity, and quality of the pain. (Guilbaud 1994, Covington 2000).

The thalamus relays nociceptive input to the limbic system. (Willis & Westlund 1997). This input joins input from the spinoreticular and spinomesencephalic tracts to mediate affective aspects of pain. (Refer to figure 1)

Immediate social and environmental context influences the perception of pain, as do past experience and culture. Consequently, a standard cause of pain (e.g., surgery) can generate enormous individual differences in pain perception.

What Is Modulation?

a. Descending pathwaysModulation of nociceptive transmission occurs at multiple (peripheral, spinal, supraspinal) levels. Yet, historically, modulation has been viewed as the attenuation of DH transmission by descending inhibitory input from the brain. Melzack and Wall’s Gate Control Theory brought this notion to the forefront in 1965 (Melzack & Wall 1965). Models of descending pain systems now include both inhibitory and facilitory descending pathways. Multiple brain regions contribute to descending inhibitory pathways. (Terman & Bonica 2001), Nerve fibers from these pathways release inhibitory substances (e.g., endogenous opioids, serotonin, norepinephrine, GABA) at synapses with other neurons in the DH. These substances bind to receptors on primary afferent and/or DH neurons and inhibit nociceptive transmission. Such endogenous modulation may contribute to the wide variations in pain perception observed among patients with similar injuries. (Basbaum & Fields 1984, Hammond 1986).

b. Clinical implications

Some analgesics enhance the effects of descending inhibitory input. For example, some antidepressants interfere with the reuptake of serotonin and norepinephrine at synapses, increasing their relative interstitial concentration (availability) (Walsh 1983 Wallace 1991), and the

activity of endogenous pain-modulating pathways. Thus, antidepressants are used to treat some types of chronic pain.

What Is Central Sensitization?

a. Definitions and features

Central sensitization refers to a state of spinal neuron hyper-excitability. (Woolf 1983). Tissue injury (inflammation), nerve injury (i.e., aberrant neural input), or both may cause it, and ongoing nociceptive input from the periphery is needed to maintain it (Covington 2000). Repeated stimulation of C-nociceptors initially causes a gradual increase in the frequency of DH neuron firing known as “wind-up.” Activation of N-methyl D-aspartate (NMDA) receptors plays a key role in this process. (MacDermott 1986, Yashpal 1995). The clinical correlate of wind-up temporal summation-refers to a progressive increase in pain experienced over the course of a repeated stimulus. Repeated or prolonged input from C-nociceptors or damaged nerves causes a longer-lasting increase in DH neuron excitability and responsiveness (i.e. central sensitization) (Woolf 1986) which may outlast the stimulus by minutes to hours. Central sensitization is associated with a) a reduction in central inhibition, b) spontaneous DH neuron activity, c) the recruitment of responses from neurons that normally only respond to low intensity stimuli (i.e., altered neural connections), and d) expansion of DH neuron receptive fields (McMahon 1984; Dickenson 1995; Cervero 1992).

Clinically, these changes may manifest as: 1. An increased response to a noxious st imulus

(hyperalgesia), 2. A painful response to a normally innocuous stimulus

(allodynia), 3. Prolonged pain after a transient stimulus (persistent pain),

and 4. The spread of pain to uninjured tissue (i.e., referred

pain). In contrast to hyperalgesia caused by peripheral mechanisms (i.e., primary hyperalgesia), such secondary hyperalgesia extends beyond the region of injury. (Ru-Rong 2000)

b. Clinical implications

Sensitization is likely responsible for most of the continuing pain and hyperalgesia after an injury (Wolf 2000). This sensitivity may be due to “normal” noxious input from injured and inflamed tissue or “abnormal” input from injured nerves or ganglia. In the former case, sensitization serves an adaptive purpose. That is, the hyperalgesia and allodynia encourage protection of the injury during the healing phase.

However, these processes can persist long after healing of the injury in the setting of chronic pain.

Central sensitization plays a key role in some chronic pain, especially pain induced by nerve injury or dysfunction (i.e., neuropathic pain). It explains why neuropathic pain

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(Woolf 1983; Covington 2000). Central sensitization also explains the long standing observation that established pain is more difficult to suppress than acute pain (Wall 1988; McQuay 1989).

In contrast to nociceptive pain, neuropathic pain is often unresponsive or poorly responsive to NSAIDs and opioids (Amer & Meyerson 1988; Chemy et al 1994). However, it may respond to antiepileptic drugs, antidepressants, or local anesthetics (Covington 1998).

CHRONIC PAIN:

Chronic pain was once defined as pain that extends 3 or 6 months beyond onset or beyond the expected period of healing (Turk & Okifuji 2001). However, new definitions differentiate chronic pain from acute pain based on more than just time.Chronic pain is now recognized as pain that extends beyond the period of healing, with levels of identified pathology that often is low and insufficient to explain the presence and/or extent of the pain. (Jacobsen & Mariano 2001).

Chronic pain is also defined as a persistent pain that “disrupts sleep and normal living, ceases to serve a protective function, and instead degrades health and functional capability.”( Chapman & Stillman 1996) Thus, unlike acute pain, chronic pain serves no adaptive purpose.

Chronic pain may be nociceptive, neuropathic, or both and caused by injury (e.g., trauma,surgery), malignant conditions, or a variety of chronic non-life-threatening conditions (e.g., arthritis, fibromyalgia, neuropathy).

In some cases, chronic pain exists de novo with no apparent cause. Although injury often initiates chronic pain, factors pathogenetically and physically remote from its cause may perpetuate it (Chapman & Stillman 2001). Environmental and affective factors also can exacerbate and perpetuate chronic pain, leading to disability and maladaptive behavior.INITIAL ASSESMENT OF PAIN:

Assessment is an essential, but challenging, component of any pain management plan. Pain is subjective, so no satisfactory objective measures of pain exist. Pain is also multidimensional, so the clinician must consider multiple aspects (sensory, affective, cognitive) of the pain experience. Finally, the nature of the assessment varies with multiple factors (e.g., purpose of the assessment, the setting, patient population, clinician), so no single approach is appropriate for all patients or settings.

Core Principles of Pain Assessment and Management

a. Patients have the right to appropriate assessment and management of pain

b. Pain is always subjective. Therefore, the patient’s self-report of pain is the single most reliable indicator of pain. A clinician needs to accept and respect this self-report, absent clear reasons for doubt.

c. Physiological and behavioral (objective) signs of pain (e.g.,

tachycardia, grimacing) are neither sensitive nor specific for pain. Such observations should not replace patient self-report unless the patient is unable to communicate.

d. Assessment approaches, including tools, must be appropriate for the patient population. Special considerations are needed for patients with difficulty communicating.

e. Family members should be included in the assessment process, when possible.

f. Pain tolerance varies among and within individuals depending on factors including heredity, energy level, coping skills, and prior experiences with pain.

g. Patients with chronic pain may be more sensitive to pain and other stimuli.

h. Pain is an unpleasant sensory and emotional experience, so assessment should address physical and psychological aspects of pain.

Information to be elicited during the initial assessment of pain includes

Characteristics of the pain (e.g., duration, location, intensity, quality, exacerbating/alleviating factors)

• Present and past pain management strategies and their outcomes

• Past and present medical problems that may influence the pain and/or its management

• Relevant family history• Current and past psychosocial issues or factors that may

influence the pain and its management• The impact of the pain on the patient’s daily life and

functioning• The patient’s and family’s knowledge of, expectations

about, and goals for pain management.Given the link between chronic pain and depression, the impact of the pain on the patient’s mood, satisfaction, quality of life, and cognitive functioning also requires thorough exploration. Key elements of this evaluation include a more comprehensive psychosocial assessment, psychiatric evaluation, psychometric testing (as appropriate), and assessment of function and any disability

COMMON ASSESSMENT TOOLS

Psychometric Instruments:

1. Assessing the sensory/discriminative component of pain

2. Assessing the affective component of pain

3. Assessing the behavioural component of pain

4. Assessing the lifestyle component of pain

5. Assessing the central control processes

Assessing the sensory/discriminative component of pain

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Category ratings may be either A) numerical (say 1-10) or B) verbal rating scale (VRS) (e.g. ‘none’, ‘mild’, ‘moderate’, ‘severe’, ‘unbearable’). In addition C) visual analogue scales (VAS) (10 cm lines with anchors at each end) represent a continuous dimension of pain intensity. (Karoly 1985).

Assessing the affective component of pain

McGill Pain Questionnaire (Melzack 1975) assesses affective component of pain. It consists of 78 pain adjectives arranged into 20 groups, each reflecting slightly different qualities of pain. Some group describe sensory experience (‘pricking’, ‘hot’ ‘scalding’) others describe affective qualities (‘sickening’, ‘fearful’, ‘punishing’, ‘cruel’) and yet others describe evaluative aspect of pain (‘annoying’, ‘miserable’, ‘troublesome’). Subjects are asked to indicate which words describe their pain.

Assessing the behavioural component of pain

Richards et al (1982) describe the development of a pain behaviour scale in which observation is recorded on 3 point scales (‘none’, ‘occasional’ ‘frequent’) of 10 verbal and non-verbal behaviour.

In most clinical settings, however, records of pain behaviour are likely to depend on patient’s self-observation.

Assessing the lifestyle component of pain

This is a broad concept but one which is of considerable importance. It is intended to refer not to specific behaviour related to the immediate experience of pain (which would be part of the behavioural component) but rather more general psychosocial factors which may be associated with chronic pain. Marital distress, social interactions, recreational activities, employment status and domestic arrangements fall within this category. Follick et al 1985 have devised a questionnaire which yields scores.

Assessing the central control processesThese aim to assess patients’ coping strategies or their use of strategies taught as part of treatment. The Vanderbilt Pain Management Inventory (Brown & Nicassio 1987) measures frequency with which patients use ‘active’ or ‘passive’ coping strategies. It comprises a mixture of cognitive and behavioural items. Passive coping is tapped by items such as wishing the doctor would prescribe better medication and restricting social activities, while active coping is assessed by items such as engaging in physical exercise, distracting oneself from the pain or staying busy. They found high scores on the active coping scale were related to low pain intensity ratings, low depression and less functional impairment, whilst high scores on the passive coping scale showed the opposite.PSYCHIATRIC DISORDERS IN CHRONIC PAIN:

Varma et al (1983) from Chandigarh have studied 2000 consecutive new cases with chronic intractable pain. In 50% of these patients, no physical illness could be detected by treating physicians (non psychiatric specialists); in another

21% of the cases, physical illnesses (arthropathies, arthritis, spondylosis) were not considered to be sufficient to explain the pain by treting specialists doctors. 72% of these 2000 cases had identifiable psychiatric illnesses, the most common being depressive disorder and anxiety disorders.

Vijay et al (1988) from Banglore have reported that 40% of patients attending the orthopedic outpatient department of a general hospital, had recognizable psychiatric disorder requiring psychiatric treatment.

Many patients learn to adopt a chronic pain life-style because they find it highly reinforcing psychologically. The spouse and other family members become quite anxious and take over many responsibilities for such patients. Some patients find the increased attention and avoidance of unwanted home and work responsibilities and family/marital conflicts highly reinforcing. These patients may enter a chronic pain stage in which their pain complaints are controlled primarily by their positive social and environmental consequences.(Gada 1991)

Typically patients with chronic pain have a history of multiple contacts with physicians for diagnosis and treatment, a long series of treatment failures, significant social and economic problems and an altered life-style.

Depression and Pain Comorbidity:

Epidemiologic studies indicate that the lifetime prevalence of pain symptoms (e.g. joint pain, back pain, headache, chest pain, arm or leg pain and abdominal pain) ranges from 24% to 37% (Regier et al 1984) and that physical symptom such as pain are leading reason that patients seek medical care (Komaroff 1990; Kroenka 2001). Major Depression is also common, with prevalence in primary care patients of 5% to 10 %. (Katon et al 1992). A growing body of literature has focused on the interaction between depressive disorder and pain symptoms (Gada 1980, 1987, Gada & Shah 2004; Bagadia et al 1973). This interaction has been labeled by some authors as depression-pain syndrome (Lindsay & Wyckoff 1981) or depression-pain dyad, implying that the conditions often coexist, respond to similar treatments, exacerbate one another and share biological pathways and neurotransmitters (Blier & Abbott 2001).

Primary care physicians fail to accurately diagnose at least 50% of patients with major depression and studies have shown that patients with major depression who present with physical symptoms such as pain are particularly likely to receive an inaccurate diagnosis. The new emphasis on pain as the fifth vital sign by Joint Commission on Accreditation of Healthcare Organization and the Veterans Health Administration highlights the importance of better understanding of the likely reciprocal links between major depression and pain.

Prevalence of Pain symptoms in patients with Major Depression:

The prevalence of pain ranged from 15% to 100% (mean prevalence 65%) in 14 studies investigating pain symptoms in cases of major depression (Bair et al 2003). A large longitudinal cohort study has shown that depressive disorder predict

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without depressive disorder at baseline (Leino & Magni 1993). Another study showed that low back pain is more than 2 times as likely to be reported by individuals with depressive disorder compared with those without depressive disorder (Croft et al 1995). In addition, the specific complaints of headache, abdominal pain, joint pain and chest pain are frequently reported by patients with depressive disorder in primary care settings (Gada 1980, 1987, Kroenka et al 1994).

Prevalence of Major Depression in Pain Patients:

Several studies have reported the association between major depression and pain, specifically addressing how the risk of depressive disorder increases as a function of different aspects of worsening pain (e.g. severity, frequency, duration and number of symptoms). Patients with multiple pain symptoms (e.g. back pain, headache, abdominal pain, chest pain and facial pain) are 3 to 5 times more likely to be depressed than patients without pain (Von Korff et al 1988) and pain symptoms are associated with at least a 2 fold increased risk for coexisting depression (Kroenka & Price 1993). Additionally population based study showed that subjects with chronic pain (defined as pain for most days for at least a month) are 3 times as likely to meet depression criteria as those without chronic pain (Magni et al 1993). The association between depression and pain becomes stronger as the severity of either condition increases (Moldin et al 1993, Carroll et al 2000).

Consistent with findings in primary care patients (Kroenka et al 1994) multiple pain complaints increase the probability of depression (Dworkin & Gitin 1991) such that patients with 2 or more different pain complaints are 6 times more likely to be depressed and patients with 3 or more pain complaints are 8 times more likely to meet depression criteria (Katon & Sullivan 1990). In addition, more frequent pain episodes (Wang et al 1999) and longer pain duration are associated with depression. An international study showed that patients with pain lasting longer than 6 months were more than 4 times as likely to have a depressive disorder as those without chronic pain (Guruje et al 1998). Migraine headaches and back pain are strongly associated with depression (Patten 2001)

Does Presence of Pain affect recognition and treatment of depression?

The “typical” depression presentation in primary care is dominated by physical (somatic) complaints as opposed to psychological complaints. More than 50% of patients with depression report somatic complaints only (Gada 1987; Kirmayer et al 1993; Cape & McCulloch 1999) and at least 60% of these somatic complaints are pain related (Gada 1980; Katon et al 1988; Kroenka et al 1994; Hollifield et al 1994).

Thus patients with depression in primary care settings are more likely to report various pain symptoms than they are to present with dysphoric mood or anhedonia. The study has shown that if all primary care patients presenting with a variety of pain conditions (e.g. abdominal pain, headache, joint pain and back pain) were evaluated for possible depression, 60% of previously undetected depression cases could have been

recognized (Katon 1984). Patients having multiple presenting physical complaints including non-specific musculoskeletal complaints and back pain, had more underlying depressive symptoms. (Gerber et al 1992).

Does presence of Depression affect clinical outcomes in patients treated for Pain?

Patients with pain and co morbid depression experienced more pain complaints (Betrus et al 1995), more intense pain (Lamb 2000), more amplification of pain symptoms (Wells 1989) and longer duration of pain (Burton et al 1995). Unfortunately patients with both conditions were more likely to have persistent pain (Gurejee 2001; Potter & Jones 1992; Reis et al 1999) and non-recovery (Gurejee 2001). Future episodes of pain, such as low back pain, chest pain, headache and musculoskeletal complaints were predicted by presence of depression.

Functional limitation (e.g. limited mobility, activity restrictions) and resulting disability, such as days in bed, ill and hospitalization, were increased in patients with pain and depression (Wells et al 1989; Burton et al 1995; Dionne et al 1997). Similarly, depression and pain produced additive impairments in social functioning (Holroyd et al 2000), higher unemployment rates, (Dolce et al 1986; Sullivan et al 1992) and diminished patient satisfaction (Cherkin et al 1996). Literature review by Linton (2000) has suggested that depression has a greater impact than other clinical factors on outcomes, especially functional impairment, in patients with pain and that neglecting to treat the depression accounts of pain treatment failure (Atkinson et al 1986; Dwarkin & Giltin 1991).

Depression is associated with an array of poor pain outcomes and worse prognosis.

Common Biological Pathways for Depression and PainThe biochemical theory of depression posits that depression is the result of a neurochemical imbalance or a functional deficiency of key neurotransmitters, the monoamines: serotonin, norepinephrine and dopamine. A common theory holds that depression and painful symptoms follow the same descending pathways of the central nervous system. The studies have described the biological link between depression and pain. Although nociceptive fibers transmitting pain signals from the periphery of the body through the dorsal horn to the medulla, midbrain, hypothalamus, thalamus, limbic cortical areas (anterior cingulated and insular cortex), somatosensory cortex and posterior parietal cortex have been carefully mapped, there is an increasing interest in neuroanatomy of a descending system of pain modulation (Kroenka & Swindle 2000). The increasing knowledge about this system allows to better understanding mechanisms of pain modulation via medications as well as psychological mechanisms such as expectation, attention and distraction, negative and positive affect.Studies have shown that brain regions involved in the generation of emotions (e.g. medial prefrontal, insular, anterior temporal cortex, hypothalamus and amygdala) send many projections to brainstem structures involved in pain modulation

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(periaqueductal gray PAG, rostral-ventromedial medulla RVM) (Fields 2000). Negative anticipation causes key brain areas to activate, and the subject then appears to focus, attend to, and rate the pain stimuli as more severe. Distraction from pain signals in experimental pain has been shown in other experiments to decrease activation of PAG and decrease pain perception (Rainville et al 1997; Sawamoto et al 2000). Perhaps, these experiments suggest how depression, which is associated with negative expectancies, may amplify pain signals by activating brain structures such as the anterior cingulated gyrus. Depression is also associated with depletion of serotonin and norepinephrine, which may decrease the modulatory effect of this descending pain system.

TREATMENT:

Engel has emphasized that the key to success lay in investigating the manner in which pain disrupted the patient’s personal, social, family and occupational life thus avoiding an artificial separation between what are regarded as organic, psychological and social factors. An interview with a spouse or relative should provide information about interpersonal pain behaviour and social reward system.

A central task in evaluation and pretreatment planning is a. to help patients redefine their problem in a manner that

ends the investigations without challenging the reality of the pain and

b. that shifts the emphasis from a curative to a rehabilitative approach

c. implicit in this change is a transfer of responsibility from physician to the patient.

COMMON ANALGESIC AGENTS:

a. Nonopioids

Mechanism of action and effects The primary mechanism of action of NSAIDs is

inhibition of the enzyme cyclooxygenase (COX) which blocks prostaglandin synthesis. Acetaminophen, another nonopioid, appears to act mostly via a central mechanism. All nonopioids have anti-inflammatory, antipyretic, and analgesic effects, but the anti-inflammatory effect of acetaminophen is essentially negligible. The analgesic effect of NSAIDs is prompt (minutes to hours), whereas the anti-inflammatory effect may take longer (1-2 weeks or longer). This latter effect can indirectly relieve some pain by reducing tissue swelling.

b. Opioids

Mechanism of action and effects

Opioids bind to opioid receptors in the central nervous system (CNS) to: 1) inhibit the transmission of nociceptive input from the periphery to the spinal cord, 2) activate descending inhibitory pathways that modulate transmission in the spinal cord, and 3) alter limbic system activity. Thus, opioids modify sensory and affective aspects of pain. The different actions of opioids (i.e., agonist and antagonist)

at various opioid receptors (e.g., mu, kappa, and delta) provide one means of classification. In this system, opioids are broadly classified as mu agonists or agonist-antagonists.

c. Antiepileptic drugs (AED)


AEDs are a type of adjuvant analgesic. The increasing use of AEDs for neuropathic pain is based on their ability to reduce membrane excitability and suppress abnormal discharges in pathologically altered neurons. However, the exact basis of their analgesic effects is unclear. It does not appear to be specifically related to their antiepileptic activity. Other drugs that suppress seizures (e.g., barbiturates) do not relieve pain, and AEDs with effective antiepileptic activity do not necessarily have good analgesic activity.

d. Antidepressants


Antidepressants exhibit analgesic properties in animal models of nociceptive, inflammatory, and neuropathic pain, and some relieve chronic and neuropathic pain in humans. These analgesic effects may reflect the ability of some antidepressants to block the reuptake of serotonin and norepinephrine in the CNS, thus increasing the activity of endogenous pain-modulating pathways. Their analgesic actions do not depend on antidepressant activity, and antidepressants are equally effective in patients with and without depression. While analgesia may occur at lower doses and sooner than antidepressant activity, maximum efficacy may require high antidepressant doses and trial duration.

e. Local anesthetics (LA)

Mechanism of action

LAs are another type of adjuvant analgesic. These drugs block sodium channels and inhibit the generation of abnormal impulses by damaged nerves to exert their peripheral analgesic effects. When used systemically, they do not produce conduction block (anesthesia) as they do with local injection and topical application but may suppress aberrant electrical activity in structures associated with pain.

PSYCHOLOGICAL INTERVENTIONS:

Contingency Management/ Operant Methods:

The development of contingency management methods for chronic pain derives from Fordyce’s view of chronic pain as an operant problem (Fordyce 1976). Fordyce considers that pain behaviours, such as complaining of pain, inactivity or taking medication, may be maintained by their reinforcing consequences. Pain behaviour may either be positively reinforced, for example, by social factors such as concern from family members or negatively reinforced for example

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from unwanted responsibilities.

The aim of operant programmes is to increase the frequency of well behaviour and decrease that of pain behaviour. The aim is to increase activity level in a graded fashion. Reduction in pain intensity per se is not specific as an aim. It is to help them cope better with it and resume normal activities despite pain. Family members give no attention to pain behaviour or requests for medication, but provide considerable social reinforcement for targeted well behaviours. Physical therapy programmes are developed to increase patient activity levels. Progress is charted graphically and attention of family member is made contingent on successful daily completion of the quota. Reducing levels of medication is also an important aim.

Outcome studies of operant methods have generally reported good results at follow-up periods. (Cinciripini & Florren 1982; Seres & Newman 1976)

Cognitive Methods:

Cognitive methods aim at altering the subjective component of pain. Turk & Genest (1979) have classified these into 1. Imaginative Inattention: Here the subject’s task is to imagine a scene generally

considered incompatible with the experience of pain for example, lying on a beach.

2. Transformation of context: Here the task is to imagine that the pain sensations the

individual feels are actually occurring in another context. The assumption appears to be that if the sensations are associated with the affective state of courage rather than fear and anxiety, pain intensity will be reduced.

3. Imaginative Transformation: The subject is instructed to relabel the sensations as

numbness or tightness or some other experience that is easier to bear and less distressing than the pain itself.

4. Attention Diversion: This involves either external diversion strategies such as

counting ceiling tiles or internal ones such as counting backwards in threes or reciting poetry.

This classification of cognitive coping strategies is by no means definitive. In practice it is important not to stick too rigidly to any classification system but allow strategies (which may be amalgamation of the above categories) to be individually developed. Cognitive methods of pain control have successfully applied (Turner 1982, Bradley 1988).

Relaxation:

Relaxation training has been widely used in the treatment of chronic pain. Relaxation training for Tension Headache report encouraging results (Gada 1984, 1988; Gada & Shah 2001; Cox et al 1975). Linton 1986 has reviewed relaxation methods for low back pain with positive results.

Biofeedback:

Feedback of electroencephalogram, electromyogram, skin temperature and pulse has all been applied to chronic pain patients with good results (Gada & Gada 1981).

ROLE OF FAMILY MEMBERS:

Family members will need to change their reaction to the patient’s pain complaints and this is likely to require considerable attention in the home environment and change in patterns of interactions.

Family members require the simultaneous avoidance of excessive caretaking or over direction with the promotion of autonomy by firmly and consistently placing responsibilities o the patient for effort, persistence and progress towards treatment goals. This must be accomplished in a manner that recognizes and respects the subjective reality of the patients suffering but that resists the natural tendency of family members to assume control or cure the problem. Spouse and family members should help the patient to resume increasingly the previous level of functioning in spite of pain. With the attitudinal change in the spouse and family members, the secondary gain is avoided and the progress in the therapy is achieved rapidly.

CONCLUSIONS:

1) The prevalence of pain in a depressed patients and the prevalence of depression in a pain patients are higher than the prevalence rates when the conditions are individually examined. On average, 65% of patients with depression experience one or more pain complaints. Depression is most prevalent in pain, psychiatric and specialty clinics.

2) The presence of pain negatively affects the recognition and treatment of depression. Depression is often under recognized and thus frequently under treated. At least 75% of primary care patients with depression present with physical complaints exclusively and seldom attribute their pain symptoms to depression. These physical complains remain medically unexplained after extensive workup. As a result, providers frequently assess for physical causes of pain and treat medically instead of exploring the pain symptoms in a broader bio-psychosocial context.

3) Primary care providers should recognize

• that pain is a common symptom of depression,

• that depression and painful conditions frequently coexist and

• that evaluation and treatment of both are important.

4) In primary care settings, the typical depression presentation is complicated more often by painful symptoms and physical complains than emotional symptoms of sad mood or anhedonia.

5) Depression complicates the management of patients with pain and is associated with poorer outcomes. In patients with pain, depression is associated with more pain

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complaints, greater pain intensity, longer duration of pain and greater likelihood of non-recovery. Additive impairments in social function, work function, and functional limitation (e.g. limited mobility and restricted activity) are seen when depression and pain coexist.

SUMMARY:

Chronic pain is now recognized as pains that extend beyond the period of healing, with levels of identified pathology that often are low and insufficient to explain the presence and/or extent of the pain. Chronic pain is also defined as a persistent pain that “disrupts sleep and normal living, ceases to serve a protective function, and instead degrades health and functional capability.” Thus, unlike acute pain, chronic pain serves no adaptive purpose.

Both cortical and limbic system structures are involved in perception of pain. Immediate social and environmental context influences the perception of pain, as do past experience and culture. Modulation of nociceptive transmission occurs at multiple (peripheral, spinal, supraspinal) levels. Multiple brain regions contribute to descending inhibitory pathways. Such endogenous modulation may contribute to the wide variations in pain perception observed among patients with chronic pain.

Environmental and affective factors also can cause, exacerbate and perpetuate chronic pain, leading to disability and maladaptive behavior. Chronic pain is the most common cause of long-term disability

Pain is often under-treated. Data surveys suggest that only 1 in 4 individuals with pain receive appropriate therapy. Under-treated pain has significant physical, psychological, and financial consequences.

Inadequate control of pain interferes with the pain sufferer’s ability to carry out activities of daily living (e.g., work, relationships, hobbies, sex). Patients with inadequately managed pain may experience anxiety, fear, anger, depression, or cognitive dysfunction, and family members report varying levels of helplessness, frustration, and “heartbreak.” These consequences are especially likely to occur in patients with chronic pain. These individuals report impairments on multiple measures of physical, social, and psychological well-being, and many experience psychiatric disorders (e.g., depression, anxiety) that adversely influence health care. Left unchecked, these psychiatric disorders can contribute to more serious consequences. Pain is also a major cause of work absenteeism, underemployment, and unemployment.

Chronic pain is a significant public health problem and frustrating to everyone affected by it. Psychiatrists should take an active role in the care of these patients. They no longer should wait to make psychiatric diagnosis by exclusion in the patient who has failed to respond to multiple treatments over a period of years.

Recent advances in the treatment of chronic pain include

• the diagnosis and treatment of psychiatric co-morbidity,

• the application of primary psychiatric treatments to chronic pain and

• development of interdisciplinary efforts to provide comprehensive health care to the patient suffering with chronic pain.

Specifically, psychiatrists provide the expertise of examining a) mental life, b) the person as a whole, and c) the socio-cultural systems in which patients interact. Psychiatrists offer skills with pharmacologic and psychological treatments now recognized as effective in the management of chronic pain. Psychiatrists as medical specialists, who are more similar to than different from other physicians, need to participate actively in the integration of the delivery of medical care.

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Acknowledgement : The author wishes to thank Dr. Dipti Gada, Consultant Psychiatrist for her help in preparation of this article

Manilal Gada Hon. Professor of Psychiatry, D.Y. Patil Medical College. Head & Hon. Psychiatrist: Rajawadi Municipal General Hospital (Retd.) Hon. Psychiatrist: Dr. L. H. Hiranandani Hospital, Powai Corresponedence: 201, Kumudini, Above Andhra Bank, 7th Road, Rajawadi, Ghatkopar East Mumbai 400077 e-mail: [email protected]

Delivered at 37th Annual Conference of Indian Psychiatric Society Western Zonal Branch, at Rajkot on 7th October 2006

Appendix:

Emotional Pathway Of Pain

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Review Article

Metabolic Syndrome- A Psychiatric Perspective Mohandas.E, Rajmohan.V

AbstractThe metabolic syndrome is used to refer to a group of modifiable risk factors that confer an increased risk for type 2 diabetes mellitus and cardiovascular disorders (CVD). The major psychiatric disorders have an independent risk of high CVD and metabolic syndrome is a forerunner of this risk. There is a variable propensity among the different atypical antipsychotics to cause weight gain, diabetes, dyslipidemia and metabolic syndrome. This review focuses on metabolic syndrome and its relevance to psychiatry.

Key words: Metabolic syndrome, Insulin Resistance, Central obesity, Atypical antipsychotics

INTRODUCTION

Metabolic syndrome refers to a group of modifiable risk factors that confer an increased risk for type 2 diabetes mellitus and cardiovascular disorders (CVD). The condition is poorly understood in terms of definition and pathogenesis and is the subject of much debate. The syndrome however is important as it represents an important target for the prevention of diabetes and CVD. The introduction of atypical antipsychotics which are associated with significant weight gain and risk of diabetes has resulted in an increased focus on this syndrome among psychiatrists. Further it is now recognized that conditions like schizophrenia and mood disorders are associated with an increased risk of cardiovascular mortality. Therefore the condition is of relevance to psychiatry in terms of the risk of metabolic syndrome posed by the psychiatric disorders and the agents used to treat them.

CONCEPTUAL CONFUSION

The coexistence of risk factors for CVD has been recognized from the 1920’s, but the description of syndrome X by Gerald Reaven in 1988 generated renewed interest in conceptualizing metabolic syndrome. Since then multiple definitions and criteria have been put forth for this syndrome. (Sarafidis and Nilsson, 2006) (Table1) There is however no empirical validation for the components that constitute metabolic syndrome and the syndrome has been criticized as one that does not offer much in terms of pathogenesis or treatment. The different factors across definitions that have been included in the definition of metabolic syndrome are: insulin resistance, abdominal obesity (increased waist circumference or waist hip ratio), dyslipidemia [increased triglyceride (TG) level and decreased high density lipoprotein (HDL) level], hyperglycemia (high fasting glucose), hypertension, and microalbuminuria. The criteria and components vary across different definitions and the two most widely used criteria are the ones proposed by World Health Organization (WHO) and the National Cholesterol Education Programme (NCEP). (Table 2)

PATHOPHYSIOLOGY

Metabolic syndrome is an entity with an unknown etiology. Some hypothesize that this condition results from insulin resistance and obesity. The mechanism of disposal of surplus calories (resulting from excess caloric consumption, a sedentary lifestyle or, as is often the case, a combination of both factors) might, ultimately, determine the susceptibility to metabolic syndrome. The link between insulin resistance and CVD is mediated by oxidative stress, which produces endothelial cell dysfunction with the resultant cardiovascular damage and atheroma formation. (Lopez-Candales, 2001) Excess visceral fat accumulation is hypothesized as the causal factor for the features of insulin resistance. The extra energy if diverted into insulin-sensitive subcutaneous adipose tissue, the individual, although in positive energy balance, will be protected against the development of the metabolic syndrome. However, in insulin resistant people with a limited ability to store the energy excess, the triglyceride(TG) surplus will be deposited at undesirable sites such as the liver, the heart, the skeletal muscle, and the visceral adipose tissue (visceral adiposity)— a phenomenon described as ectopic fat deposition. Ectopic fat deposition results in an increase of TG and small low density lipoproteins (LDL) particles and decreased protective high density lipoproteins (HDL). The factors that predispose to a preferential accumulation of visceral fat and with features of insulin resistance include smoking, stress. The genetic susceptibility and a neuroendocrine profile related to a maladaptive response to ectopic fat deposition results in visceral obesity, insulin resistance, atherogenic dyslipidaemia and a pro-thrombotic inflammatory profile— the defining features of metabolic syndrome.(Despres and Lemieux,2006). (Figure 1) Appendix

Another hypothesis suggests that abdominal obesity results from hormonal changes. The evidence to this comes from the fact that elevated levels of serum cortisol results in abdominal obesity, insulin resistance, and lipid abnormalities suggesting a link between the activation of the hypothalamic-pituitary-adrenal (HPA) axis and CVD (Bjorntorp, 2001). The etiologic

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Table 1: Conceptual EvolutionHypertension–hyperglycaemia–hyperuricaemia syndrome Kylin (1923) Metabolic trisyndrome (trisyndrome metabolique) Camus (1966) Plurimetabolic syndrome Avogaro and Crepaldi (1967) Syndrome of affluence (wohlstandssyndrom) Mehnert and Kuhlmann (1968) Metabolic syndrome (metabolische syndrom) Hanefeld and Leonhardt (1981) Syndrome X G. M. Reaven (1988) Deadly quartet Kaplan (1989) Insulin resistance syndrome DeFronzo and Ferrannini (1991) Criteria for Metabolic Syndrome World Health Organisation (1998) EGIR Criteria for Metabolic Syndrome European Group for the Study of Insulin Resistance (EGIR) (1999) NCEP/ATP III Criteria for Metabolic Syndrome National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III) (2002)AACE Criteria for Metabolic Syndrome American Association of Clinical Endocrinologists (AACE) (2003) IDF Criteria for Metabolic Syndrome International Diabetes Federation (IDF) (2005)

Table 2: Definitions of Metabolic Syndrome

Component WHO diagnostic criteria ATP III diagnostic criteria (insulin resistance plus two of the following) (three of the following)

Abdominal/central obesity Waist to hip ratio: >0.90 (men), >0.85 Waist circumference: >102 cm (women), or BMI >30 kg per m2 (40 inches) in men, >88 cm (35 inches) in women

Hypertriglyceridemia >=150 mg per dL (>=1.7 mmol per L) >=150 mg per dL

Low HDL cholesterol < 35 mg per dL (< 0.9 mmol per L) for <40 mg per dL (<1.036 mmol per L) men, <39 mg per dL (<1.0 mmol per L) for men, <50 mg per dL (<1.295 for women mmol per L) for women

High blood pressure >=140/90 mm Hg or documented use >=130/85 mm Hg or documented use of of antihypertensive therapy antihypertensive therapy

High fasting glucose Impaired glucose tolerance, impaired >=110 mg per dL (>=6.1 mmol per L) fasting glucose, insulin resistance, or diabetes

Microalbuminuria Urinary albumin to creatinine ratio: 30 mg per g, or albumin excretion rate: 20 mcg /m

uncertainty has resulted in he various definitions of this condition and has made it difficult to ascertain the clinical impact of this syndrome.M E TA B O L I C S Y N D R O M E A N D M E N TA L DISORDERS

Major mental disorders pose increased threat of CVD. The evidence though preliminary points to an association between metabolic syndrome and psychotic and mood disorders. There is however no robust causal association between mental disorders and metabolic syndrome. A study has shown that 15% of drug-naive individuals with first-episode schizophrenia have impaired fasting glucose levels, hyperinsulinaemia and high cortisol. Further it was noticed that unaffected first-degree relatives of people with schizophrenia have high rates of type

2 diabetes mellitus (19–30%), pointing to a genetic association between these two disorders. (Thakore, 2005)

The prevalence of metabolic syndrome in patients with schizophreniavaries from 22.2%-60%. (Meyer et al, 2005) A study on 171 bipolar patients showed the prevalence of metabolic syndrome to be around 30%. Among the 171 patients 49% met the criterion for abdominal obesity, 41% met the criterion for hypertriglyceridemia, 23% met the criterion for low high-density lipoprotein cholesterol, 39% met the criterion for hypertension and 8% met the criterion for high fasting glucose or antidiabetic treatment (Fagiolini et al, 2005).

The prevalence of metabolic syndrome in depression was found to be 36% and was associated with a current diagnosis of major depression (Heiskanen et al, 2006). The increasing evidence

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Table 3: Classification of AAPsSerotonin Dopamine Antagonist (SDA) Risperidone ZiprasidoneSertindole Multi-actingReceptor-Targeted Antipsychotics (MARTA) Clozapine Olanzapine Quetiapine Partial Dopamine Agonist Aripiprazole D2/D3 antagonists Sulpiride Amisulpride

therefore suggests an association between metabolic syndrome and major psychiatric disorders. So the treatment goal should be to use medications which do not alter the metabolic profile and predispose to diabetes mellitus (DM) and CVD. (Newcomer, 2005)

ATYPICAL ANTIPSYCHOTICS (AAP), WEIGHT GAIN, DIABETES, DYSLIPIDEMIA

The AAPs include a heterogeneous group of agents which differ both in terms of chemical structure and receptor profile. They can be classified based on their receptor profile into serotonin dopamine antagonist (SDA), multi-acting receptor-targeted antipsychotics (MARTA), partial dopamine agonist, and D2/D3 antagonists (Horack et al, 2006). (Table 3)

The risk of weight gain, diabetes, and dyslipidemia is most with MARTAs especially clozapine and it is much lower with agents like amisulpride, aripiprazole and ziprasidone. The average weight gain over 10 weeks varies from 4 kg with clozapine to 0.28 kg with ziprasidone. (Kroeze et al, 2003) (Table 4).

Table 4: Weight gain with AAPs

Antipsychotic Weight Gain (kg/10 weeks)

Clozapine 4

Olanzapine 3.51

Sertindole 2.92

Quetiapine 2.67

Risperidone 1.67

Amisulpride 0.8

Aripiprazole 0.71

Ziprasidone 0.28

The evidence for DM and dyslipidemia also is most with clozapine and there is almost no evidence of the same with ziprasidone and aripiprazole. (Table5) In fact, it is calculated that the decrease of deaths due to suicides

Table5: Weight gain, diabetes and dyslipidemia with AAPsAAPs Weight Risk of Worsening Gain Diabetes of Lipid ProfileClozapine +++ + + Olanzapine +++ + + Quetiapine ++ D D Risperidone ++ D D Amisulpride +- - - Aripiprazole +- - - Ziprasidone +- - - D- Discrepant results

with clozapine over a ten year period (492/100,000) is offset by the increased deaths due to the metabolic side effects over the same period (416/100,000) (Fontaine et al, 2001). The agents like amisulpride, aripiprazole and ziprasidone provide safer alternatives for those at risk of metabolic syndrome. These agents also can be used when a patient develops signs or symptoms of metabolic syndrome with clozapine or olanzapine.

MECHANISM OF AAP INDUCED WEIGHT GAIN, DIABETES AND DYSLIPIDEMIA

The exact mechanisms by which antipsychotic medications produce their effects on bodyweight is unclear. It may involve the dysregulation of satiety, metabolism and activity levels, both centrally (CNS) and peripherally (GI).

The central mechanisms are mediated by the receptor affinity profile of the different agents. The dopaminergic mechanism of weight gain involves the agonism of limbic D2 receptors and the hypothalamic level antagonism of D2 receptors. The serotonergic receptor mechanisms leading to weight gain include 5HT2a and 5HT2c antagonism and 5HT1a agonism. The antagonism of α1 and β3 receptors and the agonism of α2 also result in weight gain. Probably the most understood mechanism of AAP induced weight gain is histaminergic (H1) antagonism. The other probable mechanisms of drug induced weight gain include glutametergic agonism, estradiol agonism, leptin and ghrelin dysregulation, agonism of orexin and neuropeptide Y (NPY), antagonism of α melanocyte stimulating hormone (α-MSH) and cocaine amphetamine regulated transcript (CART), the dysregulation of TNF-%, and the endocannabinoid system (ECS) dysregulation.

The peripheral factors by which AAPs induce weight gain probably involve the glucoregulatory abnormalities especially via the alteration in insulin secretion. The increased insulin resistance is also central to the causation of metabolic syndrome. In clinical samples AAPs cause insulin resistance and glucose intolerance and it is suggested that this is mostly considered secondary to weight gain but that causality could run in the opposite direction (Elman et al, 2006; Newcomer, 2005).The mechanism of AAP induced diabetes is probably due to

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weight gain and adiposity induced insulin resistance. However in a minority of cases AAPs induce glucose dysregulation independent of adiposity. The probable mechanisms involved include: inhibition of glucose via glucose transporter GLUT 1 and GLUT 3 (especially in the case of clozapine and olanzapine); AAP induced pancreatic 5HT1a antagonism; the dysregulation of leptin by 5HT2c blockade (clozapine); the decreased ? cell function and increased glucose release from hepatocytes due to increased noradrenergic and adrenergic turnover; and the α2 induced blockade of insulin release. (Newcomer, 2005)

The mechanism of AAP induced dyslipidemia remains largely unknown as few studies have attempted to elucidate it. The probable mechanism is secondary to weight gain and adiposity. There may also be a role of adiposity induced glucose intolerance and insulin resistance. There are reports of substantial elevation of TG without much weight gain in patients taking AAPs, pointing to a hitherto undiscovered direct effect of AAPs on lipid modulation. (Newcomer, 2005)

ASSESSMENT AND MANAGEMENT OF METABOLIC RISK WITH AAP

There are no clear guidelines regarding the assessment and management of metabolic syndrome in patients with mental disorders, especially on treatment with atypical antipsychotics. The existing recommendations including those put forth by American Psychiatric Association (APA) and American Diabetic Association (ADA) require empirical validation. The tentative measures for the assessment and management of metabolic syndrome based on the existing evidence are set forth below.

Assessment

Routine psychiatric assessment of any case should include a detailed psychiatric history and medical history.. Medical history should be focused to detect co morbidities like – hypertension (HT), diabetes mellitus (DM), hyperlipidemia, coronary heart disease (CHD), cardiovascular disease, cerebrovascular disease, peripheral vascular disease, renal disease, thyroid disease, surgical history, and obesity. A family history of HT, DM, CVD, obesity, thyroid dysfunction etc is also important in this context.

The personal history should focus on diet history, an assessment of physical activity pattern and type of physical activity; with emphasis on frequency, duration, and motivation (sedentary life style).The personal habits like smoking, alcohol and substance use should be assessed. The psychiatrist should also ask for any history of use of prescription medication including oral hypoglycemics, insulin, antihypertensives, oral contraceptives, vitamins, and herbal remedies.

A detailed physical examination should be done with special focus on a comprehensive general examination including heart rate and blood pressure, evaluation of height and weight, and

evaluation of body mass index (BMI = weight (kg)/ [Height (m)]2). The waist circumference measured at the anterior superior iliac spine level is a sensitive index of visceral obesity. There is also need for a detailed systemic examination to detect existing risk factors or complications. .

The laboratory investigations should include screening of fasting and post prandial blood sugar (FBS/PPBS), lipid profile (especially TG, HDL and LDL), and glycosylated hemoglobin (HbA1C). . Others investigations which are more of research value include fasting insulin levels, uric acid and microalbuminuria assessment, liver function test (LFT) and ultrasonogram (USG) (to detect non-alcoholic steato-hepatitis), C- Reactive Protein (CRP) assessment and euglycemic clamp and homeostasis model assessment (HOMA) for detecting insulin resistance (Faulkner, 2003)

The patients should also be monitored from the first visit on in a periodic manner. The American Psychiatric Association (APA) along with the American Diabetic Association has set forth the protocol for monitoring patients on AAPs for metabolic risks. (Newcomer, 2005) (Table 6)

MANAGEMENT

Guidelines to prevent weight gain, DM and dyslipidemia in patients on AAP include the following: a) Selection of an AAP with low risk b) Counseling regarding behavioral/ lifestyle management and early institution of the same c) Preventive pharmacological management of the risk factors.

Patients who have developed metabolic consequences while on AAP should be managed by a) Switching to an AAP with low risk b) Behavioural/ lifestyle management c)Pharmacological management of the different components like weight gain, DM or hyperglycemia, hypertension, and dyslipidemia d) a review of all other agents (medications, substance use etc.) which can contribute to metabolic syndrome. The periodic review of all metabolic parameters is paramount to any intervention to prevent or correct the metabolic consequences posed by atypical antipsychotic treatment.

The evidence for the efficacy of pharmacological interventions for weight gain with AAPs has been at best mixed despite research designs including randomized controlled trials (RCT). (Faulkner and Cohn, 2006)

Current guidelines state that the use of pharmacotherapy should be restricted to those individuals who are obese (BMI of >30 kg/m2) or overweight (BMI of >27 kg/m2) with additional co-morbidities like type 2 diabetes, hypertension and hyperlipidaemia. (Faulkner et al, 2003) The different behavioral therapies also show modest improvement of weight. A review of the pharmacological and nonpharmacological interventions in patients on AAPs with metabolic syndrome concluded that short-term weight loss can occur with the addition of selective medications and (or) lifestyle interventions. However, it is recommended that more rigorous and longer-term studies are needed to prove their efficacy. (Faulkner and Cohn, 2006)

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Table 6: ADA/APA Recommendations

Baseline 4 wks 8 wks 12 wks Quarterly Yearly

Personal/family history X X

Weight (BMI) X X X X X X

Waist circumference X X

Blood pressure X X X

Fasting plasma glucose X X X X

Fasting lipid profile X X X

CONCLUSION

Metabolic syndrome is an important but unrecognized condition among psychiatric patients. The evidence regarding the association of mental disorders and metabolic syndrome, especially the evidence regarding causality is far from conclusive. The mechanisms mediating the metabolic side effects of AAP need to be elucidated. This probably would help in a better decision making as to which patient can be safely started on the AAPs and the measures to prevent the emergence of metabolic syndrome. The existing evidence regarding the risk posed by drugs like clozapine and olanzapine though significant, their therapeutic efficacy (especially clozapine) necessitates their use in many situations. The clinicians selecting the medication should therefore weigh the possible therapeutic benefits against the probable metabolic effects before starting these AAPs. Diligent monitoring is needed to detect these side effects and plan effective management..

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Fontaine KR, Heo M, Harrigan EP,et al (2001) Estimating the consequences of anti-psychotic induced weight gain on health and mortality rate. Psychiatry Res., 101:277-88.

Heiskanen TH, Niskanen LK, Hintikka JJ,et al (2006) Metabolic syndrome and depression: a cross-sectional analysis. J Clin Psychiatry., 67:1422-7.

Horacek J, Bubenikova-Valesova V, Kopecek M, et al. (2006) Mechanism of action of atypical antipsychotic drugs and the neurobiology of schizophrenia. CNS Drugs; 20: 389-409.

Kroeze WK, Hufeisen SJ, Popadak BA,et al (2003) H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs. Neuropsychopharmacology. 28:519-26.

Lopez-Candales A. (2001) Metabolic syndrome X: a comprehensive review of the pathophysiology and recommended therapy. J Med; 32:283-300.

Meyer J, Koro CE, L’italien GJ. (2005) The metabolic syndrome and schizophrenia: A review. International Review of Psychiatry, 17: 173–180.

Newcomer JW. (2005) Second-generation (atypical) antipsychotics and metabolic effects: a comprehensive literature review. CNS Drugs, 19 Suppl 1:1-93.

23


, , , , , , , ,

AppendixFigure 1 : Metabolic Syndrome - Pathogenetic Model

Physical

inactivity

Energy Rich DietNormalAdiposeTissue Smoking

GenotypeStress

MetabolicSyndrome

Altered MetabolicProfile

Fat deposits (TG)in Liver, Muscle,Heart

VisceralObesity

PositiveEnergy Blance

Source of support: None Conflict of interest: None

E.Mohandas * Senior Consultant in Psychiatry V.Rajmohan, Consultant in Psychiatry, Elite Mission Hospital, Koorkencherry, Thrissur, Kerala-680007 E-mail: [email protected] Phone: 0487-3011400 * Correspondence

Reynolds K, He J. (2005) Epidemiology of the metabolic syndrome. Am J Med Sci.; 330:273-9.

Sarafidis PA, Nilsson PM. (2006) The metabolic syndrome: a glance at its history. J Hypertens.; 24:621-6.

Thakore JH (2005). Metabolic Syndrome and Schizophrenia. Br. J. Psychiatry. 186: 455-456.

24

Subcutaneous obesity ( normal metabolic profile)


Sincere Appreciation

The Archives sincerely appreciates time and expertise of the following reviewers of this issue:

Chittaranjan Andrade

E.Mohandas

Vikram Patel

Nilesh Shah

K.S.Jacob

Ritambhara Mehta

Bharat Panchal

Parag Shah

Anurag Mishra

Param Shukla

Anuradha Sovani

Sudhir Kumar

Shivarathnamma

Rajesh Kumar

25


Dr.A.V.Shah Best Paper Award

PTSD and major depression in Children and Adolescents Four Years After the communal violence

G.K.Vankar, Girish Banwari, Viral Parikh, Hemang Shah

ABSTRACT

Introduction: PTSD and major depression are common psychiatric sequelae among children and adolescents after exposure to extreme stressors.

Methods: Children and adolescents who had lost one of their parents in communal violence in 2002 were evaluated in 2006 i.e. four years after the event for PTSD and major depression. UCLA Index for PTSD was used to screen for PTSD, while Brief PHQ was used to screen for major depression.

Results: Out of 255 subjects studied, 25 (9.8%) had PTSD , 19 (7.4%) had PTSD co morbid with major depression, and 8(3.1%) had major depression. Thus, 52 subjects (20.4%) had psychiatric morbidity 4 years post-trauma.

Psychiatric morbidity was associated with female gender, age older than 12 and residence in Ahmedabad (the worst affected city). PTSD was not associated with religious affiliation, change of residence, income or education.

Implications: PTSD occurred in about 17.2% children and adolescents even after 4 years of exposure to communal violence. Major depression was present in 10.5% children and adolescents. This emphasizes need for assessment and treatment of these disorders in child and adolescent population exposed to trauma.

Key Words: PTSD, Children and Adolescents, communal violence

INTRODUCTION

PTSD is a common sequel after exposure to a traumatic event. Non referred samples of adolescents exposed to various forms of trauma have documented that 25% to more than 90% develop PTSD depending on the type of stressor, the length of time since exposure (rates tend to rise over first several months to two years with a gradual reduction over time) and the method used to assess symptomatology. [1] Level of exposure and lack of social support tend to predict higher risk of PTSD and other psychiatric disorders. Exposure to multiple traumatic events and female gender increase PTSD risk.Several studies indicate that majority of children with exposure to trauma develop PTSD symptoms severe enough to interfere with functioning even in absence of a PTSD diagnosis. Most studies have found girls to score higher than boys on PTSD measures [2-5] while one study found girls to report greater subjective appraisal of danger. [6] With regard to age, Green et al did not find any significant difference in the diagnosis of “probable PTSD” among three age groups (2–7, 8–11, and 12–15 years) after the Buffalo Creek disaster. [7] However, there was a significant difference in the average number of PTSD symptoms, with the youngest age category showing fewer symptoms.After Hurricane Hugo, Shannon et al reported that children younger than 13 years were more likely to test positive for posttraumatic stress syndrome than older children. [4] After the earthquake in Armenia, there was no association found between the severity of PTSD and age among students 8–16

years old.[8] In a study among students exposed to the Chi-Chi earthquake in Taiwan, elementary school students experienced more severe PTSD symptoms compared to junior high school students. [9]

With regard to post disaster adversities, La Greca et al reported that “major life events” (e.g., death or hospitalization of a family member) had an additive effect on children’s post disaster reactions. [10] Lonigan et al noted that children whose parents were unemployed experienced more PTSD symptoms. [11]

End of February, 2002 struck Ahmedabad and state of Gujarat with communal violence that continued for three months and beyond. As per estimations, over 1200 people were killed, several thousands were injured, more than 30000 households were destroyed and about one lakh people were forced to take shelter in relief camps. In the wake of communal violence, magazine stories definitely talked about agony and distress of young children and adolescents who had witnessed the violence.

Self Employed Women’s Association (SEWA), one of the leading women organizations, was working with violence-affected women and their children. These children besides witnessing communal violence had lost either parent in the violence. The grass root workers of SEWA were trained by the principal author and his team to provide psychosocial care to these women and children one year after the riots. The staff felt that there was need for working with children and adolescents

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AIMS AND OBJECTIVES

· To find out frequency of PTSD and major depression among children and adolescents who were exposed to communal violence 4 years earlier

· To find out demographic as well as phenomenological characteristics of PTSD and major depression

· To find out associations of PTSD and major depression with demographic and trauma related factors

MATERIAL AND METHODS

The authors trained fifteen M.A. psychology postgraduates pursuing clinical psychology course at Kanoria Hospital, Ahmedabad to administer study instruments to children, adolescents and their parents.

The study team with data collectors visited Shantipath Centres (community centres to the road to peace) located at various places in Ahmedabad, Mehsana, Vadodara, Anand, Panchmahal and Sabarkantha. No particular sampling method was used or applied. All such children and adolescents brought to our knowledge were interviewed, so it was more of a convenient sample.

Study instruments

UCLA Child PTSD Index, UCLA Adolescent PTSD Index and UCLA PTSD Index (current version) were used as appropriate (Rodriguez et al, 2001). [12] The instruments are almost similar with minor changes in phrasing of questions for the purpose.

Part 1 of the instrument asks about exposure to a traumatic event,

Part 2 asks about what actually happened and what the child or adolescent felt at the time of the trauma itself.

The next section contains statements about PTSD manifestations (21 statements to reach the interviewee response on a score range of 0-4 (0=none, 1=little, 2= some, 3=much, 4=most). The time frame for which the question is asked is last one month. For diagnosis of PTSD, score of 3 or more on a question was considered as manifestation being present. Those having a total score of 38 or higher were diagnosed as having PTSD.

The Brief PHQ consists of nine items corresponding to the nine criteria for major depression as per DSM-IV [13] for the time frame of last two weeks to be rated on a 4-point scale (0= not at all, 1=frequently, 2= more than half of the days, 3=almost daily).

The PRIME-MD [14] was the first mental health diagnostic test that could be entirely self-administered by the patient. The shortened version of the Prime MD is called the “Patient Health Questionnaire”. It is a self-administered questionnaire that is 85% effective in suggesting the presence of a mental health problem.

PHQ consists of 9 items for time frame of last two weeks to be rated on 4-point scale (0 = Not At All, 1= Frequently, 2 =

More than half of the days, 3 =Almost Daily). Major depression is diagnosed when a person rates at least five symptoms as 2 or more with sadness of mood or lack of pleasure as essential criteria. Persons who have these essential criteria present plus 2 or 3 responses rated 2 or 3 were considered as having major depressive disorder. The ninth item related to suicidal ideas was rated as present even if it were present for less than half of the days.

In a study of 3,000 patients who used the Brief PHQ, about 30% had a mental disorder according to the questionnaire. [15] It took the doctors about 3 minutes on an average to review the questionnaire and most of the doctors agreed with the PHQ result.

This instrument is extensively used in India and has been translated in all major languages.

Demographic characteristics like name, age, religion, years in education, monthly family income, occupation of mother or father and change in residence were carefully noted.

Data analysis:

The subjects who had PTSD and major depression and those who didn’t (comparison group) were compared with regard to demographic characteristics, associated factors. SPSS X version 2002 (SPSS Institute, 2002) was used to analyze the data. [16]

Categorical data was assessed using Chi Square test and quantitative data was assessed using ‘t’ test. Correlation coefficient was calculated to find total number of trauma related events and UCLA PTSD index scores. Principal component analysis was done to delineate factor structure of PTSD.

RESULTS

1. Demographic characteristics:

Total 255 children and adolescents were interviewed whose ages ranged from 5-21 years. There were 135 boys and 120 girls (52.9 vs. 47.1%). One hundred and seventy three subjects (67.4%) had monthly income less than Rs. 1000 and a vast majority, 198 (77.6%) were Muslims. Most had mother who was a homemaker, unskilled worker or working part time as a tailor or small shopkeeper. One hundred and seventy (66.7%) children and adolescents were residents of Ahmedabad and the rest belonged to districts of Vadodara, Anand, Mehsana and Sabarkantha.

Table 1: Psychiatric Morbidity

Diagnosis N=255 n (%) Post Traumatic Stress Disorder (PTSD) 25 (9.8) MDD + PTSD 19 (7.4) Major Depressive Disorder (MDD) 8 (3.1) Total psychiatric morbidity 52 (20.4)

2. Psychiatric morbidity: Out of the 255 subjects studied, 25

27


exposure to traumatic events. (Table1). For the subsequent discussion, the subjects with PTSD are referred as index group and the rest as comparison group.

3. Psychiatric morbidity and demographic characteristics: Table 2 compares index and comparison group regarding their demographic characteristics.

Out of 120 girls, 31(25.8%) had psychiatric morbidity, while out of 135 boys, 21(15.6%) had psychiatric morbidity. There was statistically significant gender difference in the occurrence of psychiatric morbidity. Subjects living in Ahmedabad as compared to those living in other parts of Gujarat had higher morbidity. Adolescents older than 12 years of age compared to younger children also had higher morbidity. No other demographic characteristics like religion, education, family income or relocation were associated with higher psychiatric morbidity.

4. Exposure to trauma related events:

The index group was exposed to 1-8 events with mean of 4.25(SD1.86) events whereas the comparison group was exposed to 0-8 events with mean of 4.0(SD1.82).

Table 3 compares both the groups regarding the events. Seeing a dead body and getting to know about a loved one’s death or serious injury were objective trauma related events associated with higher PTSD and major depression. None of the other trauma related events were associated with higher psychiatric morbidity.

5. Number of trauma related events and PTSD score:

The number of trauma related events the subjects were exposed to was proportionately related to severity of post traumatic reaction as measured by total UCLA PTSD Index scores. This confirmed dose-response relationship (Pearson correlation: 0.227, significant at 0.01 level, 2 tailed).

6. Manifestations of PTSD:

25 subjects had PTSD while 19 had PTSD co morbid with major depression. Their score on PTSD Index ranged from 38 to 80 with a mean score of 48.1 (SD 10.1). Irritability(86.4%), physical symptoms (84.1%),reminders of trauma upset, frighten, make sad (81.8%), avoiding people, places, things related to the event (72.7%), flashback-thoughts, images, voices (70.5%),hyper arousal (70.5%), difficulty concentrating (68.2%),fear that the event would happen again (68.2%),avoiding talk, thoughts related to traumatic event (65.9%), sleep disturbance (65.9%) gloomy future outlook(65.9%), nightmares (56.8%),impending doom(56.8%), frequent quarrels(54.5%),Hyper vigilance(50.0%),trouble feeling of happiness and love (50.0%),emotional blunting (47.7%), re experience of traumatic event (38.6%), prefers being alone than in company (31.8%), loss of memory about the event (25.0%) feelings of guilt (20.5%), trouble feeling sad or angry (11.4%). Survivor guilt, emotional blunting and feeling estranged were absent.

7. Factor Structure of PTSD:

Table 4 and 5 shows factor structure of PTSD on Principal Component Analysis.

Principal component analysis revealed 4 factors with Eigen value more than 1. Factor 1 explained greatest variance i.e. 37.4% and the items Hyper vigilance, Reminder of traumatic event causing anxiety, sadness, fear, Flashback-thoughts, images, voices, Irritability, Nightmares, Re experience of traumatic event, Remaining lonely, Emotional blunting, Avoiding talk, thoughts related to traumatic event, Hyperarousal, Sleep disturbance. Difficulty concentrating, Avoiding people, places, things related to the event, Physical symptoms, Impending doom, Frequent quarrels, Gloomy future outlook and Fear that the event would happen again had high loading.

Factor 2 explains 6.5% of variance. Reduction in emotional reactivity had high loading on this.

Factor 3 explains 5.6% of variance and consists of high loading on items Emotional blunting and Feeling of happiness and love reduced, Factor 4 explains 5.1% of variance and has high loading on item Loss of memory about the event .Thus this study reveals that in child and adolescent population- re experiencing, avoidance and hyper arousal are inter related and contribute most to clinical manifestations.

DISCUSSION

Prevalence of PTSD: Although PTSD is a controversial diagnosis according to some; qualitative study of women exposed to communal violence has concluded that PTSD may be a relevant clinical construct even in Indian context. [17] This study furthers our knowledge that PTSD can occur even in children and adolescents who are exposed to traumatic events in India and possibly in some may run a chronic course. Earlier in earthquake affected and riots affected adolescent population PTSD prevalence 6-8 month post-trauma was found to be 20-22.5%. Most PTSD onset occurs soon after exposure to trauma, the manifestations gradually reduce over 2-year period and in some, they become chronic. [1] Studies have indicated that children and adolescents exposed to the catastrophic1988 Spitak earthquake in Armenia were suffering from chronic severe posttraumatic stress disorder (PTSD) symptoms years after the earthquake. [3,18] This emphasizes screening of trauma exposed children and adolescents for PTSD and adequate early intervention.

Risk Factors for PTSD:

In this work, there was significant gender difference in the rate of PTSD and major depression. This is in agreement with most other studies on gender and PTSD. [2-5]

Adolescents older than 12 years of age had higher psychiatric morbidity in this study; this is in contrast to other studies that found younger children having higher PTSD. [4,9]

Relocation did not have a negative impact on posttraumatic symptoms in this study; this is as per Armenia study after the Spitak earthquake [19] or the Chi-Chi earthquake in Taiwan.

17.2% children and adolescents had PTSD, 4 years after

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Table 2: Demographic Characteristics and Psychiatric morbidity

Psychiatric No Psychiatric Statistics Morbidity Morbidity N=52 N=203 N (%) N (%)

Age years Range 6-19 5-21 t=2.59, df=253, p=0.01 Mean 12.8 11.4 SD 3.4 3.5

Upto 12 25 (48.1) 147 (72.4) χ2=11.2, df=1, p=0.0008 >12 27 (51.9) 56 (29.6) OR= 0.35(0.18-0.69)

Gender Boys 21 (40.4) 114 (56.2) χ2=4.13, df=1, p=0.04 Girls 31 (59.6) 89 (43.8) OR= 0.53(0.27-1.03)

Education Range 0-10 0-15 t=0.00, df=253, p=1.00 Mean 5.3 5.3 SD 2.8 3.1

Religion Hindu 9 (17.3) 38 (18.7) χ2=0.05, df=1, p=0.81 Muslim 43 (82.7) 165 (81.3) OR= 0.91(0.38-2.14)

Income <1000 40 (76.9) 133 (65.5) χ2=2.47, df=1, p=0.12 (Rs/month) >1001 12 (23.1) 70 (34.5) OR= 1.75(0.82-2.79)

Change of Yes 21 (40.4) 102 (50.2) χ2=1.61, df=1, p=0.20 residence No 31 (59.6) 101 (49.8) OR= 0.67(0.35-1.30)

Residence Ahmedabad 42 (80.8) 128 (63.1) χ2=5.85, df=1, p=0.015 Other 10 (19.2) 75 (36.9) OR= 2.46(1.11-5.58)

However, among relocated students in Taiwan, those who lived with their parents had fewer acute PTSD symptoms.

Trauma related events and psychiatric morbidity:

A few objective trauma events were associated with psychiatric morbidity. This study also confirms a dose response relationship, i.e. greater the number of trauma related events, higher the PTSD score. This is also in harmony with our own work in earthquake and communal violence in adolescent population. [21,22]

Manifestations of PTSD:

The manifestations of PTSD were similar to those described in literature. [1] Irritability was the commonest manifestation reported. It has been mentioned that manmade traumatic events compared to natural disasters more often provoke anger and irritability as the manmade events are considered as eminently

controllable or willful. Flashbacks were present in 70% subjects; in children intrusive memories are more common than flashbacks. Avoidance symptoms were present in about three-fourth of the subjects.

Survivor guilt was absent in children and adolescents in this study, perhaps because the traumatic events were manmade on which they did not have control.

Factor structure of PTSD revealed the largest one factor indicating that the manifestations like re-experiencing, avoidance and hyperarousal are closely linked, dissociative feature might be considered a separate though less powerful factor contributing to clinical picture.

Reduction in emotional feeling and dissociative amnesia due to trauma emerge as distinct but less powerful manifestations contributing to overall clinical picture of PTSD.

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Table 3: Psychiatric morbidity and trauma related events

Event Psychiatric No Psychiatric Significance Morbidity Morbidity N=52 N=203 N (%) N (%)

Violence, residence in 48 (92.3) 167 (82.3) χ2=2.44, df=1, p=0.12 violence affected area OR= 2.59(0.82-9.03)

Beaten, fired at or threatened 26 (50.0) 80 (39.4) χ2=1.91, df=1, p=0.17 OR= 1.54(0.80-2.96)

Family member being beaten, 49 (94.2) 175 (86.2) χ2=1.80, df=1, p=0.18 fired at, threat of serious injury OR= 2.61(0.76-13.95)

Witnesses someone being beaten, 23 (44.2) 76 (37.4) χ2=0.80, df=1, p=0.37 fired at or killed OR= 1.33(0.68-2.57)

Seeing Dead body 24 (46.2) 61(30.1) χ2=4.83,df=1, p=0.02 OR= 2.00(1.02-3.89)

Came to know about loved 50 (96.2) 174 (86.7) χ2=6.15,df=1, p=0.013 one’s death or serious injury OR= 5.95(1.44-52.3)

Forced to live in camp 23 (44.2) 85 (41.9) χ2=0.09,df=1, p=0.76 OR= 1.10(0.57-2.12)

Damage to house 19 (36.5) 89 (43.8) χ2=0.90,df=1, p=0.34 OR= 0.74(0.37-1.44)

Table 4: Factor Structure of PTSD: Principal Component Analysis of UCLA PTSD Index

\ Component Eigen values % of Cumulative Variance %

1 8.094 36.793 36.793

2 1.405 6.385 43.178

3 1.267 5.761 48.939 4 1.125 5.111 54.050

5 1.023 4.650 58.700

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Table 5: Component MatrixVariable Component 1 2 3 4 5VAR00001 .59 .25 1.930E-02 -.12 .38VAR00002 .71 .16 5.973E-03 -.29 6.558E-02VAR00003 .67 .21 -.24= -.11 2.427E-02VAR00004 .60 -.36 -4.620E-02 -8.750E-02 7.136E-02VAR00005 .56 .20 -.28 -.19 -.16VAR00006 .64 2.184E-02 .12 -.24 -.20VAR00007 .41 -2.239E-02 .13 .19 .42VAR00008 .62 -.15 .56 -.19 -.21VAR00009 .58 1.893E-02 .18 .12 .36VAR00010 .58 -.30 .56 -.16 -.15VAR00011 .27 .56 .25 3.434E-02 .14VAR00012 .67 .15 -.21 -8.957E-02 .14VAR00013 .63 -.14 -.22 .13 -.11VAR00014 .41 .38 .10 .21 -.45VAR00015 .25 .27 .23 .70 -.10VAR00016 .64 -.28 -9.699E-02 .32 .14VAR00017 .65 .19 .12 -.12 .16VAR00018 .735 -2.684E-02 -7.950E-02 -3.311E-02 -6.012E-02VAR00019 .69 -.17 -.16 .25 -.13VAR00020 .63 -.43 -.18 7.934E-02 5.406E-02

PTSD and grief:

The more sudden, unexpected and unnatural the death, the more likely the bereavement process is to overlap with traumatic stress reactions. Indeed, in the most traumatic situations, both grief and PTSD are likely to co-occur. Investigators have reported that the sudden and unexpected death of a loved one accounted for more PTSD than any other life stress event.

Limitations of this study:

We did not have PTSD data at baseline, sooner after exposure to trauma to compare. Such data would throw more light on the natural history of the disorder, suggesting whether the PTSD was chronic or delayed onset in nature.

The traumatic event was 4 years prior to the study; this may lead to recall bias on part of children and adolescents.

This study has not explored sub threshold PTSD (which though do not meet DSM IV criteria of PTSD but cause comparable distress and disability) and psychiatric morbidities like substance use after exposure to trauma.

Implications of the study:

In India, child and adolescent population exposed to traumatic events like communal violence may suffer from PTSD and

major depression, even four years after such events

Risk factors for PTSD included female gender, being adolescent rather than child, and living in violence- torn area\severe posttraumatic stress disorder (PTSD) symptoms years after the earthquake. [3,18] This emphasizes screening of trauma exposed children and adolescents for PTSD and adequate early intervention.

REFERENCES:

1. Cohen J A. Post Traumatic Stress Disorder in children and adolescents In Sadock B. J. and Sadock V. A. (eds.) Comprehensive Textbook of Psychiatry, 8th edition, Philadelphia, Lippincott William and Wilkins: 2005; 3286-91.

2. Vernberg EM, Silverman WK, La Greca AM, Prinstein MJ: Prediction of posttraumatic stress symptoms in children after Hurricane Andrew. Journal Abnormal Psychology 1996; 105:237–48.

3. Goenjian AK, Pynoos RS, Steinberg AM, et al: Psychiatric co morbidity in children after the 1988 earthquake in Armenia. Journal of American Academy of Child and Adolescent Psychiatry 1995; 34:1174–84.

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4. Shannon MP, Lonigan CJ, Finch AJ Jr, et al: Children exposed to disaster, I: epidemiology of post-traumatic symptoms and symptom profiles. Journal of American Academy of Child and Adolescent Psychiatry 1994; 33:80–93.

5. Shioyama A, Uemoto M, Shinfuku N, et al.: [The mental health of schoolchildren after the Great Hanshin-Awaji earthquake, II: longitudinal analysis.] Seishin Shinkeigaku Zasshi 2000; 102: 481–97 (Japanese).

6. Goenjian AK, Molina L, Steinberg AM, et al: Posttraumatic stress and depressive reactions among Nicaraguan adolescents after Hurricane Mitch. American Journal of Psychiatry 2001; 158:788–94.

7. Green BL, Korol M, Grace MC, et al. Children and disaster: age, gender, and parental effects on PTSD symptoms. Journal of American Academy of Child and Adolescent Psychiatry 1991; 30:945–51.

8. Pynoos R, Goenjian A, Tashjian M, et al. Post-traumatic stress reactions in children after the 1988 Armenian earthquake. British Journal of Psychiatry 1993; 163:239–47.

9. Chen S-H, Lin Y-H, Tseng H-M, et al. Posttraumatic stress reactions in children and adolescents one year after the 1999 Taiwan Chi-Chi earthquake. J Chinese Institute of Engineers 2002; 25:597–608.

10. La Greca AM, Silverman WK, Vernberg EM, et al. Symptoms of posttraumatic stress in children after Hurricane Andrew: a prospective study. Journal of Consulting and Clinical Psychology. 1996; 64:712– 23.

11. Lonigan CJ, Shannon MP, Taylor CM, et al. Children exposed to disaster, II: risk factors for the development of post traumatic symptomatology. J.Am.Acad.Child Adolesc.Psychiatry 1994: 33:94-105.

12. Rodriguez N, Steinberg AM, Saltzman W et al. UCLA PTSD Reaction Index: psychometric analysis, in Proceedings of the International Society for Traumatic Stress Studies. Northbrook, Ill, ISTSS, 2001.

13. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC: American Psychiatric Association.

14. Spitzer RL, Kroenke K, Williams JBW. Validation and utility of a self-report version of PRIME-MD: the PHQ Primary Care Study. JAMA 1999; 282:1737-1744.

15. Spitzer R.l. Williams JBW,Kroenke et al. Validity and utility of the PRIME MD Patient Health Questionnaire in assessment of 3000 obstetric –gynecological patients: the PRIME MD Patient Health Questionnaire obstetric –gynecology study. JAMA, 183:759-69.

16. Statistical Package for Social Sciences Institute: SPSS X, 2002.

17. Mehta K, Vankar G., Patel V (2005) Validity of the construct of posttraumatic stress disorder in a low-income country. British Journal of Psychiatry. 187:585-6.

18. Goenjian AK, Karayan I, Pynoos RS, et al: Outcome of psychotherapy among early adolescents after trauma. American Journal of Psychiatry 1997; 154:536–42.

19. Najarian LM, Goenjian AK, Pelcovitz D, et al.: Relocation after a disaster: posttraumatic stress disorder in Armenia after the earthquake. Journal of American Academy of Child and Adolescent Psychiatry 1996; 35:374–83.

20. Soong T-W, Lee Y-C, Huang R-R, et al. A comparative study of post-traumatic symptoms between students living at Yu-Chih and relocating to Kaohisung after the Chi-Chi earthquake, in Proceedings of the International Workshop on Annual Commemoration of Chi-Chi Earthquake. Taipei, Taiwan, National Center for Research on Earthquake Engineering, 2000, pp 308–17.

21. Mehta K, Vankar GK, Panchal B, et al. Posttraumatic stress among adolescents in by earthquake-affected Kutch. 2002. (Unpublished work)

22. Mehta K and Vankar GK Post traumatic stress disorder among adolescent girls exposed to communal riots. 2003. (Unpublished work)

Acknowledgements : Authors thank trainees of Kanoria Hospital for collection of data and SEWA,Ahmedabad for facilitating the study

Sources of support: None Conflicts of Interest: None G.K.Vankar, Professor and Head Girish Banwari, Senior Resident Viral Parikh, Resident Hemang Shah, Assistant Professor Dept. of Psychiatry, B.J.Medical College and Civil Hospital, Ward E1, Asarwa, Ahmedabad 380016

Correspondence: Dr. G.K.Vankar, Dept. of Psychiatry, Civil Hospital, Ward E1, Asarwa, Ahmedabad 380016

e-mail: [email protected] Cell: 09904160338

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Original Research Paper

Patterns of prescription in private psychiatry : A comparison with public sector

Navneet Kumar Johri, Trupti R. Sharma

ABSTRACT

Background: There is a felt need to monitor patterns of prescription of psychoactive drugs among psychiatrist in both private and public sector in a rapidly evolving era of newer medications as against the theoretical knowledge. This is probably the pilot study of its kind in India

.Method: One hundred patients attending psychiatry out patient service at two public hospitals in Gujarat were studied. Data was collected on an unstructured performa. The source of information was prescription record (files) of private psychiatrists attended by them. This was compared with prescription patterns for the same patients seen by psychiatrist working in these public sector services.

Results: Ninety six per cent case sheets did not have a diagnosis mentioned. No patient in private sector received monotherapy. On an average there were 4.2 medications per script per patient in the private sector. Antipsychotic medications used frequently in mood and anxiety disorders. Several erratic drug combinations were observed.

Key words: Prescriptions, psychiatry, private sector, public sector

INTRODUCTION

Developed countries have long ago formulated national prescribing guidelines for medications used in psychiatric practice as a means to maintain and monitor standards of clinical practice by striving to follow them. The task force comprising of senior members of Indian Psychiatric Society published Clinical practice guidelines for psychiatrist in India in 2004(1), the first of its kind. In a country of poor resources for mental health this is still a praiseworthy effort.Polypharmacy is a global trend. Table 1 summarises several studies on polypharmacyIt is noteworthy that in several above studies polypharmacy means two or more drugs. This could commonly be a benzodiazepine with either SSRI or an antipsychotic. However, with regards to a global trend for polypharmacy there are some essential differences: When it occurs as mentioned in above studies there are measures to monitor them and it is audited. Further, the reasons of poly pharmacy are documented and it follows rationale even in the private set up (4). Finally there is a close follow up and side effects are actively looked in and reported (4, 13). There is little information of how psychiatry is practiced when it comes to prescriptions in this country of 10 billion plus population with approximately 4000 practicing psychiatrists.METHODOLOGY

This study was conducted at the out patient services of Surat Municipal Institute of Medical Education and Research (SMIMER) and Government Medical College Surat. These are Surat Municipal Corporation and Gujarat State Government run teaching hospitals respectively catering to mental health needs of people in South Gujarat. 100 consecutive patients

sector community clinic their current prescriptions were also analyzed on same parameters to provide a comparison. The current diagnosis was based on DSM IV (2).

There could have been no other source of information on private psychiatrist prescriptions than obtaining it from patients.

The following medications were available at Civil Hospital Surat:Drugs used in psychotic disorders (haloperidol, trifluoperazine, risperidone, olanzepine, clozapine, chlorpromazine and trihexipenydil HCl), drugs used in mood disorders( sodium valproate, lithium,carbamazepine, imipramine, amitriptyline, escitalopram, citalopram, fluoxetine), benzodiazepines( diazepam, clonazepam)

The following medications were available at Surat Municipal Corporation Institute of Medical Education and Research Drugs used in mood disorders (sodium valproate, lithium, amitriptyline, benzodiazepines (diazepam)

RESULTS

The demographic profile reflects that of any general hospital community settings with 60% males, average age as 36 years (range 18-65), 85% Hindus, income range 2000-40000 and average of 7000 rupees per month, literacy level ranging from being illiterate (10%) to class 10 (45%), mostly manual labourer for males and housewives for females.

The patients had following diagnostic profile: Schizophrenia

who had visited at least one private psychiatrist previously and having the follow ups mainly in form of files, were included. Since these patients were being followed up by the public

33


Study

Spanish study. De las Cuevas C et al.(3)

Australian study. Botvinik L et al.(4)

Spanish study. De las Cuevas C et al.(5)

West Indies study. Moore S et al.(6)

Helsinki study. Hemminki E (7)

Italian National Survey. Magliano L et al (8)

Austria Rittmannsberger H et al. (9)

Hungary Viola R et al (10)

Austria Rittmannsberger H (11)

Italian study Barbui C et al. (12)

Italian study. Tomasi R et al (13)

Average medication per

patient

2.22 (+/- 0.70) Range 1-6

-

1.63 (+/-0.93) Range 1-7

-

2.1 Range 1-6

-

2.2-3.3

-

-

3.2

2.7 (+/-1.1)

Rate of polypharmacy

67%

100%

41.9%

83%

69%

29%

92-78%

33.6%

63.8%

-

-

Other significant findings

34.1% received more than 2 drugs. 20.5% more than 3 drugs

11% more than two antipsychotics.57% depressed and 40% anxiety disorder patients received antipsychotics.

Same class Polypharmacy.

Traditional psychotropics more common

Reviewed 14 controlled clinical trials for use of more than one drug. No evidence to support Polypharmacy.

24% more than 2 neuroleptics

5-22% received 5 or more psychotropics.

-

1970’s 47.8% on monotherapy and in 1990’s 19.6%. 28 studies on 4 treatment facilities.

Study of trend over 20 years. Medical illness related drugs included.

15% Tardive DyskinesiaAntipsychotic Polypharmacy common.

Sample sizeand type of study

352Retrospective design

100 Retrospective design

2647 Retrospective design

132 cross sectional

694 cross sectional

682 randomly selected patients

Cross sectional study984 Retrospective study.

Literature review.

Retrospective study.

2962 cross sectional study.

Table 1: Comparison of various studies regarding polypharmacy

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an average of 4. The total illness duration ranged from 1month to 8 years, average 3 years and 8 months. Frequency of visits: range once a week to once in two months, average once in a fortnight. 12% patients received ECT. Each received anywhere between 2 to 22 sessions with an average of 7. These patients had Schizophrenia in 4 cases and rest had depressive illness. Allegedly, no explanation offered in most cases. The common thing said was, “It would be an injection in your vein and then you won’t feel any discomfort”

Most patients were explained that they suffered a ‘mental illness’ (“mansik bimari”). At the most chemical imbalance in brain was stated. 55% patients reported not being adequately explained what the illness was and what medicines would do.Patients had spent a minimum of 3000 rupees and a maximum of 4 lac rupees on treatment in the private sector. The average being 900 rupees per month of treatment sought. This includes medication and consultation cost. The common reason for change of doctor was financial exhaustion. In decreasing order: lack of adequate improvement, desire for second opinion and anger towards some behavior on the part of psychiatrist. One patient sighted doctor’s using alcohol and smoking in front of them as the reason for leaving the doctor.

The duration of treatment sought varied from single session to 4 years with an average of 7 months in the private setting. In public setting the average length varied from 2 months to 2 years with an average of 8 months.

Patients almost never had any doubt on the efficiency of their previous psychiatrists.The total number of prescriptions analyzed was 1348. Diagnosis mentioned on private prescriptions in 4% scripts in contrast to being mentioned on 72 % public sector script. For private sector the average number of medicines per script was 4.2, range 2-14. There were a few rare scripts which contained all available atypical antipsychotic in low doses along with a typical antipsychotic in a single script!

with a range from single to 5 medications. 24% public sector patients were on monotherapy.

Patients with current diagnosis of Depression:

98% private sector scripts had two or more antidepressants. Same class polypharmacy (e.g two SSRI’s) was seen in a third of them. This came down to single antidepressant in public sector in 74 % of them. Tricyclics found place in 34% of private scripts and 56% of public sector. SSRI’s were far more common with escitalopram the most popular. With regard to dosing the maximum dosage of amitryptiline or imipramine was observed to be 200 mg or more in just 2 patients in private script as against 6 patients in public sector.Low dose atypical antipsychotic like 2.5 mg of olanzapine or 2 mg risperidone, typical antipsychotic in fixed dose combinations were found to be given in 42% private scripts.

This dropped down to 13 % in public sector where invariably the diagnosis was depression with psychotic features. As previously stated there was no reason documented in private scripts for using antipsychotic medicines.

Patient with current diagnosis of Psychotic Disorder:

Typical antipsychotic was found to be used for 28% patients in the private sector. However this was invariably in addition to atypical antipsychotic. Every script had a minimum of two antipsychotic from the first consultation. The dose ranges of medications were as follows: haloperidol 5-10 mg/day, trifluperazine 5-10 mg/day, chlorpromazine 50- 100 mg/day, risperidone 2-6 mg/day, olanzapine 2.5 to 15mg/day, and aripiprazole 15mg/day and clozapine in 500mg/day in a singe patient each. Anticholinergic medications were found in 25% patients.

Common co prescribed medications in the private sector included valproate in dose range of 250 to 500 mg/day, lithium upto 600 mg/day and benzodiazepines like lorazepam, clonazepam, alprazolam and nitrazepam in decreasing order of frequency. Other medications include multi vitamins, agents for constipation were found to be given in 27% of private scripts.

Table 2: Various irrational drug use

Examples Number of people

Two SSRI in patients with Depression/ Anxiety/mixed disorders One third cases

Two or more atypical antipsychotic in psychotic disorder from first consultation All psychotic patients

Two or more benzodiazepines 12% patients across all diagnostic domains

Same medication with two different brand names Less than 5% prescriptions

Change of one medication in each follow up (Addition/subtraction) 82% of private prescriptions

No wash out period ever 100% of private prescriptions

Two mood stabilizers in Bipolar disorder from first consultation All Bipolar disorder patients in private

and related psychotic illness-18%, Bipolar disorder 12%, Depressive disorder 38%, Anxiety disorder 12%, Mixed anxiety Depression 7%, and Others (includes Epilepsy, ADHD, enuresis, sexual disorder) 13%..

The average number of doctors visited ranged from 2-7 with

In the public sector average number of medication per script 2.5

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For all these patient with psychotic illness, since they were being followed up in the public sector community setting, they received single antipsychotic medication, 48% of them getting a typical antipsychotic and rest with atypical antipsychotic. This reflects the profile of available drugs in government sector.

Patients with Bipolar disorder:

In private sector all patients were started on two mood stabilizers from the beginning, usually lithium and valproate. This was combined with olanzapine in 40% of patients. Typical antipsychotic was prescribed to 37% patients. There has been no mention of serum lithium levels anywhere in any prescription.

Interestingly carbamezapine was not found to be used except in patient with epilepsy. The doses of valproate more than 1000mg/day was seen in 2 patients only, with usual dose range 200 to 600mg/day. Similarly subtherapeutic doses of less than 600 mg were used for lithium. 900 mg/day and above was found to be given in another 2 patients only. Other drugs found to be used were lamotrigine and gabapentin.

When followed up in public sector, in nearly 70% of these patients two mood stabilizers were continued although in increased doses. Lithium invariably had a dose range 900 to 1200 mg/day. Half of patients previously treated with valproate were increased to doses above 1000mg/day. In both sector lorazepam and clonazepam were two commonly used benzodiazepines for sedation or agitation.

Across all diagnostic domains, at least one medication was changed in each follow up in 92% patients; often the brand name was changed. Uncommonly there were same medications with different brand names in a few scripts.

Another relatively common pattern was sudden introduction and sudden withdrawal of a medication in large doses. Stepping up doses was observed in rare cases, but tapering dose to cease the drug was never observed. There was never a wash out period. There were no serious drug side effects documented anywhere in the private scripts.

DISCUSSION

There are several limitations of this study. The source of information of private sector prescriptions was the records that patients carried with them. This never reflected the exact picture, as in nearly every patient several scripts were missing or lost. Another aspect can be a subjective bias in collecting and analyzing data, by the virtue of author’s working in the public sector. And finally the relatively small sample size can be argued for not being representative.

As observed, the rate of monotherapy in private sector was zero and 24% in public sector. This is a complex issue to discuss. One aspect of discussion relates to availability. Until 1950s we had no available drug, then came Chlorpromazine and ever since then newer agents have been available, more so in the last few years. The newer drugs are reportedly safer (4). This has provided clinicians with opportunity to use drugs more liberally. As observed in this study the use has been quite adventurous

to the point of being hazardous in a rare few. Polypharmacy is a global trend.

It’s worth taking in account that in several above studies polypharmacy means two or more drugs. This could commonly be a benzodiazepine with either SSRI or an antipsychotic.

However, there are some essential differences:

1) When it occurs in different countries there are measures to monitor them and it is audited.

2) Further, the reasons of polypharmacy are documented and it follows some rationale even in the private set up (4). 3) Finally there is a close follow up and side effects are actively looked in and reported (4, 13). All these have found to be missing in our study.

In favour of the poor documentation observed, it is important to note that our mental health resources are scanty, the time for which a patient is assessed is limited, more so in the private sector where there are financial benefits of compressing more patients in given time. So, it would be unreasonable to look for the same meticulous documentation.Another aspect of polypharmacy is potential financial benefits for prescribing more medications through pressures by drug companies, possibly. This can only be proved hypothetically if we have balance sheets of major pharmaceutical companies providing the amount spent for clinicians.

The fourth aspect is the rationale and evidence for polypharmacy. Both these factors would favour an undoubted preference for monotherapy as far as possible. Only when monotherapy has not been effective, which means a maximum allowable therapeutic dose for 4-6 weeks, and a trial with another drug with a different mechanism of action, augmentation, addition or supplementation strategies need to be used. Unfortunately these are not practiced as per our results.

Another interesting finding has been at least one change of medication in every follow up. This could be possibly due to that fact that patient pays the doctor every time, there is a perceived notion in people’s mind that some medication change must be done; otherwise what for is the doctor being paid for? Sudden discontinuation and sudden introduction of a new drug were also not uncommon. The rational behind this could not be understood and it would rather be described as irrational.

Medications were used in low doses across the usual indication. This has several aspects to it. With the atypical agents side effect profile and patient tolerability has greatly improved (4) Not only that these atypical antipsychotic agents are now finding their way through approval to be used for bipolar disorder and are often classified as mood stabilizers as well. The horizon is clearly expanding.

Guided by the logistics of private practice, clinicians make every effort to avoid drug related side effect to prevent loss of the patient at follow up. This is likely reason for the medications (Lithium, valproate) to be used in sub-therapeutic doses and virtually no use of carbamezapine.

36


Most surprisingly, none of the patients ever reported any symptoms suggesting Neuroleptic Malignant Syndrome, serotonin syndrome or any serious, life threatening complication of medications.

Essential basic documentation regarding prescribed medication is necessary, it gives clinician much needed information at follow up, guides future clinical decisions , and protects against malpractice or negligence suits by consumers . If Indian Psychiatric Society provides such a uniform format for such record, it can benefit both consumers as well as providers.

Finally, more than acting defensively, as a quality improving exercise, not only for ourselves but for the patients we care for, we need to provide rational for polytherapy and document it as well.

There is a reasonable scope of Indian patients having differences with regards to class of drug for a particular disorder, dosage, metabolism, potential for side effect and actual response as compared to Western world and we need not blindly follow what is stated in the textbooks. But this needs to follow a collective scientific approach to prove this with methodologically sound studies.

Conclusion:

This preliminary study highlights several sound and unsound patterns of prescription in psychiatry. It is time to review and audit our own practicing trends before being caught in a potential legal battle. Also there are likely genetic and metabolic differences in our patients with regards to the doses requirement, tolerability for various drugs, and effectiveness of various drug combinations as compared with the western world, which the private practitioners must be savouring as secrets that can be brought to the knowledge of rest of the world.

REFERENCES1. Clinical Practice Guidelines for Psychiatrists in India,

Indian Psychiatric Society, 2004.2. American Psychiatric Association (2000) Diagnostic and

Statistical Manual, Fourth Edition American Psychiatric Association , Washington.

3. De las Cuevas C, Sanz EJ, De la Fuente JA, Cueto M.

Polypharmacy in psychiatric patients as an alternative to limited mental health resources. Actas Esp Psiquiatr. 2005 Mar-Apr;33(2):81-6

4. Botvinik L, Ng C, Schweitzer I. Audit of antipsychotic prescribing in a private psychiatric hospital. Australasian Psychiatry 2004 Sep;12(3):227-33.

5. De las Cuevas C, Sanz EJ. Polypharmacy in psychiatric practice in the Canary Islands. BMC Psychiatry. 2004 Jul 5;4:18

6. Moore S, Jaime LK, Maharajh H, Ramtahal I, Reid S, Ramsewak FS, Maharaj M.The prescribing of psychotropic drugs in mental health services in Trinidad. Rev Panam Salud Publica. 2002 Sep;12(3):207-14.

7. Hemminki E. Polypharmacy among psychiatric patients. Acta Psychiatr Scand. 1977 Nov;56(5):347-56.

8. Magliano L, Fiorillo A, Guarneri M, Marasco C, De Rosa C, Malangone C, Maj M; National Mental Health Project Working Group. Prescription of psychotropic drugs to patients with schizophrenia: an Italian national survey. Eur J Clin Pharmacol. 2004 Sep;60(7):513-22.

9. Rittmannsberger H, Meise U, Schauflinger K, Horvath E, Donat H, Hinterhuber H. Polypharmacy in psychiatric treatment. Patterns of psychotropic drug use in Austrian psychiatric clinics. Eur Psychiatry. 1999 Mar;14(1):33-40.

10. Viola R, Csukonyi K, Doró P, Janka Z, Soós G. Reasons for polypharmacy among psychiatric patients. Pharm World Sci. 2004 Jun;26(3):143-7

11. Rittmannsberger H. The use of drug monotherapy in psychiatric inpatient treatment. Prog Neuropsychopharmacol Biol Psychiatry 2002 Apr;26(3):547-51.

12. Barbui C, Ciuna A, Nosè M, Levi D, Andretta M, Patten SB, Amaddeo F, Tansella M. Drug treatment modalities in psychiatric inpatient practice: a 20-year comparison. Eur Arch Psychiatry Clin Neurosci. 2005 Apr;255(2):136-42. Epub 2004 Nov.

13. Tomasi R, de Girolamo G, Santone G, Picardi A, Micciolo R, Semisa D, Fava S; Gruppo PROGRES. Drug prescription in Italian Residential Facilities. Epidemiol Psichiatr Soc. 2005 Apr-Jun; 14(2):77-90.

Conflict of interest: The authors were working at SMIMER . Sources of support: None

Acknowledgement: Special thanks to Dr. Ritambhara Mehta and Dr. Kamlesh Dave for their cooperation in conducting this study at Government Medical College Surat. Navneet Kumar Johri* Trupti Sharma** *Registrar, Adult Mental Health Armadale Hospital, WA, AustraliaEx. Assistant Professor Psychiatry, SMIMER, Surat. **Registrar, Older Adult Mental HealthArmadale Hospital, WA, Australia Ex Resident in Psychiatry, SMIMER, Surat.

Correspondence: Dr Navneet Kumar Johri 3061, Albany Highway, Armadale, WA, Australia 6112 e- mail: [email protected]

37


Original Research Paper

Depression in Diabetes Mellitus

G.K.Vankar, Viral Parikh, Girish Banwari, Minakshi Parikh

ABSTRACT

Consecutive 225 patients attending Diabetes Clinic in a general hospital were screened for Depression using Beck Depression Inventory Gujarati Version. 38.6% patients were found to have depression and 11.5% have moderate to severe depression. Female gender, illiteracy, duration of diabetes less than 5 years and complications of diabetes were characteristics associated with depression. Other demographic and disease characteristics were not found to be associated.

Key Words: Diabetes, Depression

INTRODUCTION:

Diabetes mellitus is a disorder of metabolism and vascular system, manifested by disturbances in the body’s handling of glucose, lipid and protein. The prevalence of diabetes mellitus in India is 3.8%.

A meta-analysis to estimate the odds and prevalence of clinically relevant depression in adults with type 1 or type 2 diabetes from 39 studies has concluded that diabetes doubles the odds of depression (Anderson et al., 2001). The prevalence of depression in diabetes is 2-3 times higher than general population. (Gavard et al., 1993; Asghar et al 2007) and is observed across ethnically diverse groups (de Groot et al., 2006). However, two large, population-based studies have demonstrated that people who are diagnosed with type 2 diabetes are at no greater risk of developing subsequent depression than people without diabetes, once comorbid diseases and the burden of diabetes complications were accounted for (Brown et al, 2006; Engum et al., 2005).

Furthermore, factors associated with depression in type 1 and type 2 diabetes were shared with the nondiabetic population (Engum et al., 2005).Several of the factors claimed to be linked to depression are not limited to those with diabetes and may be related to the general psychological distress of having a chronic disease (Fisher et al., 2001) Depression, on the other hand, is an independent risk factor for the onset of type 2 diabetes (Eaton et al., 1996). Brown et al. (2006) have concluded that depression increases the risk of diabetes rather than vice-versa. Various hypotheses have been put forward to support the same. Insulin resistance and reduced glucose uptake during depressive illness might contribute to the linkage between depression and type II diabetes (Timonen et al., 2005). Another hypothesis is that stress-induced disturbances of the hypothalamopituitary adrenal axis and the development of visceral obesity as a pathway to type 2 diabetes in individuals with genetic susceptibility (Rosmond R, 2003).

Significant correlates of higher depressive symptoms in diabetes include female gender (Egede et al., 2003; L Loyd

et al., 2002; Blazer DG et al., 2002; Padgett DK, 1993), less education (Egede et al., 2003; Blazer DG et al., 2002; Padgett DK, 1993), the presence of diabetic complications (de Groot et al., 2001; Egede et al., 2003; Miyoka et al., 1997; Padgett DK, 1993) and longer duration of the disease (Garduno Espinosa et al., 2002; Miyoka et al., 1997; Padgett DK, 1993). Comorbid depression has been found to be associated with greater functional disability (Egede LE, 2004), more hospital days and days off of work (Egede LE, 2004),decreased adherence to dietary measures, exercise, medication, and self-monitoring of blood glucose recommendations (Ciechanowski et al, 2000, Lin et al, 2004), worsened diabetes complications (Lustman et al, 2000) and increased health care costs (Ciechanowski et al, 2000, Egede et al, 2002).In addition, the coexistence of diabetes and depression is associated with a significantly increased risk of death from all causes, beyond that due to having either diabetes or depression alone (Egede et al., 2005, Zhang et al, 2005).Although depression is common in diabetics, its relation with glycemic control is poorly understood. A host of studies and meta analyses have concluded that depression severity is associated with poor glycemic control. (Lustman et al., 2000; Gross et al., 2005). On the other hand, Georgiades et al. (2007), Engum et al. (2005) and Ciechanowski et al. (2000) did not find an association between severity of depressive symptoms and glycemic control in patients with diabetes. Kruse et al. (2003) found that people with diabetes and affective disorders were more likely to have adequate glycemic control; and another study reported somewhat lower glycosylated hemoglobin (HbA1c) levels in patients with type 2 diabetes and major mood disorders (mostly depression) compared with primary care diabetic patients without serious mental illness. (Dixon et al., 2004).Interestingly, treatment for depression results in reduction of HbA1c levels. (Lustman et al., 2000).Goldney et al. (2004) and Brown et al. (2000) have indicated

38


addition of depression to diabetes has a severe impact on quality of life, and this needs to be managed in clinical practice.

The present study aims to find out the frequency of depression and its severity, as well as sociodemogaphic and clinical correlates of depression in diabetes mellitus.

METHODOLOGY:

Consecutive 225 patients attending diabetic clinic at Civil Hospital, Ahmedabad were studied.

Each patient was asked about demographic details like age, sex, domicile, income, education, marital status and also about disease characteristics like duration, type, medication, complication and co morbidity like hypertension, ischemic heart disease, hypothyroidism, osteoarthritis.

They completed Beck Depression Inventory (BDI) Gujarati Version which is a 4 point scale containing total 21 items. According to total score of BDI, depression was found out. >40 profound depression, 31-40 severe depression, 21-30 moderate depression, 17-20 mild depression, 11-16 borderline mood disturbances, 0-10 normal. In this study, patients having BDI score more than 20 were considered as having depression.

Statistical analyses included calculation of means, frequencies and percentages of the variable as descriptive measures. The results were analyzed using chi square test and also appropriate Fisher’s exact t test to find out any significant difference.

RESULTS:

The prevalence of depression (BDI >20) was 11.5%. Table 1 shows socio demographic characteristics of the depressed and non-depressed diabetics. Mean age for depressed and non-depressed was same (56.6). Among 26 depressed diabetics 19(73.1%) were women, 15(57.7%) were uneducated, 22(84.6%) were married, 26(100%) were residing in urban areas and 13(50%) had family income less than Rs.1000./month. Among the 199 non-depressed diabetics 90(45.2%) were women, 51(25.6%) were uneducated, 177(88.9%) were married, 176(88.4%) were residing in urban areas and 61(30.7%) had family income less than Rs.1000./month.

Being woman , being uneducated , living in city were associated with more frequent depression.

Table 2 shows diabetes characteristics of the depressed and non-depressed diabetics. Among 26 depressed diabetics 6(23.1%) had duration less than 5 years, 21(80.8%) were on oral medication, 2(7.7%) were having type I diabetes mellitus, 15(57.7%) had no complication and 13(50%) had no comorbid medical disorder. While among 199 non depressed 94(47.2%) had duration less than 5 years, 160(80.4%) were on oral medication, 9(4.5%) were having type I diabetes mellitus, 153(76.9%) had no complication and 102(51.3%) had no co morbidity.

Presence of complications of depression and 5 years or longer duration after diabetes diagnosis were significantly associated with more frequent depression. Other disease variables like

type of diabetes and treatment were not associated with more frequent depression.

DISCUSSION:

The present study is an attempt to find out frequency of depression in diabetics and also correlation with socio demographic details like age, sex, domicile, income, education, marital status. We have also correlated depression with diabetes characteristics like duration, type, medication, complication and co morbidities.

In our study we found frequency of moderate to severe depression 11.5%. But if the patients with borderline mood disturbances and mild depression were also taken into account the frequency works out to be 38.6%, which is about thrice the frequency of moderate to severe depression. This indicates that although many diabetics may not have full-blown major depression but they do suffer from mood disturbances, which may affect the life in many adverse ways. So, it is wisely said to train our physician friends to identify such mood disturbances in diabetes patients and help them by counseling or referring to a psychiatrist.

In our study we found significantly high rate of depression in women (17.4%) compared to men (6.03%). This finding is in agreement with other studies (Egede et al., 2003; L Loyd et al., 2002; Blazer DG et al., 2002; Peyrot et al., 1997). This probably reflects the higher prevalence of depression in women in general population.

Depression was seen more frequently in patients who had no formal education. This finding is consistent with other studies (Egede et al., 2003; Blazer DG et al., 2002; Peyrot M et al., 1997). Lack of knowledge and understanding in uneducated about the illness may lead to poor disease control, thereby increasing the burden of the illness and difficult adjustment with the same, thereby leading to higher rates of depression.

Diabetics with less than 5 years duration were found to have lower rate of depression compare to more than 5 years duration. Similar findings were found in Garduno Espinosa et al study. It is obvious that as the disease become chronic various factors may contribute to depression. These are poor glycemic control, increase dosage, occasional shifting from oral to injectable medication, leading to complication of disease and financial burden of illness.

Patients with Diabetics Mellitus having no complication were found to have lower rate (8.9%) of depression compared to diabetics having complication like neuropathy, retinopathy, nephropathy, hypothyroidism or skin ulcer (24.4%). This finding is in agreement with other studies (Egede et al., 2003; Miyoka et al., 1997; Peyrot M et al, 1997). It is understandably clear that complications add to burden of the existing illness and result in increase frequency of depression.

14.7% of urban patients were found to be suffering from moderate to severe depression while no rural diabetics had depression. This finding may be incidental as majority of the

39


Table 1: Demographic characteristics

Depression Comparison Statistical present Group significance N=26 N=199 n (%) n(%)

Age years Range 40-70 21-80 NS Mean 56.6 56.6 SD 8.7 12.1

Gender Men 7 (26.9) 109(54.8) χ2= 7.14 Women 19(73.1) 90(45.2) p=0.007

Education Uneducated 15(57.7) 51(25.6) χ2=11.43 Primary 7(26.9) 90(45.2) df=2 Secondary 3(11.5) 44(22.1) P=0.003 >secondary 1(3.8) 14(7.0)

Marital Status Married 22(84.6) 177(88.9) Fisher exact test Unmarried 0 3(1.5) 2 tailed p=0.51 Divorced 0 1(0.5) Widowed 4(15.4) 18(9.0)

Residence Urban 26(100) 176(88.4) Fisher exact test Rural 0 23(11.6) 2tailed p=0.08

Income(Rs/month) <1000 13(50) 61(30.7) χ2=3.90 1001-2000 8(30.8) 86(43.2) df=2 >2000 5(19.2) 52(26.1) P=0.14

an urban setting; a similar study if carried out in rural area will throw more light over the frequency of depression in rural diabetics.

This study did not find any significant correlation with sociodemographic characteristics like age, marital status or income. Also, we did not find any association of depression with type of diabetes, type of medication or co morbidity. Certain limitations of study need to be mentioned here. It was conducted only on patients coming in diabetic clinic in our hospital. So this sample might have selection bias. Also, the sample size was not adequate

Depression complicates the diabetes by promoting poor glycemic control and increase risk of complication. Treatment has favorable effect on mood and quality of life as well as beneficial effect on glycemic control. So it is better to diagnose and treat depression in diabetics. But unfortunately depression is recognized and treated only in one third of cases (Lustman et al., 2005).

In summary, our study found that 11.5% of diabetes mellitus patients had moderate to severe depression. Higher risk of depression was found in women and the uneducated. Longer the duration of diabetes, greater was the risk of depression. Diabetes patients having complications were associated with higher risk for depression. No significant association was

found with age, marital status, income, type of diabetes, type of medication and co morbid medical disorders.

REFERENCES :1. Lustman PJ, Clouse RE. Depression in diabetic patients:

the relationship between mood and glycemic control; J Diabetes Complications. 2005 ,19(2): 113-22

2. Garduno-Espinosa J, Tellez-Zenteno JF, Hernandez-Ronquillo L Frequency of depression in patients with diabetes mellitus type 2; Rev Invest Clin. 1998, 50: 287-91.

3. Egede LE, Zheng D Independent Factors Associated With Major Depressive Disorder in a National Sample of Individuals With Diabetes; Diabetes Care. 2003; 26:104-111

4. Lloyd CE, Brown FJ Depression and Diabetes; Curr Womens Health Rep. 2002; 2:188-193

5. Blazer DG, Moody-Ayers S, Craft-Morgan J Depression in Diabetes; Psychosom Res. 2002; 53:913-916

6. Miyaoka Y, Miyoaka H, Kitamura S, et.al., Impact of sociodemographic and diabetes related characteristics on depressive state among non insulin dependent diabetic patients; Psychiatry-Clin-Neurosci. 1997 Aug; 51(4):

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Table 2: Diabetes characteristics and Depression Psychiatric Control Statistical morbidity Group significance N=26 N=224 n (%) n(%)

Substance use Nil 20(76.9) 157(78.9) χ2=0.04 Tobacco 3(11.5) 27(13.6) df=3 Smoking 3(11.5) 13(6.5) P=0.84 Alcohol plus smoking 0 2(1.0)

Diagnosis since Years Upto 5 years 6(23.1) 94(47.2) χ2= 10.82 5-10 years 11(42.3) 33(23.2) df=2 >10 years 9(34.6) 72(29.6) p=0.004

Medication Oral 21(80.8) 160(80.4) χ2=0.09 Injectable 3(11.5) 26(13.1) df=2 Combined 2(7.7) 13(6.5) P=0.95

Type I 2(7.7) 9(4.5) Fisher exact test II 24(92.3) 190(95.5) 2 tailed p=0.37

Complications Nil 15(57.7) 153(76.9) χ2= 4.48 Neuropathy 9(34.6) 38(19.1) df=5 Retinopathy 1(3.8) 7(3.5) P=0.03 Skin Ulcer 1(3.8) 2(1.0) Nephropathy 0 1(0.5) AMI 1(3.8) 01(0.5)

Comorbidity Nil 13(50) 102(51.3) χ2=0.24 Hypertension 13( 50) 93(46.7) df=5 IHD 1(3.8) 13(6.5) P=0.62 Thyroid 1(3.8) 1(0.5) COPD 0 1(0.5) Osteoarthriris 0 3(1.5)

anxiety symptomatology among diabetic adults; Diabetes Care. 1997 Apr; 20(4): 585-90

8. Asghar S, Hussain A, Ali SM et. al., Prevalence of depression and diabetes: A population-based study from rural Bangladesh. Diabet Med. 2007 Apr 2; [Epubahead of print]

9. Padgett DK, Sociodemographic and disease-related correlates of depressive morbidity among diabetic patients in Zagreb, Croatia. J Nerv Ment Dis. 1993; 181(2): 123-9.

10. Anderson RJ, Kenneth BA, Freedland E, Clouse RE, Lustman PJ. The Prevalence of Comorbid Depression in Adults With Diabetes: A Meta-Analysis. Diabetes Care. 2001 Jun; 24(6): 1069-1078

11. De Groot M, Anderson RJ, Kenneth BA, Freedland E, Clouse RE, Lustman PJ Association of Depression and Diabetes Complications: A Meta-Analysis. Psychosom Med 2001; 63:619-630

12. Brown LC, Majumdar SR, Newman SC, Johnson JA. Type 2 diabetes does not increase risk of depression. CMAJ, 2006 July 4; 175(1): 42-46.

13. Egede LE: Diabetes, major depression and functional disability among U.S. adults. Diabetes Care 2004; 27:421– 428

14. Ciechanowski PS, Katon WJ, Russo JE: Depression and diabetes: impact of depressive symptoms on adherence, function, and costs. Arch Intern Med 2000;160: 3278–3285

15. Lin EHB, Katon W, Von Korff M, Rutter C, Simon GE, Oliver M, Ciechanowski P, Ludman EJ, Bush T, Young B: Relationship of depression and diabetes self-care, medication adherence, and preventive care. Diabetes Care 2004; 27:2154–2160

16. Lustman PJ, Anderson RJ, Freedland KE, de Groot M, Carney RM, Clouse RE: Depression and poor glycemic control: a meta-analytic review of the literature. Diabetes Care 2000; 23:934 –942

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Sources of support: None Conflicts of Interest: None

HS: Depressive symptoms and mortality among persons with and without diabetes. Am J Epidemiol 2005; 161: 652–660

18. Egede LE, Nietert PJ, Zheng D: Depression and All-Cause and Coronary Heart Disease Mortality Among Adults With and Without Diabetes. Diabetes Care 2005; 28:1339–1345

19. Egede LE, Zheng D, Simpson K: Comorbid Depression is Associated With Increased Health Care Use and Expenditures in Individuals With Diabetes. Diabetes Care 2002; 25:464–470

20. Gavard JA, Lustman PJ, Clouse RE: Prevalence of depression in adults with diabetes: an epidemiological evaluation. Diabetes Care 1993; 16:1167–1178

21. Engum A, Mykletun A, Midthjell K, Holen A, Dahl AA: A large population-based study of sociodemographic, lifestyle, and clinical factors associated with depression in type 1 and type 2 diabetes. Diabetes Care 2005; 28:1904–1909.

22. Timonen M, Laakso M, Jokelainen J, Rajala U, Meyer-Rochow VB, Keinanen-Kiukaanniemi S: Insulin resistance and depression: cross sectional study. BMJ 2005; 330:17–18

23. Gross R, Olfson M, Gameroff MJ, Carasquillo O, Shea S, Feder A, LantiguaR, Fuentes M, Weissman MM: Depression and Glycemic Control in Hispanic Primary Care Patients with Diabetes. J Gen Intern Med 2005; 20:460–466.

24. Kruse J, Schmitz N, Thefeld W. On the association between diabetes and mental disorders in a community sample: results from the German National Health Interview and Examination Survey. Diabetes Care. 2003; 26:1841–6.

25. Dixon LB, Kreyenbuhl JA, Dickerson FB, et al. A comparison of type 2 diabetes outcomes among persons

with and without severe mental illnesses. Psychiatr Serv. 2004; 55:892–900.

26. De Groot M, Pinkerman B, Wagner J, Hockman E: Depression treatment and satisfaction in a multicultural sample of Type 1 and Type 2 diabetic patients. Diabetes Care 2006; 29:549–553

27. Lustman PJ, Griffith LS, Freedland KE, et al: Fluoxetine for depression in diabetes. Diabetes Care 2000; 23:618–623

28. Brown GC, Brown MM, Sharma S, Brown H, Gosum M, Denton P: Quality of life associated with diabetes mellitus in an adult population. J Diabetes Complication 14:18–24, 2000

29. Goldney RD, Phillips PJ, Fisher LJ, Wilson DH: Diabetes, Depression, and Quality of Life-A population study. Diabetes Care 2004; 27:1066–1070

30. Rosmond R: Stress induced disturbances of the HPA axis: a pathway to type 2 diabetes? Med Sci Monit 2003; 9:35–39.

31. Fisher L, Chesla CA, Mullan JT, Skaff MM, Kanter RA: Contributors to depression in Latino and European-American patients with type 2 diabetes. Diabetes Care 2001; 24:1751–1757

32. Eaton WW, Armenian HA, Gallo J, Pratt L, Ford DE: Depression and risk for onset of type 2 diabetes: a prospective, population-based study. Diabetes Care 1996; 19:1097–1102

33. Egede LE: Effects of depression on work loss and disability bed days in individualswith diabetes. Diabetes Care 2004; 27:1751–1753

34. Georgiades A, Zucker N, Friedman KE, Mosunic CJ, Applegate K, Lane JD, Feinglos MN, Surwit RS: Changes in depressive symptoms and glycemic control in diabetes mellitus. Psychosom Med. 2007; 69: 235-41

G.K.Vankar, Professor and Head *

Viral Parikh, Resident Girish Banwari, Senior Resident Minakshi Parikh, Associate Professor Dept. of Psychiatry B.J.Medical College and Civil Hospital, Ward E1,Asarwa, Ahmedabad 380016

Correspondence: G.K.Vankar, Professor and Head Dept. of Psychiatry, Civil Hospital, Ward E1, Ahmedabad 380016 e-mail:[email protected] Cell: 09904160338

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Brief Research Communication

A Clinical study in Childhood Trichotillomania

Avinash De Sousa

ABSTRACT

Childhood onset trichotillomania is a poorly understood disorder , with only a few Indian studies. This study examines the clinical profile, family history, severity of hair pulling and response to various treatment modalities in 26 children and adolescents with childhood onset trichotillomania presenting to a private psychiatric clinic in Mumbai. No differences in severity of hair pulling behavior was noted in both sexes. 76.9% of subjects pulled hair from their scalp. Majority of the subjects were treated using behavior therapy and medication was the second choice. Moderate improvement was noted in both groups with no sex differences.

Key Words : Childhood onset trichotillomania, children, trichotillomania.

INTRODUCTION

Trichotillomania (TTM) is a poorly understood disorder in children defined by the irresistible urge to pull out one’s hair accompanied by a build up of tension and subsequent sense of relief. The prevalence of TTM in children is probably underestimated due to its secretiveness as well as due to an under recognition by health professionals. Current evidence suggests that there is a higher prevalence than realized. (1)

Though the disorder is gaining recognition there are few studies of large groups more so in the pediatric population .(2) Some authorities even state that the disorder in children has a milder form and a shorter course. (3)\

Hair pulling is a behavior that occurs along a continuum from a very benign form of hair pulling that provides no cosmetic damage to a very severe form of hair pulling that leads to disfiguring and personal suffering. (1, 4) Upto 10% of people have engaged in hair pulling at some time in their lives. DSM IIIR TTM prevalence rates range from 0.6-1.6% while when subthreshold hair pulling is included the rate goes up to 3.4% .(5-6) The true prevalence of TTM in children and adolescents is unknown but is most probably < 1%. The mean age of the onset of the disorder is 9-13 years while hair pulling without any emotional distress may occur in smaller children (< 5 years). (7-8). Children with TTM report urges to pull their hair that occurs many times a day. The act of hair pulling reduces the tensions that these urges produce. They often scrutinize, tug and stroke their hair\before pulling it. Many pull out single or tufts of hair and spend at least 1 hour a day in hair pulling activity. (9) The management of childhood onset TTM is a difficult task. There are no pharmacological trials of drugs in childhood onset TTM. There are no FDA approved drug therapies for the same. Selective serotonin reuptake inhibitors (SSRIs), typical and atypical antipsychotics have all been used in anecdotal case reports with no success in any major drug class. (10-11) Among the SSRIs, fluoxetine has been the most widely used . (12) Behavior therapy and habit reversal have been used effectively with modest success .(13-14)

Research techniques have included genetic, comorbidity studies, neuropsychological testing and structural or functional

neuroimaging. Cerebrospinal fluid, pain thresholds and pharmacological probes have also been studied. Many of these studies lend support to a biological relationship between TTM and obsessive compulsive disorder. (15-16) Studies on childhood onset trichotillomania suggest a balanced sex distribution or even a male preponderance. (17-18) Hair may be pulled from a variety of sites, most frequently from the scalp but also from the eyelashes, eyebrows, chest, axillary and pubic hair. Associated behaviors may include nail biting (onychophagia) and / or eating of the hair (trichotillophagia). (3) In children with trichotillomania there is an elevated family history of disorders like trichotillomania, obsessive compulsive disorder and affective disorders. (19) Finally it is also noted that many patients with childhood onset trichotillomania present to non mental health professionals like pediatricians, general practitioners and dermatologists while they may present to mental health professionals for comorbid disorders like OCD and depression. (3)

Studies on childhood onset trichotillomania have increased our knowledge about the psychiatric comorbidity and phenomenology of the disorder but data still remains inconclusive. This study assesses the demographics, phenomenology, comorbidity and treatment history in 26 children and adolescents with trichotillomania seen in Mumbai schools over the past 3 years.

METHODOLOGY The parents of the children with trichotillomania were administered a semistructured questionnaire that inquired about demographics, clinical profile, other psychiatric disorders in the child and the family and treatment history. The parents were explained the aim of the study and anonymity of the information was assured. A written valid informed consent was obtained from all the parents. In some cases where the child was old enough both the parents and the child filled the questionnaire.

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The severity of hair pulling was rated on a 5 point scale (0 = none, 1 = mild, 2 = moderate, 3 = severe, 4 = extreme) for each of the six listed hair pulling sites viz. eyelashes, eyebrows, scalp, pubic area, body and face. Subjects were asked to report only formally diagnosed psychiatric disorders in the child and the family in order to minimize self diagnosis. The professional qualification of the doctor diagnosing the disorder was taken into account. Treatment history was obtained for medications, behavior therapy and psychotherapy. Effectiveness for each was rated on a 7 point scale (1 = very much improved, 2 = much improved, 3 = mildly improved, 4 = unchanged, 5 = mildly worse, 6 = much worse and 7 = very much worse). Names and dosages of each medication, effectiveness, duration of therapy was rated separately. RESULTS There were a total of 26 children and adolescents in the study. Of these 14 were boys and 12 were girls. The mean ages of the boys and girls were 10.3 and 9.6 years respectively. All lived with both parents and in nuclear families. The age of onset of symptoms in most children was between 6-9 years. The mean age of onset in boys was 7.9 years and for girls 6.6 years. On enquiring about the area of hair pulling and its severity, 20 out of the 26 subjects (76.9%) reported pulling hair from the scalp. There was no difference between severity of hair pulling in both the boys and girls group. One patient reported pulling hair from the body i.e. chest and axillary hair while 5 reported pulling hair from the eyebrows and eyelashes (19.2%). Surprisingly none of the subjects reported hair puling from multiple sites. Here too there were no differences amongst boys and girls in the severity of hair pulling. None of the subjects reported pulling pubic hair .

Table 1: Site of Hair Pulling

Site of Hair Pulling Incidence N = 26 n(%)Scalp Hair 20(76.9)Eyebrows and Eyelashes 05(19.2)Body Hair 01(3.8)

Table 2 : Gender and severity of hair pullingSeverity Boys Girls (N = 14) (N = 12) Mean (SD) Mean (SD)Scalp Hair 3.3 (0.8) 3.4 (0.7) Eyebrows /Eyelashes 2.8 (0.7) 2.9 (0.9)Body Hair 1.9 (0.8) 2.0 (0.9)

Among the subjects, 4 had a comorbid diagnosis of obsessive compulsive disorder (15.4%). 3 had a diagnosis of childhood depression (11.5%). In their families, only 1 had a family history of trichotillomania. 4 had a parent that suffered from major depression and 2 had parents that suffered from panic disorder (Table 2).

The most common treatments used were behavior therapy (84.6%) and medication with behavior therapy (46.1%). The later group included some children from the behavior therapy group. Parents had in early treatment refused medication but later agreed for the same after some time. Their improvement was analysed before the start of medication (while on behavior therapy alone and were included in the improvement analysis for the behavior therapy group alone. The most common class of medications used was the SSRIs with fluoxetine and sertraline being the favorites finding use in 5 subjects each. Paroxetine and clomipramine was used in one subject each. The mean improvement scores for all treatments were similar for boys and girls on the CGI-Improvement scale (Table 3).

Table 3 : Degree Of Improvement With The TreatmentsDegree of Improvement Boys Girls (N = 14) (N = 12) Mean (SD) Mean (SD)Behavior Therapy 3.7 (1.2) 3.5 (1.1) Medication + Behavior Therapy 3.0 (1.0) 3.1 (0.9)CBT 4.6 (0.8) -

Amongst the subjects that received behavior therapy alone, all had refused medication as treatment. The behavior therapy techniques used was positive reinforcement for restriction of hair pulling and graded habit reversal training. Two children were started on cognitive behavioral therapy. Though widely used in trichotillomania children have to have a certain level of psychological mindedness and understand cognition before we can start CBT hence just two children who the author felt would benefit were started on the same. Incidentally both of them were boys.

DISCUSSION

This study derives all its information via a semi-structured questionnaire from patients of childhood onset trichotillomania and their parents who presented to our clinic. These children were original seen in Mumbai schools where they had presented with their parents and the chief complaint was hair pulling. They were evaluated in detail at the author’s clinic who is a visiting psychiatrist to various schools in Mumbai. Self and parental report data are vulnerable to distortion and inaccuracy. No statistics were used as the groups were small in number and the scales used were not qualified enough for parametric statistics. The findings from this study does not apply to the community population as it is a selective group that actually presented for treatment probably indicating that severity of disorder was more than in many subjects that do not present for treatment. One must note that childhood trichotillomania lies on the continuum of obsessive compulsive spectrum disorders and hence very often similar treatment options involving the serotonergic system predominantly are used in both disorders

Findings on the site and severity of hair pulling are consistent with other studies. (2) The lack of involvement of pubic hair pulling was due to maturational aspects of hair growth. This

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also raises the question whether children change in symptom profile once they progress with the disorder into adulthood. The patterns of comorbidity and family history in the study are consistent with previous reports. (3) The treatment modality used reflect the current pharmacological strategies in vogue i.e. the SSRIs and behavior therapy. The moderate response noted in the study is however not in keeping with certain reports of SSRI use in trichotillomania. (10,12)

Despite its limitations this study adds to the relatively scarce literature on childhood onset trichotillomania in India. The study may replicate reports from abroad and add to anecdotal case reports but on its own supports the need for controlled and large studies on the epidemiology, phenomenology, co-morbidity, family constellation and treatment strategies and algorithms of childhood trichotillomania.

REFERENCES

1. Christensen GA, Pyle RL, Mitchell JE. Estimated lifetime prevalence of trichotillomania in college students. Journal of Clinical Psychiatry 1991 ; 52 : 415-417.

2. Swedo SE, Rappaport JL. Annotation : trichotillomania. Journal of Child Psychology & Psychiatry 1991 ; 32 : 401-409.

3. Swedo SE, Leonard HL. Trichotillomania : an obsessive compulsive disorder ? Psychiatric Clinics of North America 1992 ; 15 : 777-790.

4. Graber J, Arndt WB. Trichotillomania. Comprehensive Psychiatry 1993 ; 34 : 340-346.

5. Azrin NH, Nunn RG. Habit Control in a Day. New York, Simon & Schuster ; 1977.

6. Tay YK, Levy ML, Metry DW. Trichotillomania in childhood – a case series and review. Pediatrics 2004 ; 113(5) : 494-498.

7. King RA, Scahill L, Vitulano LA. Childhood trichotillomania – clinical phenomenology, comorbidity and family genetics. Journal of the American Academy of Child & Adolescent Psychiatry 1995 ; 34 : 1451-1459.

8. Christenson GA. Trichotillomania – from prevalence to

comorbidity. Psychiatric Times 1995 ; 12(9) : 44-48.

9. Reeve E. Hair pulling in children and adolescents. In Trichotillomania, Edited by Christenson GA, Hollander E. Washington DC, American Psychiatric Press ; 2000.

10. O’Sullivan RL, Christenson GA, Stein DJ. Pharmacotherapy of Trichotillomania In Trichotillomania, Edited by Stein DJ, Christenson GA, Hollander E. Washington DC, American Psychiatric Press ; 1999.

11. Orange AP, Peereboom-Wynia JDR, DeRaeynaecker DMJ. Trichotillomania in childhood. Journal of the American Academy of Dermatology 1986 ; 15 : 614-619.

12. Koran LM, Ringold A, Hewlett W. Fluoxetine for trichotillomania : an open clinical trial. Psychopharmacology Bulletin 1992 ; 28 : 145-149.

13. Friman PC, Finney JW, Christophersen ER. Behavioral treatment of trichotillomania : an evaluative review. Behavior Therapy 1984 ; 15 : 249-265.

14. Azrin NG, Nunn RG, Frantx SE. Treatment of hair pulling : a comparative study of habit reversal and negative practice timing. Journal of Behavior Therapy and Experimental Psychiatry 1980 ; 11 : 13-20.

15. Bienvenu OJ, Samuels JF, Riddle MA, Hoehn Saric R, Liang KY, Cullen BA, Grados MA, Nestadt G. Relationship between obessessive compulsive disorder and other obsessive compulsive spectrum disorders – a family study. Biological Psychiatry 2000 ; 48(4) : 287-293.

16. Stein DJ. Neurobiology of Obsessive Compulsive spectrum disorders. Biological Psychiatry 2000 ; 47 : 296-304.

17. Dawber R. Self induced hair loss. Seminars in Dermatology 1985 ; 4 : 53-57.

18. Muller SA. Trichotillomania. Dermatology Clinics 1987 ; 5 : 595-601.

19. Leane MC, Swedo SE, Rappaport JL. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania – a research note. Journal of Child Psychology & Psychiatry 1991 ; 3 : 925-933.

Sources of support : None Conflict of interest: None

Dr. Avinash Desouza Director and Consultant Psychiatrist Get Well Clinic, Carmel, 18 St. Francis Avenue, Willingdon Colony, Santacruz (West), Mumbai 4000020 Tel:: 91-22-26460002 / 9820696828 e-mail: [email protected]

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Verbal Learning difficulty in schizophrenia and epilepsy : implications for retraining

Shweta Kadaba, Anuradha Sovani

ABSTRACT

In a two group matched comparison design, 13 people each, respectively diagnosed for temporal lobe epilepsy and for schizophrenia, were assessed using a verbal memory test, viz the CVLT(California Verbal Learning Test) , which measures list learning under various conditions. Results show significant differences between the two groups in trials 1 and 2 (p< 0.01); and on trials 3 and 4 (p< 0.05). Although the interference trial yielded a significant difference between the two groups, there was no longer any statistically significant difference in Delayed recall, Cued recall and Recognition, nor in the amount of Retroactive interference seen in the two groups.

People with schizophrenia show slower learning and poorer encoding as compared to people with TLE. However once the material was well learnt it is retained, albeit with mild retrieval difficulty. Hence, there is difficulty with registration of information but not with retention. Retraining efforts must provide repetitions, and contextual cues.

Key Words : Verbal Tranning, schizophrenia, epliepsy, cognitive retraining

INTRODUCTION

People with schizophrenia experience a range of neuropsychological deficits, mainly in attention, executive dysfunction and memory, the latter linked to functional outcome. The issue of the relationship between attentional and memory deficit needs further empirical study and scrutiny. Attentional processes mediate the selection of stimuli for further processing and storage, and thus it is clear that impairment in attention is likely to produce a deficit in information acquisition. Poor encoding strategies, conversely, may cause attentional disruption as a by-product of failure to employ effective retrieval strategies and resultant failures of memory. In particular, investigations of working memory, as a construct at the intersection between attentional and mnemonic processes may help to elucidate what is likely to be a very close relationship. (Gur et al 2000)

This study focuses on assessing verbal learning deficits in people with two disorders, one with now emerging neurophysiological underpinnings, i.e. schizophrenia, and one with a clear neurological basis, viz. epilepsy. It was found that patients with temporal lobe epilepsy show deficits in long-term memory and not short-term memory. Specifically left temporal lesions yielded comparatively greater impairment for verbal long-term memory tasks, whereas right temporal lesions were more disruptive for spatial long-term memory tasks. (Ladavas et.al. 1979) Using a comparison group of people with epilepsy, where the locus of the problem is known, may help clarify the deficits of schizophrenia, and may also help us generalize well established retraining paradigms from one disorder to the other.

The left temporal lobe structures that have been reported be abnormal in schizophrenic subjects (hippocampus, amygdala, parahippocampal gyrus, and superior temporal

gyrus) are thought to be involved in verbal memory and language processing. A dysfunction of the verbal memory system, in the form of aberrant activation or over-activation of representations, could lead to symptoms such as thought disorder and verbal hallucinations. The hippocampus and related temporal lobe structures are thought to be important in the storage, retrieval and consolidation of memory in cortical areas. Impairments in encoding and consolidation have been associated with hippocampal and temporal lobe dysfunction (Squire et al 1991). The dorsolateral portion of the prefrontal cortex is thought to be involved in the maintenance of working memory representation. Working memory may rely on memory representations established and processed by the hippocampal system (i.e., the hippocampus and related structures), and hence a failure or dysfunction of the hippocampal system could result in a lack of normal activation of the prefrontal cortex during task performance. These data may be consistent when functional interactions between brain areas are taken into account. When assessing the role of prefrontal versus temporal cortex abnormalities in schizophrenia, it is important to be clear about the role of evidence from neuropsychological tests, physiological activation measures, and morphological measures, and their implications for brain function. Structural abnormalities, including cell loss, in the temporal lobe may lead to a disconnection between temporal and frontal areas, with both structural and functional consequences in the prefrontal cortex. It is also possible that structural abnormalities in the temporal lobe could lead to functional abnormalities in the prefrontal cortex without any functionally significant structural and/or chemical defects in the prefrontal cortex. For example, during the performance of tasks that include a memory component, and thus presumably activate medial temporal areas, it is possible that a failure or dysfunction of temporal lobe structures could cause a failure to activate, or aberrant

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AIMS AND OBJECTIVES:

The purpose of this study was to choose two groups, respectively with a well documented neurological and psychiatric ailment, assess them on a test of verbal learning which has implications in real life activities of daily living, in this instance list learning, and highlight the differences observed. The objectives were to find pointers for effective rehabilitation, and to look for possible strategies to combine rehabilitation efforts in order to save on the scant resource of trained personnel.

METHOD

In a two group matched comparison design, to compare people with Schizophrenia and Temporal lobe epilepsy respectively, a verbal memory test was used which assessed list learning over several conditions.: the California Verbal Learning Test(CVLT).

Sample

This sample was part of a larger group evaluated on a variety of tests including those mentioned below. A total of 25 subjects per group were administered the CVLT.

From this group, 13 subjects matched on the basis of age, education and socio-economic status were selected for comparison. Hence, the N was restricted to 13 per group in this study. E1 refers to people with schizophrenia and E2 to people with epilepsy. There were about equal males and females and the age ranged from 21 to 45, and availability sampling was used.

Schizophrenia Group ( Group E1)

The group of people with schizophrenia, who were evaluated, was drawn from patients at the Institute for Psychological Health, Thane. Most were unemployed and part of a self-help group and some were from the out patient department on follow up. The group was currently relatively symptom free and in partial remission. The socio economic status ranged from the middle to lower middle class. All were on some form of anti-psychotic medication, which was noted down. The commonly prescribed drugs were Chlorpromazine, Haloperidol, Risperidone and Trifluperazine. The duration ranged from 1 to 5 years. All patients had some active symptoms, and none were residual.

Mesial Temporal Sclerosis Group (Group E2 )

Subjects from the current study were selected from patients that sought treatment for their epilepsy at the King Edward Memorial Hospital, and, visited the E-Cell, an epilepsy support group that is part of the Indian Epilepsy Association. All the subjects were diagnosed having temporal lobe epilepsy with mesial temporal sclerosis, by the attending neurologist. All subjects who participated in the study were receiving anticonvulsant medications. The commonly prescribed drugs were carbamazepine, sodium valproate, phenobarbitone and phenytoin.

Tools (Spreen and Strauss 1998 / Lezak 1995)

California verbal learning test

The California verbal learning test (CVLT) is a test which assesses the various strategies, and processes that are involved in verbal learning and memory. The test items consist of two shopping lists for Monday (list A) and Tuesday (list B) respectively which contain 16 items each from four different semantic categories. Two of the semantic categories are the same on both lists, these are the “shared” categories whereas two of the categories are different or “nonshared”.

The Monday shopping word list (list A) is presented over 5 learning trials, each followed by a free recall. The interference list, Tuesday’s list (list B) is presented and followed by a free recall trial, subsequent to which there is a free recall of list A without presentation of the items. After a 20-minute delay, free and cued recall (semantic categories) of list A are followed by a recognition trial (using a yes/no paradigm) of list A items with distracters.

RESULTS

Performance on list learning was poorer in the group with schizophrenia (p<0.01), who showed reduced learning initially till the fifth trial. However, once the material was learnt there was no difference in the scores across two groups. The two groups showed similar performance on delayed recall, cued recall and recognition. The group with schizophrenia showed an improvement on cued recall.

A look at the following test results show clear differences between the two groups on the process of verbal learning. This test is a measure of verbal learning, recall and recognition. There is a significant difference between the groups from the on the 1st and 2nd trial. The Schizophrenia group shows poorer performance than Epilepsy group.

The level of significance is highest at the first trial at 0.01 and comes to 0.05 at trial 4. The fifth trial shows an equalizing in performance. This means that the rate of learning of the E1 is slower than E2.But with repeated exposure they can catch up. The trial B also indicated a significant difference between groups at the 0.05 level.

This could be attributed to the proactive interference effect, which means that old learning hampers the acquisition of new material. The interesting thing here is that once the learning took place and equalized there was no difference between the groups either on recall or recognition.

Thus the process, which discriminated between the two groups the most, was verbal learning. Recent studies of patients with schizophrenia have consistently demonstrated marked deficits on measures of initial learning. When initial learning levels were matched between patients and controls no subsequent drop was found on delayed recall. The initial learning was found to be more impaired than accelerated forgetting as when the effects of learning were matched the differences between groups disappeared. (Gold et al 2000)

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CONCLUSIONS

The group with schizophrenia showed slower learning andpoorer encoding as compared to the TLE group. However once the material was well learnt it was retained, albeit with mild retrieval difficulty. There is difficulty with registration of information but not with retention. Retraining efforts would have to focus on enriching stimuli during encoding. Repetition would be an extremely important tool and providing contextual cues could enhance retrieval.

The general findings can be summed up as: The E1 showed a slower verbal learning rate than the E2 ,the pattern of memory

Table 1 : CVLT scores Schizophrenia ( E1) and Epilepsy (E2) Patients

E1 E2 Mean (SD) Mean (SD) t= p

Trial 1 5.67 1.56 7.92 2.1 3.03 0.01

Trial 2 8.58 1.83 11.23 2.62 2.9 0.05

Trial 3 9.92 2.47 12.38 2.47 2.49 0.05

Trial 4 10.92 2.39 13.08 2.5 2.2 0.05

Trial 5 12.42 3.29 13.77 2.42 1.18 NS

Trial B 4.75 1.42 6.54 1.94 2.61 0.05

Trial 6 10.42 3.25 11.85 4.26 0.94 NS

Delayed Recall 10.92 3.6 12.31 4.42 0.86 NS

Cued Recall 12.08 2.84 12.38 4.57 0.2 NS

Recognition 43.75 3.33 44.15 3.69 0.29 NS

Retroactive interference 2 1.47 1.92 2.46 0.94 NS

Trial

Schizophrenia --- TLE

Scor

e

1614121086420

1 2 3 4 5 B 6

Graph 1 : Verbal learning curve: CLVT scoresin Schizophrenia and Epilepsy CVL scores are displayed on the Y axis.

deficits was similar and both groups are equally susceptible to interference effects.

Implications

The need for rehabilitation is evident for both these groups, people with epilepsy and schizophrenia. Rehabilitation requires human resources and there is a scarcity of resources for such time intensive training. Using two groups like the above studied samples together would be very cost effective. Being similar on so many parameters, it would be beneficial in more ways than one, to train them together. Current rehabilitation attempts are hindered by problems like lack of trained personnel, space

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This would also help larger goals like reducing stigma about each other’s conditions and promoting empathy. A task force with two groups having a common end in mind would be more effective to approach policy makers for changes to be made. Training caregivers too would be an important way to begin to reduce individual burden. The eventual goal would be to identify leaders within the groups to serve as peer counselors, thus reducing dependence on the caregivers.

This would provide much needed relief to them, as the job of a caregiver is a 24-hour job. The Rehabilitation council of India has emphasized the need to focus on groups in need of long-term care. Both the above-mentioned groups fit this profile and using human resources in an optimum way is the key to resolving some part of this concern.

Hence, the implications for Rehabilitation which emerge from this study are as follows:

Considering rehabilitation using both these groups together would be a good idea after keeping a few pointers in mind.

1. Repetition is indispensable

2. Amount of information in a session would be limited keeping in mind the limited memory capacity of the groups.

3. To ensure effective encoding visual aids and other mnemonics be used; special emphasis on mnemonic strategies be used with people with schizophrenia. Maybe training before the actual rehabilitation only for this mnemonic use could be held for them, to make them use these techniques more effectively. Other studies have shown that visual learning is fairly good

4. Short modules with lots of breaks for relaxation should be

planned

5. Feedback after each learning with preferably more memory enhancing tips also to be used

6. Minimal interspersing of new type of material on a single day

7. Rehearsal at the end of every module

Limitations

The sample size in this study was small, since the sample was limited by the matching carried out for demographic variables such as age, gender, educational level, SES etc.

REFERENCES

1. Gold, J.M, Rehkemper, G., Binks, S.W. 3rd., Carpenter, C.J., Fleming, K., Goldberg, T.E., & Weinberger, D.R. (2000). Learning and forgetting in schizophrenia. Journal of Abnormal Psychology. 109(3): 534-8.

2. Gur, R. E., Turetsky, B. I., Cowell, P. E., Finkelman, C., Maany, V., Grossman, R. I., Arnold, S. E., Bilker, W. B., & Gur, R. C. (2000)Temporolimbic volume reductions in schizophrenia. Archives of General Psychiatry. 57: 769-775.

3. Ladavas, E., Umilta, C., Provinciali, L. (1979) Hemisphere dependent cognitive performances in epileptic patients. Epilepsia. 20: 493-502.

4. Lezak, M. (1995). Neuropsychological Assessment. (3rd ed): 445-448. New York, Oxford: Oxford University Press.

5. Spreen, O., & Strauss, E.A. (1998) A Compendium of Neuropsychological tests. (2nd ed). Oxford, U.K: Oxford University Press.

6. Squire, L.R. & Zola Morgan, S. (1991) The Medial Temporal Lobe memory system. Science. 253: 1380- 1385.

Sources of support: Nil Conflict of interest: Nil Shweta Kadaba Ph.D. Clinical Psychologist Anuradha Sovani * M.Phil., Ph.D. Reader, Department of Applied Psychology, University of Mumbai Trustee, Institute for Psychological Health, Maharashtra

Correspondence : Dr. Anuradha Sovani “Om”, 31, Shreesh Society, LIC cross Road, Off Eastern Express Highway, Thane 400 604, Maharashtra, India Phone: 2 5833661 (M) 98210 50528

e -mail: [email protected]

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and finances. Pooling of resources by having two groups like this join up, would therefore be beneficial.



Aripiprazole in Autism

Hemang Shah, G.K.VankarAbstract:

Atypical antipsychotics especially risperidone, olanzepine and clozapine are quite effective in behavioral control as well as for reducing hyperactive symptoms seen in autism. Sometimes these agents are not effective for same purpose. Moreover there is growing concern about serious side effects of these drugs.

We report four children with autism treated with flexible doses of aripiprazole over a period of six months. The change was measured on a clinician rated scale of behavioral symptoms in autism.

Aripiprazole effectively controlled behavioral problems especially hyperactivity, self-stimulatory behavior and sleep problems in this case series. Major advantage of Aripiprazole is minimum side effects.

Key Words: Autism, Aripiprazole

INTRODUCTION

Though the incidence rate for autism is 3 to 4 per 10000 (1) in past the current estimated prevalence of autistic disorder ranging from 0.7 to 72.6 per 10 000(2). Mostly it is associated with behavioral problems and these behavioral problems may lead parents or caregiver to think regarding some thing unusual with their child. The main presentation is usually with abnormal movements: flapping, jumping; less socialization with poor understanding.

Usually the treatment modality includes use of drugs, which control the behavioral problems instead of underlying disorder (3). Because of higher susceptibility for side effects of typical antipsychotics, first choice is Risperidone.(4, 5, 6) . Risperidone is an atypical antipsychotic which calms down the patient and has less side effects than typical antipsychotics(7). A multisided, randomized, double-blind trial of risperidone as compared with placebo for the treatment of autistic disorder accompanied by severe tantrums, aggression, or self-injurious behavior in children 5 to 17 years old was conducted. It concludes that risperidone was effective and well tolerated for the treatment of these behaviors in children with autistic disorder, (risperidone vs placebo, 69% vs 12%) (4). FDA also made new guideline for dosage and administration of risperidone in Autistic Disorder for children between age 5 to 16 years(8).

Aripiprazole is effective in management of schizophrenia with favorable safely and tolerability profile with low potential for EPS, weight gain, prolactin elevation, QT(c) prolongation, and sedation(9). Aripirazole is an atypical antipsychotic having unique mechanism of partial agonist activity at dopamine D2 receptors. It has D2 antagonist activity under hyperdopaminergic conditions, which is believed to be associated with control of psychotic or positive symptoms, and D2 agonist acitivity under hypodopaminergic conditions, which is thought to be associated with improvement of negative symptoms and cognition, and minimal EPS and prolactin changes. It has also potent partial agonist at serotonin 5-HT 1A receptors, and an antagonist at 5- HT2A receptors. Partial agonist activity at 5- HT1A receptors has been linked to anxiolytic action, and may also

be associated with improvement in depressive, cognitive and negative symptoms.

Aripiprazole occupies similar proportion of D2 receptors that of other antipsychotic. Also blocks stereotypy induced by apomorphine as do other antipsychotic. It has also effect of partial agonist at 5 HT1A that can reduce the anxiety symptoms. (10) Autism is frequently manifested by abnormal body movements, repetition, lack of play with other kids, lack of preference for socialization, schizophrenia like symptoms like laughing with out reason, crying without reason, smelling things, as well as anxiety symptoms. Aripiprazole reduces all of these symptoms effectively as determined by a Clinical Global Impressions-Improvement (CGI-I) scale and no significant adverse effects emerged during these short-term trials on five patients (11).

We report four children having diagnosis of Autism as per DSM- IV- TR who were prescribed Aripirazole in flexible doses, after routine investigations. After consent from parent the medication was started.

For better understanding we used a clinician rated scale constructed by us. (Appendix).

The scale is slightly different from routinely used Conner Autism Rating Scale (CARS) (12). CARS is a standardized tool for assessment of severity and treatment response with children with autism. It should be filled after detailed observation of child by the therapist, which required plenty of time. Our scale included items on sleep related problems and laughing and crying spells without reason which are not included in CARS. As the used tool is parent oriented, simplified form of CARS and is to reduce subjective bias by the therapist.

With each item, parents described severity and frequency of the problem or symptoms based on which clinician rated the items. We discussed with parents and assessed each child in detail on every visit to the OPD.

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Here we provide the case summaries .

CASE 1

A male child, aged 5 and half years brought by mother with main complaints of not speaking, not able to understand, hyperactivity, screaming, smelling things, not sleeping till late nights, laughing and crying spells without reason with repetition of particular play several times a day. In his past history he was totally normal up to age of one and half year, at that age he had severe diarrhea and was hospitalized. After that illness he lost all his acquired skill including speech and developed above-mentioned behavioral problems. Parents consulted several psychiatrists and neurophysicians who advised medications including atomoxetine, olanzapine, methylphenidate but without any significant improvement.

He was diagnosed as having autism and given aripiprazole. For initial one month he was given 5 mgs of aripiprazole at bed time. With this, the only significant improvement was in sleep, Smelling things, screaming and repetition of act. After one month the dose of aripiprazole was increased to 10 mgs. More improvement was noticed in hand and body movements, he started playing with other kids and also identifying parents and close relatives after another month.

His follow up was continuous for last seven months and there was some waxing and waning in the symptoms of smelling, the other symptoms are under control and parents were happy with the improvement.

At one time there was salivation with aripiprazole and the dose was reduced to 7.5 mg and added with trihexyphenidyle, but with that the main behavioral problems reemerged and patient was again put on 10 mgs with reassurance and he became fine.

The improvement was minimal in manifestations of speech, understanding of emotions and developmental progress in terms of cognition.

CASE 2

A male child aged 10 years was brought by mother for the complaints of restlessness, delayed development, sleep problem, poor eye contact, not speaking, not playing with other kids. He was diagnosed as autism and aripiprazole was given with 5 mgs per day. After 15 days his sleep became normal, and his restlessness also reduced by 40%.So the dose was increased to 10 mgs. Over next month further improvement was observed in form of restlessness was reduced to 70% and the child started mixing with other children and eye to eye contact improved. To achieve still more response the dose was increased to 15 mg but there was restlessness, and the dose was re adjusted to 10 mgs.

At 6 months of treatment, the improvement was minimal in manifestations of speech, irritability, repetition, understanding of emotions and developmental progress in terms of cognition.

CASE 3

A male child aged 5 years was brought by parents with complains of smelling things, not playing with other kids, not sitting at one place, not recognizing parents, sleepiness in day time. The onset was after fever at 10 months of age. Parents consulted several doctors and the child given variety of medicines but no improvement was noted.

He was diagnosed as having autism with mental retardation and aripiprazole was given in 2.5 mgs per day dose. In first 15 days 25% improvement was reported in restlessness, sleep became normal, occasionally he played with other kids, recognized parents and began to speak monosyllables . The dose was increased to 5 mgs. And after a period of another 45 days further improvement was observed in playing with other kids, improvement in eye contacts, understanding the emotions and marked reduction in the behavior of smelling things.

At 5 months of treatment, the improvement was minimal in manifestations of repetition and developmental progress in terms of cognition. The marked improvement was in smelling things, hyperactivity, speech and play with other children.

CASE 4

A male child aged 9 years was brought by parents with the chief complaints of hand movements, jumping, head movements, restlessness and not sitting at one place, not mixing with other kids, absence of eye contact, not understanding emotions.

As his motor development was normal, he was diagnosed as autism. He was given variety of medication for his behavioral problems including atomoxetine, clonidine, risperidone, and fluoxetine. But none of the medications was effective in reduction of symptoms and had side effects. He was given aripiprazole 5 mgs per day. Some improvement was observed in body movements, hand movements and jumping. Parents reported 30% reduction in hyperactivity. Child started understanding emotions. The dose of aripiprazole was increased to 10 mgs. Further improvement was noted again in movements.

Because of his medical illness i.e. common cold and fever, parents stopped the treatment leading to recurrence of the symptoms. Again aripiprazole was stared and slowly the dose was raise up to 15 mgs. At seven months follow up, he has 50% improvement in movements, restlessness, has improved eye contacts, and stared understating some emotions. However a new symptom emerged after 3 months of treatment. Child cried continuously particularly when forced to go to school. This can be explained by the social anxiety features of autism.

At seven month follow up since aripiprazole treatment, the marked improvement was in head and body movements, restlessness, eye contact and repetition and understanding of emotions. The improvement was minimal in manifestations of self-injurious behavior, speech development, and recognition of family members.

DISCUSSION

Aripiprazole as a novel antipsychotic drug when given to the

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patients having diagnosis of developmental disability(13) and autism with behavioral problems was quite effective in mean dose of 10 mgs per day with effective duration of minimum 4 weeks(9). However the improvement is likely to be reported as the dose and the duration is increased with very minimal side effect like extra pyramidal symptoms.

In these cases the scores ranges from 71, 55, 51 and 61 respectively which reduced to 33, 46, 28 and 47 suggestive of improvement ranges from 23 % to 46 % over a period of average four to six months.

In all of these cases the major improvement is observed in areas of like hyperactivity was reduced, understanding of emotions improved, started playing with other kids and indication for toilet need, stopped smelling things, sleep became regular, while minimal response was observed in the area of speech development and cognitive development.

Further study is needed to corroborate finding of these case series.

Implications for care:

Aripiprazole is effective and well-tolerated drug for behavioral symptoms of autism especially sleep problems, hyperactivity and self-stimulatory behaviors.

REFERENCES

1. Hawline Patricia (1998), Practitioner Review: Psychological and education treatment of Autism, Journal of Child Psychology and Psychiatry, 39: 307-332.

2. Williams J G, J P T Higgins, C E G Brayne (2006) Systematic review of prevalence studies of autism spectrum disorders Arch. Dis. Child. 2006; 91;8-15.

3. .Sloman Leon (1991), Use of medication in Pervasive developmental disorders, The psychiatric clinic of North America, 14, 165-182.

4. Research Units on Pediatric Psychopharmacology Network

(2002). Risperidone in children with autism and serious behavioral problems. New England Journal of Medicine, 347(5): 314-321.

5. Morgan Susan at el. Antipsychotic drugs in children with autism, British Medical Journal; 2007;334:1069-70

6. Riddle Mark et al (2001), Pediatric psychopharmacology, Journal of Child Psycholo. Psychiatry, 42 (1): 73-90

7. Wolraich Mark (2003), Annotation: The use of psychotropic medications in children: An American view, Journal of Child Psychology and Psychiatry, 4: 159–169.

8. Food and Drug Administration. Risperidone labelling. www.fda.gov/cder/foi/label/2006/021444s008s015, 020588s024s028s029, 020272s036s041lbl.pdf

9. Marder SR, et al, (2003). Aripiprazole in the treatment of schizophrenia: safety and tolerability in short-term, placebo-controlled trials. Schizophr Res. 61(2-3):123-36.

10. Van Kammen Daniel P., Marder Stephen R. (2004), Biological therapies: Serotonin dopamine antagonist (Atypical or second generation Antipsychotics). In Kaplan and Saddock (Eds.) Comprehensive Textbook of Psychiatry, Eighth edition, (pp 2914-2938) Philadelphia, Pa. Lippincott, Williams and Wilkins.

11. Stigler KA at el. (2004), Aripiprazole for maladaptive behavior in pervasive developmental disorders J Child Adolescent Psychopharmacology. 14 (3):455-63.

12. Schopler E., Reichler R J.at el.(1980) Toward objective classification of childhood autism: Childhood Autism Rating Scale (CARS). Journal of Autism and Developmental Disorders. 10, 91 – 103.

13. Shastri M, Alla L, Sabaratnam M (2006) Aripiprazole use in individuals with intellectual disability and psychotic or behavioural disorders. : a case series. Journal of Psychopharmacology: On line First, Published On August

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Sources of support: None Conflict of interest: None Hemang Shah MD Assistant Professor G.K.Vankar MD Professor and Head Dept. of Psychiatry, B.J.Medical College and Civil Hospital, Ahmedabad 380016

Correspondence: Dr.Hemang Shah 87 Laxmigruh, Near Mahadev t emple, Char Rasta, Maninagar, Ahmedabad 380008 e-mail: [email protected]

Cell: 09825271454

Appendix :Name of Patient: Age: 1= never2=occasionally (3 out of 10 times)3=usually (5 out of 10 times)4=more than usually (7 out of 10 times)5= always

Table 1 Change in manifestations of Autism with Aripiprazole

Case 1 Case 2 Case 3 Case 4 Main complains 0 28 wks 0 24 wk 0 26 wk 0 28 wkDose of Aripiprazole 2.5mg 7.5mg 5mg 10mg 2.5mgs 5 mgs 5 mg 15 mg

Hand movements, i.e. clapping, flapping 3 2 1 2 1 1 4 2Body movements, i.e. rocking, jumping 3 1 2 2 1 1 4 2Head movements, i.e. banging, 3 1 1 1 1 1 4 2Smelling things 3 3 3 2 3 1 1 2Hyperactivity, restlessness 5 1 5 4 4 3 5 3Sleep disturbances 5 1 3 1 2 1 1 1Self injurious behavior 1 1 3 2 1 1 3 3Not Playing with other kids 5 2 5 4 5 3 5 4Irritability, aggression 1 1 3 3 1 1 2 4Less Developmental progress 5 3 4 3 4 3 5 3No Eye contact 4 1 5 3 2 1 5 3Shouting, screaming 5 1 2 2 2 1 1 2Repetitions of movements 4 1 5 4 1 2 4 2Perfections 1 1 1 1 3 1 1 1Speech developmental problems 5 5 5 5 4 2 4 3No Understanding emotions 5 3 2 2 4 2 5 3Not Recognize parents, caretakers, relatives 5 2 2 2 1 1 5 4Laughing spells 4 2 1 1 1 1 1 1Crying spells 4 1 2 2 1 1 1 2

Total score 71 33 55 46 51 28 61 47

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Case Report

Schizotypal Personality Disorder: a diagnosis often missed

Bimal Tamakuwala, Parag Shah, Kamlesh Dave, Ritambhara Mehta

Abstract

Personality disorders are interesting psychiatric entities that merit special clinical attention. In psychiatry clinics, majority of the cases with personality disorders are either undiagnosed or misdiagnosed. Here is a case of a person presenting with features of schizophrenia spectrum disorders, diagnosed as Schizotypal Personality Disorder and treated with psychotherapy as mainstay of treatment along with low dose antipsychotics.

Key words: Schizotypal personality disorder, Schizophrenia spectrum disorders

INTRODUCTIONThe essential feature of Schizotypal Personality Disorder (StPD) is ‘a pervasive pattern of social and interpersonal deficits marked by acute discomfort with, and reduced capacity for, close relationships as well as by cognitive or perceptual distortions and eccentricities of behavior’1. Schizotypal Personality Disorder (StPD) which is found in 3% of population is characterized by magical thinking, peculiar notions, ideas of reference, illusions, derealization, vivid imaginary relationships and child like fears and fantasies. It is a chronic condition which typically begins in early adulthood and endures throughout life. StPD is often difficult to differentiate from Schizoid and Avoidant Personality Disorder but is diagnosed on the basis of oddities in the behavior, thinking, perception and communication and a family history of schizophrenia1. Although StPD and Schizophrenia belong to the same group ‘Schizophrenia spectrum disorders’ the former differs from the later by absence of psychosis. While schizotypal personalities may experience brief psychotic episodes with delusions or hallucinations, they are not as pronounced, frequent or intense as in schizophrenia. Retrospective studies show that many patients thought to have schizophrenia actually had StPD1. Here by, we present a case which was earlier diagnosed as Schizophrenia, but finally turned out to be StPD and with appropriate therapy showed improvement.

CASE REPORT

A 30 years old hindu male, working off and on in a power-loom factory and belonging to lower socio-economic class presented with complaints of involuntary movements of cheeks, eyes, ears, nose and other facial structures with rotatory movements of body from waist and neck region for last 10 years. He also had complaint of hearing ‘Classical Music’ at workplace along with the power-loom machinery noise, which made him unaware of surrounding and caused disturbances in work for last 15 years. He also complained of nervousness and anxiety in social settings and he avoided social occasions. He reported that he had a ‘sixth sense’ and got vision of future events. He used to remain in fantasies about few women taking very good care of him and he desired for considering them as mother and sisters. He reported that all these problems were present from his early adolescence and his major concern and

reason for psychiatric contact was that he was not able to work properly. He believed that he may be having mental illnesses like schizophrenia, hysteria, OCD or depression as he had read several magazines with descriptions of mental illnesses. He had history of consultation with several psychiatrists and all of them had diagnosed him of having Schizophrenia and treated mainly with typical or atypical antipsychotics with poor response.

He had studied up to 7th Standard. At the age of 13 years he left his home-town without telling his parents and started working (although irregular) at Bombay. After few years he had a wish to restart his studies but his father did not agree. He reported that he was not having friends in his school or close relationships in any social settings and that others perceived him as odd and strange. Since his adolescence he had decided not to marry in spite of being asked frequently by parents, for no obvious reason. Since then he was living alone, his mother and sisters had come in contact with him for a very brief time during his entire life time. His father who died before 8 years was very authoritarian. . He said that his parents considered him as a burden and useless person for the family.

On mental status examination, patient had a low volume stuttering speech and was anxious about his physical symptoms. Though there were no noticeable involuntary movements on examination, patient insisted on having them around the eyes, and said people notice the changes in his eyes. He chuckled at times, which was not appropriate to the situation. On asking he said he gets funny thoughts so he laughs. Unusual perceptual experiences and referential ideas were elicited. Detailed interview of the patient revealed his odd thinking patterns, fantasizing whenever in stress, dissatisfaction for self worth and an introvert personality with cold emotional tone.

Intensive interviews using IPDE (ICD-10 International Personality Disorder Examination, 1997) and DSM IV criteria as well as Zimmerman’s positive and negative questionnaire for StPD were carried out. Inspite of multiple requests, patient disagreed repeatedly with the idea of calling relatives from his

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distant hometown and came for consultations alone. The patient was in contact with the authors for one year and contents of history and examination remained very consistent throughout the period. In medications, low dose antipsychotics were given. Long-term management involved psychotherapy dealing with issues like emotional instability, lack of ability to maintain long-lasting relationships, magical thinking and cognitive dysfunction; along with a friendly and supportive relationship with the patient. The patient maintained some rapport despite psychopathology and continued with psychotherapy sessions for almost a year with mild improvement.

DISCUSSION

The unusual perceptual experiences, magical thinking, ideas of reference, odd thinking and speech, peculiar behaviour, lack of close friends and excessive social anxiety in this patient fulfilled the diagnostic criteria for StPD. The abnormal involuntary movements were part of StPD. Force and variability of motor response in StPD is related to the positive and negative symptoms and is associated with increased salivary cortisol2. Patient’s fantasies revealed a wish to have supportive, soothing and pleasant relations with his own sisters and mother and fantasies were thus used as a defense mechanism. He never reported of having heard any voices, and the musical illusions he said were not his major problems nor did they appear to be basic psychopathology. There were no clear cut episodes of positive symptoms like delusions or hallucinations as seen in schizophrenia or deterioration severe enough to meet criteria for schizophrenia. On the other hand patient fulfilled all the criteria required to diagnose Schizotypal Personality Disorder according to DSM IV diagnostic criteria.

Biological markers in StPD like genetic, cognitive, biochemical, electrophysiological and organic markers are suggestive of links with schizophrenia3. From biological and clinical data schizoid personality disorder and schizotypal personality disorder are included in schizophrenia spectrum disorders and thus related to Axis I disorders4. But even then, pharmacotherapy

(e.g. neuroleptics and antidepressants) has its limited role in management of StPD. Psychopharmacological treatment may be directed to dimensions that underlie the personality: cognitive/perceptual organization (low-dose antipsychotics); impulsivity and aggression (serotonin blockers); affective instability (cyclic antidepressants or serotonin blockers); and anxiety/inhibition (serotonin blockers and MAOI agents). Individuals with StPD may get help from low dose neuroleptics, reducing the tendency to blame others, unwarranted suspicion, outbursts of rage, and repeated interpersonal conflict. However, these individuals are inclined to experience medication as causing odd side effects and compliance is usually a problem. While on the other side, StPDs are most often wrongly diagnosed as having Schizophrenia and treated thus. It results into patient’s continuing complaints and the treatment for years without much gain.

This case emphasizes the importance of detailed and thorough interview for the accurate diagnosis of Schizotypal personality disorder. Otherwise diagnostic errors can occur.

REFERENCES

1. Sadock BJ, Sadock VA, editors. Kaplan & Sadock’s Synopsis of Psychiatry. New York: Lippincott Williams & Wilkins; 2003.

2. Neumann CS and Walker EF. Motor dysfunction in Schizotypal personality disorder. Schizophrenia Research 1999;17:38(2-3): 159-68.

3. Ajamieh A, Ansseau M. Biological markers in schizotypal & borderline personality disorder. Encephale 2000;26(6):42-54.

4. Sass H , Junemann K. Etiological and therapeutic aspects of Schizotypal personality disorder. Fortschr Neurology and Psychiatry 2001;69 Suppl 2:120-6.

Sources of support: None Conflict of interest: None Parag Shah, Assistant Professor Bimal Tamakuwala, Resident Ritambhara Mehta, Professor and Head Kamlesh Dave, Associate Professor Govt.Medical College and New Civil Hospital, Surat

Correspondence :

Dr.Parag Shah, A-404, Jeevandham Towers, Nr. Bimanagar, Satellite Road, Ahmedabad – 380 015

Cell : 094261 38318 e-mail: [email protected]

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Case Reports

Tardive Dystonia: Two cases

Sachin K. Sinha, Ramesh R. Parmar, Mukesh J. SamaniABSTRACT:

Tardive dystonia is a rare movement disorder. It has been reported in association with the use of neuroleptics. We report two cases of tardive dystonia with features of opisthotonus and sidewards bending at the axial level. The response to clozapine and clonazepam in these cases has been discussed.

Key Words: Tardive Dystonia, Tardive Dyskinesia, clozapine, clonazepam

INTRODUCTION:

Tardive dyskinesia is a well known and much dreaded side effect of typical antipsychotic drugs. It presents with more axial than appendicular involvement. Tardive dystonia is much rarer and not so well recognized side effect. It is important to be aware of occurrence of tardive dystonia because it has poorer outcome than tardive dyskinesia. Keeping this in mind and to highlight different outcomes, we report these cases.

Following the introduction of .dopamine receptor antagonists, several authors reported patients who developed chronic, persistent dystonia after treatment with these drugs, but such cases were included under tardive dyskinesia. In 1973, Keegan and Rajput first reported a female patient with torticollis and retrocollis and introduced the term ‘dystonia tarda’.

Although tardive dystonia is defined as sustained muscle contraction that develops following at least one month of antipsychotic treatment, usually tardive phenomenon develops months to years after exposure to this class of drugs.

Tardive dystonia can be differentiated from idiopathic dystonia by improvement with voluntary movement and a combination of retrocollis, arching backwards and internal rotation of arms with extension of the elbows and flexion of the wrist.

CASE 1

A 28 year old Hindu female patient suffering from schizophrenia since 1999 received various traditional and atypical antipsychotics since 2003 in moderate therapeutic doses. She had only moderate improvement with any drug. There was no further improvement so she was given injection zuclopenthixol depot. She developed rigidity and gait impairment in few months which gradually worsened and within one year she developed severe rigidity with body’s upper half arched backwards (opisthotonus). She was brought to Civil Hospital, Rajkot where she was diagnosed as a case of tardive dystonia by one of the authors (MJS). All the ongoing antipsychotics were stopped and patient was put on clozapine. The dose was gradually titrated to 100 mg/day. Tocopherol was also added. In six months, patient showed improvement in rigidity and she was able to walk and sit without support. Now, after two years of clozapine and tocopherol she is better with no psychotic symptoms and is able to work and sleep comfortably. Few months back clonazepam was added to

clozapine and tocopherol was stopped. Patient showed more than 90% improvement in two months.

CASE 2

A 30 year old male patient suffering from schizophrenia since five years was on various traditional and atypical antipsychotics since the onset of his illness. He always improved markedly with drugs but he used to stop the ongoing drugs on his own. One year back while on 4 mg risperidone, he developed pleurosthotonus towards right side. He stopped drugs on his own and recovered fully in one month but his psychotic symptoms worsened. He was again prescribed 15 mg of olanzapine. His psychotic symptoms improved but in one month or so he again developed pleurosthotonus towards the right side which was diagnosed by one of the authors (RRP). He was admitted in the psychiatry ward where olanzapine was stopped and patient was put on clozapine with gradual dose titration to 300 mg/day. His rigidity improved fully within a month and his psychotic symptoms also improved. He even started to work in few months. Now after nine months he has no psychotic symptoms.

DISCUSSION:

Mean age of onset reported is 38.3 years (Kiriakakis et al 1998). Both of our patients also developed tardive dystonia at or near the age of 30 years. Kiriakakis et al (1998) showed that cumulative percentage of patients developing tardive dystonia after receiving dopamine receptor antagonists increased linearly with age. In men, the mean age of onset was 33.5 years. In women, the mean age of onset was 43.7 years. Prevalence of tardive dystonia in men and women was found to be 1.2:1.

Complication such as tardive dystonia is very rare in the treatment with both typical and atypical antipsychotics.Chakraborty and Chand (2002) have shown that lithium can also cause tardive dystonia. Recovery in such cases may depend on the early detection as found in our male patient who recovered spontaneously in one month after stopping the ongoing antipsychotic. With clozapine, there was no relapse of tardive dystonia in this patient. But the female patient whose dystonia was recognized one year after the onset the improvement was gradual and delayed , not more than 80%

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for long time. Addition of clonazepam to clozapine in this patient led to further improvement in two months.

Shapleske, Mickey et al (1996) in their case series found that clonazepam when used as an adjunct to clozapine led to greater improvement than clozapine alone.

Tetrabenazine and reserpine can be used in the treatment of tardive dyskinesia as well as tardive dystonia with good results .They control the psychotic features as well.

Another strategy employs GABAergic medications such as baclofen, clonazepam or valproic acid which is particularly useful in patients with tardive dystonia when used along with botulinum injections (Mahlon and Jorge (2005))

REFERENCES:

1. Goetz CG, Horn S. Tardive Dyskinesia. In. Watts RL, Koller WC (eds.) Movement disorders: Neurologic Principles and Practice 2nd edition New York: McGraw Hill Medical Publishing; 2004: 629 - 637.

2. Kang VJ, Burke RE, Fahn S. Natural History and Treatment of Tardive Dystonia. Move Dis.1986; 1:193- 208

3. Jankovic J, Beach J. Treatment of dystonia. In: Watts RL, Koller WC (eds.). Movement disorders: Neurologic Principles and Practice 2nd edition New York: McGraw Hill Medical Publishing; 2004: 527 - 539.

4. Jankovic J., Orman J. Tetrabenazine therapy of dystonia, chorea, tics and other dyskinesias. Neurology 1998;38: 391-394

5. Shapleske J., Mickay P., et al. Successful treatment of tardive dystonia with clozapine and clonazepam. British Journal of Psychiatry 1996 Apr; 168(4): 516-518

6. Mahlon R., Jorge L., Parkinson’s disease and other movement disorder. In.Kasper D., Fauci A.,Longo D.,Braunwald E., Hauser S.,Jameson J.(eds.) Harrison’s Principles of Internal Medicine 16th ed.New York:McGraw Hill; 2005:2406-2418

7. Kiriakakis V., Bhatia K., Quinn N., Marsden C.Natural History of Tardive Dystonia: A long term follow-up study of 107 cases Brain 1998; 121(11):2053-2056

8. Chakraborti S., Chand P. Lithium induced Tardive Dystonia. Neurology India 2002; 50(4):473-475

Sources of support: None Conflict of interest: None Sachin K. Sinha, Resident* Ramesh R. Parmar, Resident Mukesh J.Samani , Professor and Head Dept.of Psychiatry Deen Dayal Upadhyay Medical College, Rajkot

*Correspondence

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Letter to the editor

ECT is effective not only when it is adminis-tered but also when merely recommended !Sir,Case 1 A 52-year-old male patient having recurrent depression since last 8-10 years was brought with one more episode of depression for last 3 months n ot responding to escitalopram (20 mg/day), reboxetine (8 mg/day) and lithium (900 mg/day). Apparently, previous episodes, which used to occur at a frequency of once in 2 years to 2 episodes in a year, had shown either spontaneous remission or had responded to antidepressant therapy in 6 to 8 weeks period. But this time, in spite of regular medication for 3 months patient had persistent symptoms of retarded form of depression and was unable to go out home for work or any other recreational purposes. In view of this, the option of ECT was explained and recommended and patient was called for ECT a day-after with the required investigations. On the day of ECT, relatives happily called up to cancel the appointment as patient started going to work from the very next day. On subsequent follow-ups over next 3 months, it was observed that the sudden improvement in the symptoms which was observed on recommending ECT was maintained and patient showed remarkable improvement in the other symptoms of depression as well.Case 2 A 24-year-old female patient having post-psychotic depression, was brought by her parents as she was irregular at her college since last 2 months and had stopped going to college altogether for last 2 weeks. According to the patient, since last 2 months, she was feeling very sad and depressed, did not feel like going to college, was unable to concentrate at her studies and had lost confidence that she would be able to appear and pass her upcoming exams. In spite of adding sertraline (200 mg/day) and venlafaxine (225 mg/day) to maintenance Risperidone therapy, even after 2 months, her depressive symptoms had persisted. In view of her upcoming exams a week later, the option of ECT was explained and recommended. The patient and her parents appeared reluctant for ECT and decided to wait for a couple of weeks more before considering this option. On next follow-up after 15 days, it was learnt that a substantial improvement was observed in the patient’s symptoms after the recommendation for ECT. The patient started going to college, appeared in the exam and secured highest marks in one of the practical exams! Placebo effect is very well known with the drug treatment. Response rate with placebo has been reported to be as high as 30-40% in some drug trials. Placebo literally means ‘I please you’. The very fact that some medication is given to the patient, itself brings about improvement in symptoms. In the above reported cases there is similar phenomenon, but in stead of ‘I please you’ it is ‘I scare you’ a ‘scarebo effect’ which is evident. Due to wrong ideas associated with ECT, such as it is a ‘shock therapy’ and may be very painful and ghastly, many of the patients and their relatives are scared, frightened and reluctant

of ECT. Ironically, this faulty attitude towards ECT may be unintentionally gets exploited when ECT is recommended and some patients may show a substantial improvement in their symptoms when ECT is merely recommended.

Dr. Nilesh Shah Professor, Department of Psychiatry, L. T. M. Medical College & General Hospital, Sion, Mumbai 400 022

Being cautious about using spirituality as a psychiatric treatment tool Sir, Quite some emphasis was put on spirituality and its use in psychiatric practice in the last issue by Dr. Mrugesh Vaishnav[1], Dr.Russell F. D’souza[2].

The efforts to make it more scientific and give it a place in the academics are commendable but I would like to make a few points about it. Spirituality is such a wide, all encompassing subject with no rules as to what is right or wrong, that it cannot be tied down to rules or words or scores and scales. It has a different meaning for each individual-if one has thought about it, if one has understood oneself, if one is mature enough to be clear about it. Moreover, there can be no argument over it; one simply has to “BELIEVE”. It is such a potent weapon if in the right hands who know how to apply it on whom because it necessarily has to be tailor made for each individual, by each individual and let me tell you it is in practice since time immemorial. But in the wrong hands, who only half understand it, who would wrongly apply it to the wrong candidate; it is a potently and potentially destructive weapon. Youngsters having a psychotic breakdown after getting intensely involved with one or the other Guru/Cult/Ashrams, are examples of this. So, sir, I feel that it is imperative that these factors be kept in mind while championing for spirituality as a psychological treatment tool for one and all. Not that it shouldn’t be, it must be-its parallel use gets results where all else has failed, it is the end-answer where all questions stop and one cannot have a holistic approach while excluding it but its judicious use is something that all of us need to work upon.

Dr. Minakshi Parikh Associate Prof. of Psychiatry B. J. Medical College, Ahmedabad-380016, India E-mail: [email protected] 1. Mrugesh Vaishnav. Spirituality & Psychiatry-

complimentary or contradictory? Archives of Indian Psychiatry 2006; 8(1):1-9

2. Russell F. D’souza. The Spirituality Augmented Cognitive Behavioral Therapy-A meaning therapy for sustaining mental health and functional recovery. Archives of Indian

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QuizFill in the Blanks1. King George suffered from which _________________disease ?2. According to Emil Durkheim ,an unmarried man ,prone to commit suicide is an example of _____________

suicide.3. The author of The book “Sanity,madness and the family” was ___________.4. Schizophrenia is caused by early interpersonal difficulties especially faulty, overanxious mothering. This is the

concept of ___________________________.5. Denial of hemiparesis is called______________________.6. A debilitating cycle of “yuns” and “crushes” is a common pattern of _________________.7. “Haptic hallucination” is ___________________.8. “Ailurophobia” is__________________________.9. _______________________ wrote the book “Anatomy of Melancholy” in 1621.10. “Unipolar depression” was described by______________________.11. ___________________ described “thought disorder” 12. Ribot’s law is______________________________________________________.13. D2 blockade by antipsychotics in tuberoinfundibular areas causes_____________.14. 330(2) Cr PC deals with _____________________________________________.15. deja entendu is____________________________________________________ .16. Partialism is_______________________________________________________ .17. “Floccillation” is___________________________________________________ .18. ______________________ is the author of Brief Psychiatric Rating Scale (BPRS).

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Contributor:Dr.T.AsokanAssistant Professor of PsychiatryInstitute of Mental HealthChennai 600010e-mail:[email protected]

59


Written after remission from an acute episode of Psychosis this poem vividly brings to life the anguish that the patient experiences in the pursuit of an increasingly elusive hope in a world that is becoming increasingly unreal. She describes about her life being enslaved and captivated by the dreadful disease. Getting affected at such a young age makes her life full of despair and hopelessness. She narrates about her efforts to remain functional in spite of incapacities and the need to seek help. She feels that destiny has been cruel to her, that just when the life was about to begin, she succumbed to the illness and was devoid of fulfilling her dreams and living a happy life. The title ‘Freedom’ denotes her wish to get her heart free from the pain and misery of the illness she suffers from.The 32 years woman is suffering from Undifferentiated Schizophrenia since last 8 years. She has stood among top 10 winners in the world in Global Essay writing competition for mentally ill patients in 2005. She has written several poems and essays, before as well as after suffering from the disorder

Commentary

Dr. Parag Shah MD,Asst.Prof. of Psychiatry Medical College Vadodara e-mail: [email protected]

Poetry

Freedom

My little heart, biting heart,Peeps n skips in nature’s part Where are you? Oh! my tottling tot! Freedom of knot.I wondered for you, for penny denied, in spite fragile tries, for food rotted, in spite ploughed & harvested, for roof tossed, in spite walls tokenedSo to rest in bind hoop, for home to find.I wondered for you, for mount melted, before I climbed, for storm flew, before silt settled, for rain wondered, before earth appearedSo to rest in eyes keen, for destiny seen.I wondered for you, lit a little, though you are blind, sing a little, though squeezed throat side by side, fly a little, though chained and sickledSo to rest in art, for melodial light apart.My little heart, biting heart,Peeps n skips in nature’s part Which way are you? Oh! my tottling tot! Freedom of knotI wondered for you, in toppled leaves, for coffin’s cover in crusty night, for lighting life in rainbow arc, for skipping skySo to rest in calm, in your palm.I wondered for you, in meadows, for your shadow, in sea shores, for your roars, in blue sky, for your wings flySo to rest in ecstasy, in thunder night.I wondered for you, to rid off, starry hell, that hooks my, every shell, to rid off, thorny days, that pokes my, happy ways, to rid off, weary life, that shook my, little joy for every whileSo to rest in “U” oh my freedom, I cried n cried.My little heart, biting heart,Peeps n skips in nature’s part Where are you? Oh! my tottling tot! Freedom of knot.

Anonymous

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Obituary

Dr. Nalinkant S. Vahia(1916-2007)

From rural Gujarat came a son of a postmaster,To be fondly called later by his students as Vahia Master.

For medical education, Dr.Vahia walked into Bombay city,Wearing spotless white attire and admirable simplicity.

Patients having symptoms but no signs made him ponder,Noyes and Kolb inspired him to solve this wonder.

After stint at Haffkine Institute as a research officer,He flew out to Connecticut, USA, with help of a well-wisher.

In August 1948 this young man set up at KEM Hospital Dept. of Psychiatry,And lived long enough to see it grow into a gigantic tree.

Patient care was always close to his heart,While teaching, he developed into a fine art.

Courtesy and manners took the centre stage,When the subject of psychiatry was considered a craze.

Humility and coolness he converted into power,Students and colleagues getting astonished at this tower.

Research on meditation he carried out with scientific dedication,For this he got from here and abroad lot of admiration.

Presidentships and honours came his way,Glamour and showmanship he kept at bay.

With wit and humour that is very subtle,Mr.and Mrs.Vahia made a complementary couple.

He has spent major period of life in Psychiatric den,Being blessed with brilliant and successful sons and grandchildren.

To work day and day out was his trend,And he kept up the show till the very end.

A voracious reader keeping knowledge up to date,In unison all his students proclaim, ‘Sir is great!’

Dr.J.S.Apte, Mumbai

61

Archives of Indian Psychiatry April 2007

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