Facial pain non odontogenic causes-part1

FACIAL PAIN-NON ODONTOGENIC FACIAL PAIN-NON ODONTOGENIC CAUSESCAUSES

Prof. A.V. SRINIVASAN,MD, DM, Ph.D, D.Sc(hon)F.A.A.N, F.I.A.N.

Emeritus Professor

The Tamilnadu Dr. M.G.R. Medical University

Former Head

Institute of Neurology, Madras Medical College

Prof. A.V. SRINIVASAN,MD, DM, Ph.D, D.Sc(hon)F.A.A.N, F.I.A.N.

Emeritus Professor

The Tamilnadu Dr. M.G.R. Medical University

Former Head

Institute of Neurology, Madras Medical College

Ragas dental college-7-09-11

Understanding, Impact and Understanding, Impact and AwarenessAwareness

Facial PainFacial Pain

We learn by thinking and the quality of the learning outcome is determined by the quality of our thoughts

R.B. Schmeck

“Pain May be Inevitable, but Misery is Optional”

Dee Malchow

Pain constitutes nearly 40% of the total of patient visits to doctors.1

1 Mäntyselkä et al. Pain as a reason to visit the doctor: a study in Finnish primary health care. Pain. 2001 Jan;89(2-3):175-80.

“By Nature All Men/ Women are alike butby Education widely different”

- Chinese

Pain is undertreatedPain is undertreated In 2001, Barry Furrow wrote “Pain is undertreated” in the American health-care

system at all levels.2

The term "opiophobia" has been coined to describe this remarkable clinical

aversion to the proper use of opioids to control pain.

The possible reasons for health-care providers' failures to properly manage pain are

many;

– Occasional lack of knowledge about appropriate treatment choices for pain

management

– A reflection of a Culture hostile to drug use

– Threats of legal action.

– Worry about tolerance and addiction and other adverse drug effects

– Something as trivial as the lack of insurance cover, can lead to patients

suffering unnecessary pain as a result.2. R.M. Marks and E.J. Sachar, "Undertreatment of Medical Inpatients with Narcotic Analgesics,"Annals of Internal Medicine, 78 (1973): 173.

Indian ScenarioIndian Scenario Despite an essentially stoic and less demanding Indian patient; the

obligation to manage pain comes to the fore not only to complete the

perfection of a clinicians management.

But also, it is an independent entity with physical and psychological

components that in adherence to best practices can neither be ignored nor

treated such that adverse effects eclipse the malady.

This importance of pain management is further increased when benefits for

the patient are realized,

– Early mobilization which tends to prevent the more dangerous

complication of a deep vein thrombosis;

– Shortening hospital stay

– Reducing costs

Decade of Pain Control and ResearchDecade of Pain Control and Research

In late 2000, US Congress passed into law a provision, which the president signed , that declared the 10 year period beginning Jan 1st 2001, as the Decade of Pain Control and Research.

The American Pain Society has actively supported the Decade of Pain Control Research, and it has been a focal point for the development of numerous programs to advance awareness and treatment of pain and funding for research.

What is Pain?What is Pain?• Pain is always a subjective experience

• Everyone learns the meaning of “pain” through

experiences usually related to injuries in early life

• As an unpleasant sensation it becomes an emotional

experience

• Pain is a significant stress physically, emotionally

(American Society of Anesthesiologists, 2002; Loeser et al, 2001; Merskey H et al, 1994; Portenoy et al, 1996)

The International Association for the Safety of Pain (IASP) defines pain an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage, or both.

Qualities of PainQualities of Pain Organic vs. psychogenic Acute vs. chronic Malignant or benign Continuous or episodic

Perceiving Pain• Algogenic substances – chemicals released at the site of the injury

• Nociceptors – afferent neurons that carry pain messages

• Referred pain – pain that is perceived as if it were coming from somewhere else in the body

Acute vs. Chronic PainAcute vs. Chronic Pain

ACUTE CHRONIC

Function To warn None (destructive)

Etiology Usually Clear Complex/obscure

Pt. Mood Anxiety/fear Depression/anger

MD impact Comforting Frustrating/draining

Role of Rx Control/cure Improve function/QOL

Categorization of Chronic painCategorization of Chronic pain

Types of PainTypes of Pain

Pain arising from pain receptors

[Nociceptive Pain]

Pain arising from pain receptors

[Nociceptive Pain]

(Psychogenic)

Pain with NO apparent cause(e.g. Low back pain or some

pelvic pain in women)

(Psychogenic)

Pain with NO apparent cause(e.g. Low back pain or some

pelvic pain in women)

Pain arising from Nervous system[Neuropathic Pain]

Pain arising from Nervous system[Neuropathic Pain]

Central(Brain and Spinal cord)

Central(Brain and Spinal cord)

Peripheral (Peripheral nervous

system)

Peripheral (Peripheral nervous

system)

Superficical / SomaticSuperficical / Somatic Deep / VisceralDeep / Visceral

Keay, KA; Clement, CI; Bandler, R (2000). "The neuroanatomy of cardiac nociceptive pathways". in Horst, GJT.  The nervous system and the heart. Totowa, New Jersey: Humana Press. p. 304

Different types of painDifferent types of pain

Nociceptive descriptors Neuropathic descriptors

Cramping, tender Shooting

Gnawing, heavy Hot-burning

Aching Sharp

Splitting Stabbing

Multidimensional Classification of Pain Multidimensional Classification of Pain

IASP (International Association for the Study of Pain) expert multi-axial classification of chronic pain

Axis I: Anatomical location Axis II: Systems Axis III: Temporal Characteristics (intermittent, constant, etc.) Axis IV: Patient’s Statement of Duration/ Intensity / severity Axis V: Etiology Example:

Mild post-herpetic neuralgia of T5 or T 6; 6 months’ duration = 303.22e

Axis I: Thoracic regionAxis II: Nervous system (central, peripheral, or autonomic); physical

disturbance/dysfunctionAxis III: Continuous or nearly continuous, fluctuating severityAxis IV: Mild severity of 1 to 6 monthsAxis V: Trauma, operation, burns, infective, parasitic (one of these)

(Loeser et al, 2001; Merskey et al, 1994)

Dimensions of Chronic PainDimensions of Chronic Pain

Loneliness

HostilitySocial

Factors

Anxiety

DepressionPsychological

Factors

Pathological ProcessPhysical

Factors

TIM

E

A.G. Lipman, Cancer Nursing, 2:39, 1980

Chronic pain has a psycho-

social component that must

be dealt with before

depression becomes a part of

the clinical picture. Chronic

pain should be recognized as

a multi-factorial disease state

requiring intervention at

many levels.

Pain: Social and Psychological FactorsPain: Social and Psychological Factors

Chronic pain has high co-morbidity– Depression– Anxiety disorders– Sleep disorders

All diminish function and quality of life Addressing these issues is essential to optimal pain

management

Give us the GRACE to accept with serenity the things that cannot be changed the COURAGE to change the things that should be changed and the WISDOM to know the

difference

Current Understanding of PainCurrent Understanding of Pain

Chronic pain is NOT a normal part of aging. Emotions play a key role in painful experience Pain sounds a warning, signaling damage to tissues, and has survival value so pain receptors do not adapt

to prolonged stimulation and pain sensation may intensify as pain thresholds are lowered by continued stimulation.

The 19th Century viewed pain as a solely physiological entity with two theories dominating – the “specificity” & the “summation” theories. 8

Paradigm Shift: – Pain perception impulses are modified by ascending and by descending pain-suppressing systems

activated by various environmental and psychological factors. – 1965 Melzack & Wall: Gate Theory of Pain marked a turning point in understanding transmission

and modulation of nociceptive signals, and recognition of pain as a psychophysiological phenomenon.

The concept of Neuroplasticity was recognized and accepted adding dynamism to neuronal & brain structure with neuroimaging of the central nervous system in three domains; anatomical, functional, and chemical imaging helping measure changes in chronic pain.

Taken together these three domains have changed our thinking on pain; now considered an altered brain state in which there may be altered functional connections or systems and components of degenerative aspects of the CNS. 9

8) 11. J.A. Paice, C. Toy, and S. Short, "Barriers to Cancer Pain Relief: Fear of Tolerance and Addiction," Journal of Pain and Symptom Management, 16 July 1998): 1-9.9) Quick Reference Guide for Clinicians No. 1a. AHCPR Publication No. 92-0019: February 1993

Understanding Pain Understanding Pain PathophysiologyPathophysiology

What causes pain?What causes pain?

Trauma/ injury initiates immediate nerve impulses to brain

Injury to cells result in chemical release H+

K+

Substance P Bradykinin 5HT Phospholipids Prostaglandins

Blood vessels leak resulting in inflammation

Stimulate C-fibres (slow response)

Peripheral and Central Pathways for PainPeripheral and Central Pathways for PainAscending TractsAscending Tracts Descending TractsDescending Tracts

Cortex

Midbrain

Medulla

Spinal Cord

Thalamus

Pons

(Brookoff, 2000)

Pain PathwayPain Pathway

Nerve FibresNerve Fibres

( A delta) Myelinated Fast conductors Gentle pressure and pain

(A beta) Thinner – but still

myelinated Fast conductors Heavy pressure &temp

C - very thin Slow conductors PAIN, Pressure, temp &

chemicals

Pathophysiology of Chronic PainPathophysiology of Chronic Pain

In chronic pain, the nervous system remodels continuously in response to repeated pain signals

– nerves become hypersensitive to pain

– nerves become resistant to anti-nociceptive system

If untreated, pain signals will continue even after injury resolves

Chronic pain signals become embedded in the central nervous system

(Marcus, 2000)

Pain-Sensing System in the Malfunction in Chronic Pain

(Illustration: Seward Hung, 2000)

Acute pain:

Pain-sensing signals are initiated in response to a stimulus

• They elicit a pain-relieving response

Chronic pain:

Pain signals are generated for no reason and may be intensified

• Pain-relieving mechanisms may be defective or deactivated

Pain Sensing

In chronic pain, pain signals are generated without physiologic significance

Role of Serotonin and NorepinephrineRole of Serotonin and Norepinephrine

Reticulospinal fibers from raphe nuclei project to dorsal horn of spinal cord and release serotonin which stimulates interneurons to release enkephalin

Enkephalin inhibits transmission of pain and temperature signals in second order neurons

Reticulospinal fibers from locus coruleus also project to dorsal horn of spinal cord and release norepinephrine which inhibits pain and temperature signals by an unknown mechanism

Mental illnesses such as depression decrease serotonin and norepinephrine and lower pain thresholds while antidepressant drugs and therapies (e.g., exercise) which increase serotonin and norepinephrine levels raise pain thresholds

Pathophysiology of PainPathophysiology of Pain

Inferred from characteristics, etiology or pathophysiology

Types

– Nociceptive

– Neuropathic

– Idiopathic

Therapeutic implications

(Portenoy et al, 1996)

Nociceptive PainNociceptive Pain

Presumably results from ongoing activation of primary afferent neurons responding to noxious stimuli Pain consistent with degree of tissue injury

Described as aching, squeezing, stabbing, throbbing

Subtypes:

– Somatic: related to activation of somatic afferent neurons

– Visceral: related to activation of visceral afferent neurons

(Loeser et al, 2001; Portenoy et al, 1996)

Neuropathic PainNeuropathic Pain

Initiated by a primary lesion in the nervous system; believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system

Independent of obvious ongoing nociceptive activation

Burning, shooting, electrical quality; may be aching, throbbing, sharp

Subtypes:

– Presumed “central generator” deafferentation pain (central pain, phantom pain) Sympathetically-maintained pain

– Presumed “peripheral generator” Polyneuropathies and mononeuropathies

(Portenoy et al, 1996)

Idiopathic and Psychogenic PainIdiopathic and Psychogenic Pain

Idiopathic Pain

Usually exists in the absence of an identifiable physical or psychologic pathology that could account for pain

Uncommon in patients with progressive illness

Psychogenic Pain

Presents positive evidence of a predominant psychologic contribution and may be labeled with a specific psychiatric diagnosis

(Loeser et al, 2001; Merskey et al, 1994; Portenoy et al, 1996)

Recent Developments In Pain ManagementRecent Developments In Pain Management

Greater understanding of the pathophysiology underlying chronic pain syndromes

Scientific breakthroughs in molecular biology; insight into pain at the molecular level

Advances in drug therapy (drug delivery technologies)

Multimodal therapy

Multidisciplinary teams, shared decision-making that includes patients

Patients’ rights movement

(JCAHO, 1999; Loeser et al, 2001)

Therapeutic Modalities for

Chronic Pain Management

Assessment

Progress in Chronic Pain Management:Progress in Chronic Pain Management:

“Describing pain only in terms of its

intensity is like describing music only in

terms of its loudness”

von Baeyer CL; Pain Research and Management 11(3) 2006; p.157-162

Pain AssessmentPain Assessment

Characterize the pain

Characterize the disease, relationship between pain and disease and potentially treatable etiologies

Clarify syndromes and infer pathophysiology

Determine need for urgent therapy

Identify other needs

Develop a therapeutic strategy

(Portenoy et al, 1997)

Pain AssessmentPain AssessmentComponents History: temporal features, intensity, topography, quality,

exacerbating/alleviating factors Physical Exam: determine existence of underlying pathology Lab and Radiographic Tests: appropriate to pain syndrome

Assessment Tools Pain Intensity Scales: VAS, NAS, “faces” scale Multidimensional Pain Measures: Brief Pain Inventory, McGill

Pain Questionnaire

(Portenoy et al, 1997)

Pain Intensity Rating ScalesPain Intensity Rating Scales• Visual Analogue Scale (VAS)

No painNo pain ----------------------------------- ----------------------------------- Worst painWorst pain

•Categorical Scale None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10) None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10)

• Numerical Rating Scale0 0 -------------------------------------------------------------------------- 10 10

No painNo painWorst pain Worst pain imaginableimaginable

(Cleeland, 1991; Jacox et al, 1994)

00

No No hurthurt

22

Hurts just a Hurts just a little bitlittle bit

44

Hurts a little Hurts a little bit morebit more

66

Hurts even Hurts even moremore

88

Hurts a whole Hurts a whole lotlot

1010

Hurts as much Hurts as much as you can as you can

imagineimagine

• Pain Faces Scale

• Brief Pain Inventory Shade areas of worst pain. Put an X on area that hurts mostShade areas of worst pain. Put an X on area that hurts most

Progress in Chronic Pain Management

Therapeutic Modalities for Chronic Therapeutic Modalities for Chronic

Pain ManagementPain Management

TreatmentTreatment

Therapeutic Options for Chronic Pain ManagementTherapeutic Options for Chronic Pain Management

Pharmacotherapy (Analgesics) Non-opioids Adjuvant Analgesics

Antidepressants Anticonvulsants

Opioids Rehabilitative Approaches Psychologic Interventions Anesthesiological Approaches Neurostimulatory Techniques Surgery Complementary/Alternative Approaches Lifestyle Changes

(Cashman, 1996; Portenoy et al, 1997; Hanks et al, 1998; Galer, 1998; Stein, 1995)

Status of antidepressants in chronic pain managementStatus of antidepressants in chronic pain management

Best evidence: TCAs – Inhibit both NA and 5-HT reuptake

TCAs are superior to SSRIs in pain management

TCAs are superior to the anticonvulsant

There is no consensus regarding which of the many TCA

derivatives is most effective.

The choice of TCA is therefore dictated largely by adverse

effects

Neurologic Complications of Cancer Therapy Current Treatment Options in Neurology 1999, 1.428-437

Litsedge, A Double-Blind Comparison of Dothiepin and Amitriptyline for the Treatment of Depression with Anxiety, Psychopharmacologia (Berl.) 19, 153--162 (1971)

INTRODUCTIONINTRODUCTION

Major reason for seeking medical care.

90% is vasculr headache.

10% is mixture of inflammation,traction or dilatation of pain sensitive structure.

A true commitment is a heart felt promise to yourself from which you will not back down

- D. Mcnally

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Pain Referred pain

– Pattern of referred pain

Success in life is a matter not so much of talent and opportunity

as of concentration and perseverance

- C.W. Wendte

CLINICAL ASSESSMENTCLINICAL ASSESSMENT

History– Hx of present illness

– Past medical hx

– Family hx

– Social hx

Physical examination

We possess by nature the factors out of which personality can be made, and to organize them into effective personal life is every man’s primary responsibility

- Harry Emerson Fosdick

CLINICAL ASSESSMENTCLINICAL ASSESSMENT

Clinical features suggesting serious cause– Crescendo– Early morning– Vomiting– Fever– Seizures & other neurological symptomes– Worst headache in my life– Known malignancy– Tenderness

Facial painFacial pain

Typical Neuralgias1) Trigeminal neuralgia

• Characterized by recurring paroxysmal severe pain, brief duration (seconds) in the territory of the trigeminal nerve, spontaneously or initiated by chewing, talking, touching the affected side of the face.

• Unknown aetiology, an arterial loop pushing on the sensory root in the posterior fossa.

• Females affected more than males• Analgesics, surgery, destruction of the sensory

neuron, division of nerve root.

Facial painFacial pain

Typical Neuralgias2) Glossopharyngeal neuralgia

• Unknown cause• Equal both sexes• Severe, sudden episodes of pain in the

tonsil region one side only, ipsilateral ear.• Pain - severe for 1-2 hours, recur daily• Treated like trigeminal

Facial painFacial pain

Typical Neuralgias3) Sluder’s neuralgia and Vidian neuralgia

• Intractable pain in the nose, eye, cheek and lower jaw.

• Could be due to lesion of the sphenopalatine ganglion, or vidian nerve.

• Analgesics, vidian neurectomy

Facial painFacial pain

Posttraumatic neuralgia– Neuroma

– Parietal & occipital

– 90% recovery

Experience can be defined as

yesterday’s answer to today’s problems

Facial PainFacial Pain

Atypical facial pain Pain felt over the cheek, nose, upper lip or

lower jaw Usually bilaterally symmetrical Aching, shooting, burning, accompanied by

reddening of the skin and lacrimation or watering of the nose

Lasts for hours, days or weeks Psychological consultation, analgesics

Symptomatic NeuralgiasSymptomatic Neuralgias

Intracranial lesions1) Central lesions

• Tumours of the brain stem, M.S., thrombotic lesions, metastasis, occult naso-pharyngeal ca.

• No precipitant, sensory loss.2) Post herpetic neuralgia

• Herpes zoster may affect trigeminal nerve ganglion

• Vesicular rash covers one division commonly the 1st with severe pain.

Symptomatic NeuralgiasSymptomatic Neuralgias

Extracranial lesions1) Sinus disease

• Infective and neoplastic lesions of the paranasal sinus.

• Facial pain & dental pain, loss teeth.• Clinical suspicion.• Treatment

2) Dental neuralgia• Dental carries• Dental extraction

3) Temporomandibular joint pain

HeadacheHeadache

Headache is one of the commonest symptoms in medical practice.

Aetiology:

1) Raised intracranial pressure Due to tumours, abscesses, subdural

haematoma, brain haemorrhage.

2) Inflammation of the brain and meninges e.g. meningitis, cerebritis, others

HeadacheHeadache3) Migraine

Congenital predisposition Triggered by hunger, certain foods, sleep - too much or too

little, hormonal variations, stress. Pathology-vascular dilatation Females affected more than males ? Proceeded by aura usually visual, paraesthesiae of hands,

weakness Headache is unilateral or bilateral, affects any area of the

head, aching or throbbing often accompanied by nausea and vomiting

Diagnosis - by history alone Treatment - prevention by avoiding precipitating factors,

appropriate medication.

HeadacheHeadache

4) Tension headache More common in adult females Positive family history (40%) Maybe associated with migraine Produced by persistent contraction of the

muscles of the neck, head and face Caused by emotional tension, secondary to

other headaches, posture habit Treated by analgesics, muscle relaxants,

physiotherapy

HeadacheHeadache

5) Cluster headache 90% are men Age 20 - 30 Attacks occur in groups, no aura Caused by vascular dilatation of branches of

external carotid Triggered by histamines, alcohol Treated by analgesics, anti-histamine, steroids

Pains from head and neck Pains from head and neck musclesmuscles

Pain from temporalis muscles Can arise from grinding teeth at night

(bruxism), impacted wisdom teeth, temporomandibular joint dysfunction, anxiety when the patient clenches the jaws too tightly

Treatment: Refer to interested dental surgeon.

Pains from head and neck Pains from head and neck musclesmuscles

Pain from upper neck muscles Can radiate over the head

Treatment by physio-therapist or rheumatologist

Pain from frontalis muscles Usually due to bad posture at work or

while drivingTreatment: physio-therapy

Pains from head and neck Pains from head and neck musclesmuscles

Cervical spondylosis Pain mediates upwards from the neck to the

occiput or vertex to the front of the head, down to the shoulders

Due to cervical discs prolapse Diagnosis - x-ray

Treatment: Physio-therapy, referral to rheumatologist

Pains from head and neck Pains from head and neck musclesmuscles

Temporal arteritis Due to acute inflammation of the artery, the cause

unknown, affects men and women over the age of 60

Pain over the temples and frontal region, intense, throbbing, tenderness over the scalp, swelling and redness of the overlying skin with general malaise, partial or complete loss of vision.

ESR Elevated

Treatment: Cortisone, analgesics

Pains from head and neck Pains from head and neck musclesmuscles

Psychologic headache Usually accompanied by depression,

anxiety

No organic lesion

It is a great misfortune not to possess sufficient wit to speak well

nor sufficient judgment to keep silent

La Broyers character

Dedicated to my family for making everything worthwhile

Thank youThank you

THANKYOUTHANKYOU

My sincere thanks to P.Sampath

READ not to contradict or confute

Nor to Believe and Take for Granted

but TO WEIGH AND CONSIDER

Cerebrovascular Cerebrovascular EmergenciesEmergencies

Is survival a mere stroke of Luck?

“My Opinions are founded on knowledge but modified by experience”

Every minute matters: ‘time is brain’Every minute matters: ‘time is brain’

Expert is one who think to his chosen mode of ignorance

INTRODUCTIONINTRODUCTION

Perceptual Sense (Observation) Word Sense (Recording) Common Sense (Thinking)

– Will lead you to get - Clinical Sense

“ He who cannot forgive others destroys the bridge over which he himself must pass” - Annoy

Cerebrovascular disease – Cerebrovascular disease – Mind boggling factsMind boggling facts

CVD is the most disabling of all neurologic diseases. 50% of survivors have a residual neurologic deficit.

Greater than 25% require chronic care.

World wide incidence: 2/1000 population/annum1

Incidence in people aged 45 – 84 years: about 4/10001

Incidence in India: was 36/100,000 for the year 1998-19993 in a study in Calcutta

Incidence of mortality due to stroke (India: WHO study): 73/100,000 per year2

1.A practical approach to management of stroke patients; 1996; 360-3842. Epidemology of cerebrovascular disorders in India; 1999; 4-19

3. Neuroepidemiology 2001;20:201-207

If you think you can or you can’t You are always right

• CVD 6.7 %

• MI 2.5 %

• Death 7.2 %

• CVD, MI, Vascular death 8.6 %

• CVD, MI, Death 10.3 %

Annual risk CVD, MI, vascular Annual risk CVD, MI, vascular death following TIA, minor CVDdeath following TIA, minor CVDAnnual risk CVD, MI, vascular Annual risk CVD, MI, vascular

death following TIA, minor CVDdeath following TIA, minor CVD

Experience can be defined as yesterday’s answer to today’s problems

Indian scenario

1880 death / daydue to stroke in India

Equal to 6 Boeings 737 crashes every dayEqual to 6 Boeings 737 crashes every day

22 times that due to malaria 4 times that due to RHD 1.4 times that due to TB Almost equal to deaths due to IHD

Indian scenarioIndian scenarioNumber of deaths due to strokeNumber of deaths due to stroke

Indian immigrants to England have higher risk or dying due to stroke than local population

ComparisonComparisonIndia vs. established market economiesIndia vs. established market economies

(Age adjusted stroke mortality)(Age adjusted stroke mortality)

2 to 3 times stroke 2 to 3 times stroke mortality higher in Indiamortality higher in India

– Increase life expectancy (aging population)– Urbanization

ComparisonComparison USA – stroke mortality decline since 1940’sUSA – stroke mortality decline since 1940’s

India likely to increaseIndia likely to increase

Stroke units Aspirin Thrombolysis Heparin

Acute stroke interventions – Acute stroke interventions – reasonable evidencereasonable evidence

Neurologists

StrokeStroke

Vascular event due to atherosclerosisVascular event due to atherosclerosis

CardiologistsCardiologists PhysiciansPhysicians

Relevant to all of usRelevant to all of us

Limb weakness – 77% Urinary disturbance – 48% Dysphagia – 45% Cognitive deficit – 44%

Stroke disability worldwideStroke disability worldwide

35% functionally dependent at 1 year35% functionally dependent at 1 year

Stroke care units vs general wards– 9% relative risk reduction– 56 deaths or dependency avoided / 1000 acute

strokes treated / year Aspirin

– 3% relative risk reduction– 12 deaths or dependency avoided / 1000 active

strokes treated / year

Acute stroke interventions – Acute stroke interventions – evidence based medicineevidence based medicine

Thrombolysis – (even in USA only 1% of strokes are thrombolysed)– 10% relative risk reduction– 63 deaths or dependency avoided

(91 early deaths due to haemorrhage) Heparin

– No benefit

Acute stroke interventions – Acute stroke interventions – evidence based medicineevidence based medicine

People who survive stroke – 90% are left with deficit – minimal / mild / moderate / severe

None of the presently available therapy has any major impact hence prevention is critical

ConclusionConclusion

New role of doctorsNew role of doctors

““Managers of Change”Managers of Change”

““Preventors of Change”Preventors of Change”(Health ill health)(Health ill health)

GlobalGlobal

15 million deaths globally 15 million deaths globally every year due to vascular disease every year due to vascular disease

(30% of all deaths) (30% of all deaths)

GlobalGlobal

By 2020 – stroke and myocardial By 2020 – stroke and myocardial infarction will constitute leading cause infarction will constitute leading cause

of death / disabilityof death / disability

Lowering blood pressure Primary prevention – 17 randomised trials –

reduction of 5 to 6 mmHg diastolic and 10.12 mmHg systolic BP – 38% reduction of stroke

Secondary prevention – have we made PROGRESS

Common Stroke MimicsCommon Stroke Mimics Hypoglycemia Post ictal state Drug overdose Concussion with neck injury Migrainous accompaniment Encephalopathies with focal signs Hyponatremia Subdural hematoma, Empyema Focal Encephalitis: Herpes

Being ignorant is not so much a shame as being unwilling to learn

Level of Evidence

Level A: Based on RCT or Meta analysis of

RCT

Level B: Based on Robust Experiment or Observation Studies

Level C: Based on Expert opinion.

“The True Art of Memory is The Art of Attention” - S.Johnson

Guidelines for 24 hrs – MandatoryGuidelines for 24 hrs – Mandatory

1. History And Examination

a. Stroke clerking Performa (1994) R.C.P.1. Improved patient Assessment2. Improved Management - not clear3. Improved outcome - not clear

b. Examination1. Secure Diag of Stroke2. Specify Impairment3. Identify sub type of Ischemic stroke4. Rule out stroke mimics

“ We Sometimes think we have forgotten something when in fact we never really learned it in the first place”

Imp.Your Memory Skills

Guideline: 3 (B) - CPR– CPR is rarely successful in the setting of stroke – Sneeder

1993.

Guideline: 4(B) Investigations:(Sagar 1995)-435 PTS)– Chest x-ray 16% ABN – Only 4% change clinical management– Order x-ray chest if weight loss or chest symptoms

present

Through Action You Create your Own Education - D.B. ELLIS

Guideline 5: (B) ECG:– Cardiac cause of Death (30 days) Ebrahim 1990.– All conscious patients to have ECG

Guideline 6: (C) CT:– Routine CT Head is a must– King’s fund forum(1988) gives useful framework– Weir 1994 Clinical scoring cannot distinguish – CT done if: a) Uncertainty of Stroke

b) If Anticoagulation or Anti Platelet treatment contemplated

c) IV rtPA

Thought is the labour of the intellectReverie is its pleasure

Guideline 7:(B) M.R.I.

– Mohr 1995, - Unclear for Implications for clinical practice

– 2004 – PWI > DWI – IV rtPA very useful

Whatever the Mind can conceive and Believe, the mind can Achieve -Napoleon Hill

Imagination is more Important than KnowledgeImagination is more Important than Knowledge

Guideline 8: (B) ECHO no Routine

– Echo in Acute Stroke – Cardiac cause/Thrombus LV– TEE is superior to TTE– Amer Heart Asson (1997) - same conclusion– Yield is very low. (Leung 1993; Chambors 1997)– Only when abnormal ECGS - change clinical management

Guideline 9: (A) – Doppler scan for selected patients – > 80% stenosis benefits from Endarterectomy– Subst Storke -Good recovery - do doppler– Useful in posterior circulation

A open foe may prove a curse ; but a pretended friend is worse

Guideline 10: (B) Management:

– Fever (Worst Prog.) Reith 1996 – Hypoxia (Moroney 1996) - Exac. by seizures

Pneumonia and Arrythmias - Worst outcome

– Hyperbaric O2 ineffective (Nighoghossaln 1995)

– Haemodilut. Plasm Expanders; venesection – No evidence for efficacy (As plund - 1997)

Check ABG only if Hypoxia suspected.

It is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent - La Broyers character

Guideline 11: (A) Steroids and Hyperosmolar agents Unproven treatment –

– Tumor oedma responds but not cytotoxic stroke oedma qialbash 1997 - No effect on survival or improv. In funct. Outcome

– Mannitol - (Boysen 1997) - short term effective statistically in conclusive

You are what you think and not what you think you areYou are what you think and not what you think you are

We learn by thinking and the quality of the learning outcome is We learn by thinking and the quality of the learning outcome is determined by the quality of our thoughtsdetermined by the quality of our thoughts

R.B. SchmeckR.B. Schmeck

Guideline 12: (B) - Blood Pressure

– Defer - acute reduction of BP - 10 days unless HT Encephalopathy or aortic dissection present

– Moris 1997 - Increase BP - falls in 10 days– UK - 5mm in D.B.P. 1/3 storke - Low BP prompt correct of

hypovoll. and withdrawal of hypotonic drugs– Collins 1994 - HT - Prim. stroke prevent– Neal 1996 (Current RCT) - HTs in stroke survivors -study

needed– Acute reduction of BP only if thrombolysis considered

Guideline 13: (A/B) – AF

– AF / ISCH Stroke/ Mild disability - Warfarin after 48 Hrs (Longer for larger)

– Aspirin for others EAFT 1995 Less than 2 PT - No effect SPAF 1996 > 5 - Bleeding

Discipline Weighs ounces; Regret weighs Tons

A great many people think they are thinking when they are A great many people think they are thinking when they are merely re arranging their prejudicesmerely re arranging their prejudices

W. JamesW. James

Guideline 14:(B/C) - Blood sugar

– Weir (1997) > 8 mm d/Lit - Poor outcome– Acute MI + 11 mm d/Lit - Intensive Insulin - improved

(Malmberg 1997)

Many Ideas grow better when transplanted into another mind than Many Ideas grow better when transplanted into another mind than in the one where they sprang UPin the one where they sprang UP

O.W. HolmosO.W. Holmos

Guideline 15: (A) Cholesterol

– Prosp. Study collob.: 1993 - Epidem study do not support

– Blaun 1997: Metranauetic - Chollest & statin 30% decrease - stroke in CAHD patients.

– Sacks 1996 - Tot chol: decrease to 4.8 mmol/Lit benefits

Guideline 16: (A/C) Deep vein thrombosis

– Kalra 1995 - 10 days - stroke Pts - 50% – Sandercock 1993 - Pul embol 6-16% only– Ist 1997 - 5000 IV or 12500 twice daily - Hemorrage greater– Gradual stocking value - useful in Surg - pts but its value not

evaluated - (Wells 1994)– Use with caution - if periph artery insuf. is present hence do

not use heparin on stockings.

A woman’s desire for revenge outlasts all her other emotions

Every discovery contains an irrational element or Every discovery contains an irrational element or 4 creative intuition4 creative intuition

Guideline 17: (A/B) Pressure sure

– Event health care (1995) specialised low pressure mattress systems to be used than stand Hospital - mattress

I have never let my Medical schooling interfere with my education I have never let my Medical schooling interfere with my education Mark TwainMark Twain

Management of infarction– Guideline 18: (A)

Aspirin 75 - 150 /Day 3 yrs 40% reduces of vascular events in 1000 pts (APTC -

1994) Stroke sub type value ? (TACI, PACI, LACI, POCI) Dienners - 1996, synergy possible with Clopidogrel

Ticlopidine etc.

Anti CoagulationAnti Coagulation Warfarin - AF

– In sinus rhythm - uncertain – Spirit 1997 low dose ABP + Warfarin in TIA &

Minor stroke - Stopped of HE– Heparin (IST 1997) – Significant reduction in

early death (12 fewer in 1000) not better than aspirin

– So avoid Heparin (A)

“ He who cannot forgive others destroys the bridge over which he

himself must pass” - Annoy

When they tell you to grow up, they mean stop growing When they tell you to grow up, they mean stop growing PiccasoPiccaso

Thrombolysis (A)

Warlow 1997 - Uncertain clinical benefit 2004 – NINDS – Thrombolysis

conclusively proved its efficacy – first 3 hrs

A (Neurologist’s) life is like a piece of paper on which everyone who A (Neurologist’s) life is like a piece of paper on which everyone who passes by leaves an impressionpasses by leaves an impression

- Chines proverb- Chines proverb

Guideline 20: (I) Hemorrhage

– Hankey and hon 1997: Supra tentorial evacuation for ICH is controversial - Avoid

– Infra tentorial - Yes– Main Indication - Deteriorating or depressed

consciousness

A medical school should not be a preparation for life. A medical school should not be a preparation for life. A school should be lifeA school should be life

3 D ied

3 4 R ed tag

7 D ied

2 1 d isch ton ver h om e

3 D ied

8 D isc fo rp a llim a

1 D iscH om e

6 4 D isch ar 6 7 D ied

1 3 1In tu b a tion

9 3N ot In tu b

2 2 4 P ts

Guideline 21 : Ventilation -Decreased level of consciousness - increased mortality and poor final outcome - Absent pupillary light responses - poor prognosis

PITFALLSPITFALLS Basing treatment of stoke on brain imaging

along without a vascular work-up Missing early infarct signs on CT Underestimating the time of symptom onset

for patients who wake up with a stoke Overtreatment of hypertension in acute

stoke

Three can be seen in the divisions of a human in mind, body and spirit

PITFALLSPITFALLS Overuse of carotid endarterectomy in

asymptomatic patients Not investigating both extracranial and

intracranial circulations Failure to distinguish severe cartid stenosis

from total occlusion Not obtaining spinal fluid for patients with

suspected subarachnoid hemorrhage

“Social Isolation is in itself a pathogenicFactor for disease production”

PITFALLSPITFALLS Not treating patients with large artery

ischmic stroke indefinitely with antiplatelet terapy

Failure to recognize lacunar stoke Inadequate use and dosing ofHMG Co-A

reductase inhibitors (statins) inpatients with cerebrovascular disease

Through Action You Create your Own Education - D.B. ELLIS

PROGNOSTIC PEARLSPROGNOSTIC PEARLS Flaccid Paralysis for more than 96 hrs When tendon reflexes recover without return of voluntary

movement – prognosis poor Recovery of sensory less in usual to a degree. Postion sense

recovers but not pain and temperature Recovery from Dysphasia is never complete Dysarthria usual improves and Dysphagia never improves Diplopia due to brain stem is usually permanent Conjugate gaze – recovers Vertigo improves but hearing loss is permanent Pseudobulbar palsy permanent

“By Nature All Men/ Women are alike butby Education widely different”

STOKE MYTHOLOGYSTOKE MYTHOLOGY

GENERAL MYTHS DIAGNOSTIC MYTHS THERAPEUTIC MYTHS

Serious, sincere, systematic study surely secures supreme success

GENERAL MYTHSGENERAL MYTHS

PHYSICIAN + MRI = NEUROLOGIST MINISTROKE CVA

CHAOTIC

COMMUNICATION

Discipline Weighs ounces Regret weighs Tons

DIAGNOSTIC MYTHSDIAGNOSTIC MYTHS

Self evident cause Ischaemic stroke + AF Lacunes, Lacunar infarcts and small vessel

disease Cryptogenic stroke PFO and Cardiogenic stroke

Experience can be defined as

yesterday’s answer to today’s problems

Ultrasound DiagnosisUltrasound Diagnosis

In skilled hands, ultrasound may show:• Carotid occlusion or stenosis• MCA occlusion or stenosis• Vertebrobasilar occlusion• Extracranial dissection

The secret of walking on water is Knowing where the stones are

UCLA Stroke CT ProtocolsUCLA Stroke CT ProtocolsSequence Time CT

WWOCT

Stroke

CT Stroke WWO Diamo

x

CT Stroke reduced Dye

CT Stroke

reduced Dye

WWO Diamox

SCOUT 0’15” ++ ++ ++ ++ ++

CT 0’30” ++ ++ ++ ++ ++

CTA-COW

16’

-- ++ ++ ++ ++

CTA-Neck

-- ++ ++ ++ ++

CTP 20’ -- ++ ++ ++ ++

CTP W diamox

30’ -- -- ++ -- ++

Post-contrast

0’30” ++ -- -- -- --

Magnetic Resonance Imaging (MRI)Magnetic Resonance Imaging (MRI)11

High level of anatomic detail for precisely locating the stroke and determining the extent of damage.

Especially useful for small blood vessels due to high sensitivity

Advances in the early detection of stroke involve using diffusion and perfusion weighted imaging. 

1. Curr Opin Neurol. 2004 Aug;17(4):447-51

Memory, the daughter of attention, is the teeming mother of knowledge - Martin Tupper

UCLA Stroke MRI ProtocolsUCLA Stroke MRI ProtocolsSequence Time Brain

WWOTIA Stroke Thromb

olysis 1Thrombolysis 2

SCOUT 0’25” ++ ++ ++ ++ ++

MRA-Neck 6’44” -- ++ ++ - ++

DWI 0’40” -- ++ ++ ++ ++

T2 3’42” ++ ++ ++ ++ ++

MRA-COW 6’12” -- ++ ++ ++ --

FLAIR 2’41” ++ - ++ ++ --

GRE 2’35” - - ++ ++ ++

PWI 2’ - - - ++ ++

T1 3’ ++ - - - -

T1 post Gad

3’ ++ - - - -

Other Diagnostic Tools-1Other Diagnostic Tools-1

Magnetic Resonance Angiography1

(MRA) Carotid Duplex Scanning2: Transcranial Doppler (TCD)3

Xenon CT Scanning4

1.Neurol Res. 2004 Jun;26(4):429-342. J Vasc Surg. 2003 Sep;38(3):422-30. 3. .Neurology. 2004 May 11;62(9):1468-81,4. Keio J Med. 2000 Feb;49 Suppl

1:A25-8

Science is below the mind; Spirituality is beyond the mind

Other Diagnostic Tools -2Other Diagnostic Tools -2

Radionuclide SPECT Scanning1

PET Scanning2

Transesophageal Echocardiography3

1. AJNR Am J Neuroradiol. 2001 May;22(5):928-36

2.Neuroimaging Clin N Am. 2003 Nov;13(4):741-583. Heart Dis. 2003 Sep-Oct;5(5):320-2

Success is a prize to be won. Action is the road to it. Chance is what may lurk in the shadows at the road side.

THERAPEUTIC MYTHSTHERAPEUTIC MYTHS

Evidence based medicine = Randomized Clinical Trials– Best Research Evidence– Clinical Expertise– Patient Values

Systematic Escalation of anti thrombotic therapy Brain Hemorrhage Demands Neuro surgical

Consultation

Dead/dependent follow-upDead/dependent follow-up

Deaths by day 14Deaths by day 14

Deaths during follow-upDeaths during follow-up

Deaths ordered by antithromboticDeaths ordered by antithrombotic

Deaths ordered by thrombolyticDeaths ordered by thrombolytic

Deaths ordered by stroke severityDeaths ordered by stroke severity

Symptomatic ICH by 14 dysSymptomatic ICH by 14 dys

Fatal ICH by 14 dysFatal ICH by 14 dys

Dead/dependent follow-up < 3 hr.Dead/dependent follow-up < 3 hr.

Dead follow-up < 3 hr.Dead follow-up < 3 hr.

62% vs 69% s.62% vs 69% s.

22% vs 12% s.22% vs 12% s.

22% vs 19% s. 22% vs 19% s.

40% 30% 17% 10% 40% 30% 17% 10%

3% 20% ns.3% 20% ns.

11% 29% ns.11% 29% ns.

9.3% vs 2.5% s.9.3% vs 2.5% s.

6% vs 1% s.6% vs 1% s.

55% vs 71% s.! 55% vs 71% s.!

20% vs 25% ns.20% vs 25% ns.

Thrombolysis in acute strokeThrombolysis in acute strokeThrombolysis in acute strokeThrombolysis in acute stroke

NATURE, TIME AND PATIENCE are the 3 great physicians

NINDS ConsensusNINDS Consensus

Door to MD evaluation 10 min

Door to CT completion 25 min

Door to CT read 45 min

Door to treatment 60 min

Access to neurological expertise 15 min

Access to neurosurgical expertise 2 hrs

Admit to monitored bed 3 hrs

Memory, Pity and Beauty are short lived in life; But tinged with emotion persist in life

CONCLUSION CONCLUSION

• MYTHS

• PITFALLS

• PROGNOSTIC PEARLS

It is the disease of not listening, the malady of not marking,

that I am troubled withal - Shakespeare

CVD – Prevention or Cure?CVD – Prevention or Cure?

While number of curative methods are available, preventive therapy is undoubtedly the main strategy

in the management of CVD

Lijec Vjesn. 2003 Nov-Dec;125(11-12):322-8

The sign wasn’t placed there

By the Big Printer in the sky

Where are we ……?Where are we ……?

6-8 HO

UR

S

Call Call emergencemergency servicesy services

ER stroke teamER stroke team

ActivatedActivated(15 minutes)(15 minutes)

NeuroprotectivNeuroprotective drug infused e drug infused during during transporttransport

Brain scanBrain scan

Drugs Drugs administered administered

‘stroke-‘stroke-treatment’ treatment’

cocktailcocktail

Full Full recoveryrecovery

Stroke onsetStroke onsetSecondarySecondarypreventionprevention

The art of medicine is caring for the heart of the patient

Dedicated to my family for Dedicated to my family for making everything worthwhile making everything worthwhile

READ not to contradict or confute

Nor to Believe and Take for Granted

but TO WEIGH AND CONSIDER

THANK YOUMy sincere thanks to Thudhimugan .K for

his meticulous computer work My sincere thanks to Thudhimugan .K for

his meticulous computer work