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JC ONAdvances In The Mechanisms, Diagnosis And Management Of

Neuropathic Pain : Current Opinions And Future

PerspectivesDr. Ashok Kumar Saxena,

Dr. Raman AzadIndian J. Anaeshesia,2006;50(4), 249- 257

Trigeminal neuralgiaA review

Dr. Priti Shah , Dr Hetul Patel , Dr. Mona Shah , Dr. Kevin Parikh; B U J O D, Vol. 4 Issue-1 January 2014

Introduction

Definition by International Association for the Study of Pain (IASP)

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

Neuropathic pain It refers to all pain initiated or caused by a primary lesion or dysfunction

or transitory perturbation in the peripheral or central nervous system.

Chronic pain is pain that persists more than 1 month and might be reasonably expected following an inciting event and is sustained by aberrant somatosensory nervous system processing. Chronic pain can last for months, years, and even decades.

Brian Hainline , Chronic Pain: Physiological, Diagnostic, and Management Considerations, Psychiatry Clin N Am 28 (2005) 713–735.

It would seem logical to restrict the diagnosis of neuropathic pain in conditions in which there is demonstrable evidence for a peripheral nerve lesion.

First, clinical examination and electrodiagnostic tests may fail to detect nerve lesions, e.g. trigeminal neuralgia, is commonly classified as neuropathic pain on clinical grounds, even though nerve damage cannot in most cases be formally verified.

Second, tissue trauma will almost invariably result in damage to nerve terminals, but it is unclear how severe the damage must be or how far along the proximodistal projection of a sensory neuron the lesion must be located before neuropathic pain appears.

Griffin JW, McArthur JC, Polydefkis M. Assessment of cutaneous innveration by skin biopsies. Curr Opin Neurol 2001; 14: 655-59.

Third, electrophysiological studies have shown that nonlesioned unmyelinated nociceptors projecting into a damaged peripheral nerve start to develop a low level of ongoing discharge and can acquire a novel sensitivity to catecholamines.

Finally, it is difficult to establish a casual relationship between a lesion and the pain in an individual patient. For example, in patients who have suffered a stroke, the pain may be caused by the central lesion or alternatively by multiple conditions affecting a paralyzed extremity.

This review provides an overview of differential diagnosis and efficacy of pharmacologic and interventional strategies for the treatment of Neuropathic Pain.

Ali Z, Ringkamp M, Uninjured C-fibre nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. J Neurophysiol 1999; 81: 455-66

Mechanical, heat, thermal, and chemical stimuli ↓

pain in the peripheral nervous system ↓

Primary afferent neurons (nociceptors) ↓

Myelinated or unmyelinated nerves↓

Afferent transmission of signals into the spinal cord ↓

Both nociceptive- specific neurons and more nonspecific, wide-dynamic-range cells can be

activated from these afferent sensory pathways ↓

Nociceptive- specific cells in the spinal cord ascend to the contralateral thalamus by way of the

neocorticospinal thalamic tract ↓

Afferent pathways then activate both primary and secondary somatosensory cortices

From the midbrain periaqueductal gray matter↓

Serves the endogenous opiate system. ↓

The endogenous opioids comprise endorphins and enkephalins

↓Regulates the pain response, homeostasis ,

immune function, and the normal stress response

↓Activation of periaqueductal gray matter

↓Inhibition of dorsal horn neurons

↓Analgesia

↓Excitatory connection with the dorsal raphe

nucleus ↓

Dorsal raphe nucleus ↓

Brainstem centers are modified by cortical,Subcortical, and limbic pathways

Noxious stimuli ↓

Somatotropic activation of the contralateral primary and secondary somatosensory cortex.

↓

Additional activation occurs in the contralateral insular cortex.

These diverse but interlinked pathways demonstrate that simple physical pain processing is an outdated concept; pain perception is mediated by attentional, cognitive, emotional, and motor planning brain responses.

Peyron R, Schneider F, Faillenot MS, et al. An fMRI study of cortical representation ofmechanical allodynia in patients with neuropathic pain. Neurology 2004;63:1838–46.

Allodynia Allodynia is evoked by peripheral stimulation. In response to ongoing nociception or

overstimulation, changes in spinal cord dorsal horn cells can occur, resulting in central sensitization or central reorganization and finally leading to allodynia.

E.g.-trigeminal neuralgia

Hyperalgesia Hyperalgesia refers to an exaggerated pain response produced by a normally painful

stimulus (ie, pinprick) Hyperalgesia can arise from peripheral and/or central mechanisms.

Stimulus-Independent Pain Stimulus-independent, or spontaneous, pain by definition occurs without

provocation, so symptoms can occur constantly or at any time.

Mixed Pain Syndromes In most neuropathic pain syndromes, stimulus-independent pain occurs along with

stimulus-evoked pain; for example, spontaneous burning pain and mechanical allodynia in complex regional pain syndrome (CRPS)

Types e head and neck regions are the most common sites of the Neuropathic pain which is a chronic pain condition,

Trigeminal neuralgia,

Glossopharyngeal neuralgia

Post herpetic neuralgias and

Atypical odontalgia (phantom tooth pain),

Burning mouth syndrome,

Traumatic neuropathies,

Complex regional pain syndrome

Are neuropathic pain conditions in the orofacial region that can be encountered in dental clinics. The majority of time any of the problem is misdiagnosed by the dentist, which can lead to unnecessary treatments include endodontic treatment and extraction of the tooth or teeth in the same region.

Peyron R, Schneider F, Faillenot MS, et al. An fMRI study of cortical representation ofmechanical allodynia in patients with neuropathic pain. Neurology 2004;63:1838–46.

ODONTOGENIC PAIN

Dull ache or occasionally sharp.

Response to stimuli, such as hot, cold

or percussion is predictable and

proportionate.

Inconsistent and tends to get better or

worse over time.

Often disrupts sleep.

Often an identifiable source (i.e.,

Caries, deep restoration, periodontal

disease, fracture line).

Local anesthesia of the suspect tooth

eliminates the pain.

NEUROPATHIC PAIN

Dull, sharp, shooting or burning.

Response to hot, cold or percussion

does not reliably relate to the pain and

may be disproportionate.

Persistent and remains unchanged for

weeks or months.

Rarely disrupts sleep.

No obvious source of local pathology.

Response to local anesthetic is

ambiguous.

Felt in multiple areas or teeth.

Repeated dental therapies fail to

resolve the pain.

Pain Characteristics

Intensity

Quality

Location

Onset

Associated events at onset

Duration and timing of pain

Course of symptoms since onset

Factors that increase pain

Factors that decrease pain

Associated symptoms (e.g. altered sensation, swelling)

Previous treatments and their effects

Following are the tests dentists can perform in their clinics which provides

information regarding peripheral sensory nerve function and help to accurately

diagnose patients and can aid in follow-up.

The pin-prick test,

Temperature sensitivity test,

Static touch detection test,

Direction of movement test,

Visual analogue scale.

Trigeminal neuralgia

Synonyms- tic douloureux, Fothergill’s

disease; IASP- ‘sudden and usually

unilateral severe brief stabbing recurrent pain in the distribution of one or more branches of the fifth cranial nerve’.

4.3 per 100,000

Female predominance: 1.74 to 1

Peak incidence 50-70 yrs

Unusual before age 40

Higher incidence with Multiple Sclerosis &

HTN

Spontaneous remission possible

Episodic attacks over many years

2 Types- Classical & SymptomaticClassical Criteria

When it is not associated with an underlying neurological disease

Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1 or more divisions of the trigeminal nerve.

Pain has at least 1 of the following characteristics: Intense, sharp, superficial, or stabbing Precipitated from trigger zones or by trigger factors,

Attacks are stereotyped in the individual patient

No clinically evident neuro deficit.

Not attributed to another disorder.

The clinical examination, imaging studies, and laboratory tests are unremarkable.

Symptomatic Criteria

Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, with or w/o persistence of pain between paroxysms, affecting 1 or more divisions of the trigeminal nerve

Pain has at least 1 of the following characteristics: Intense, sharp, superficial, or stabbing Precipitated from trigger zones or by trigger factors

TN without neurological disorder.

The signs and symptoms are secondary to another disease process affecting the

trigeminal system.

stereotyped attacks in the individual patient

A causative lesion, other than vascular compression, has been demonstrated by

special investigations &/or posterior fossa exploration.

PRIMARY

Occurs in the absence of an identified cause;

Most common.

In such cases, the underlying disorder presumably leads to ectopic electrical activity caused by direct pressure or demyelination

>50 yrs age

Evaluation must include CT or MRI of the head and brain.

SECONDARY Occurs by identified abnormality,

such as an intra- or extracranial tumor or other space-occupying lesion, multiple sclerosis (MS), or trauma

In younger individuals.

Etiology and Pathogenesis

10% of cases showed underlying pathology such as a tumor, multiple sclerosis or a vascular malformation.

The most frequent tumor is a meningioma of the posterior cranial fossa.

The most widely accepted theory is that a majority of cases of TN are caused by an atherosclerotic blood vessel (usually the superior cerebellar artery) pressing on and grooving the root of the trigeminal nerve.

This pressure results in focal demyelinization and hyperexcitability of nerve fibers, which will fire in response to light touch, resulting in brief episodes of intense pain.

Evidence for this theory includes the observation and neurosurgery that removes the pressure of the vessel from the nerve root by use of a micro vascular decompression procedure eliminates the pain in a majority of cases.

Rappaport Z, TN: the role of self-sustaining discharge in the trigeminal ganglion. Pain 1994; 56:127–38.

Additional evidence for this theory was obtained from a study using tomographic

magnetic resonance imaging (MRI), which showed that contact between a blood

vessel and the trigeminal nerve root was much greater on the affected side.

Wall PD, Devor M. Sensory afferent impulses originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats. Pain 1983;17:321.

In a recent study of 1,185 patients who had micro vascular decompression surgery for

TN that did not respond to drug therapy, 70% of the 328 Orofacial Pain and

Temporomandibular Disorders patients were pain free 10 years after the surgery.

Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of trigeminal neuralgia: double-blind study and long-term follow-up. Ann Neurol 1984;15:240–4.

Evidence against this theory includes the finding by neurosurgeons that

manipulation of the area of the nerve root may eliminate the painful episodes

even when an atherosclerotic vessel is not pressing on the nerve root.

Other investigators believe that a major factor in the etiology of TN is a

degeneration of the ganglion rather than the nerve root.

Meaney JF, Eldridge PR, Dunn LT, et al. Demonstration of neurovascular compression in trigeminal neuralgia with magnetic resonance imaging. J Neurosurg 1995; 83:799–805.

Glossopharyngeal neuralgia

IASP- ‘Sudden severe recurrent pain in the distribution of the glossopharyngeal nerve’.

Clinical features

Shares many of the features of trigeminal neuralgia, with a few notable exceptions.

The pain location is in the distribution of the glossopharyngeal nerve, specifically the posterior tongue and lateral oropharynx.

The pain is less intense than that of trigeminal neuralgia, though still paroxysmal and episodic in nature,

Provoked by swallowing or contact with the mucosa overlying the region innervated by the glossopharyngeal nerve.

It is a rare disorder, Affecting approximately 0.5 to 1 person per 100,000.

Etiology and Diagnosis

Tumors and vascular abnormalities that result in nerve compression and ectopic nerve impulses, demyelization, and trauma.

Clinical diagnosis based on the history and examination.

A complete cranial nerve examination is essential for detecting other abnormalities that might support an underlying illness, such as multiple sclerosis or a tumor.

Computed tomography and MRI are appropriately prescribed to detect related intra or extracranial disease.

Post herpetic neuralgia

Clinical features

Unlike trigeminal and glossopharyngeal neuralgia, post herpetic neuralgia

(PHN) is not a paroxysmal neuropathic pain, rather it is a continuous

burning or stinging neuropathic pain that persists for more than 3 months

in the distribution of a previous outbreak of herpes zoster or shingles.

Post herpetic neuralgia shares with other neuropathic pains the features

of hyperalgesia and allodynia.

Christopher L; An Update on the Treatment of Postherpetic Neuralgia; J of Pain, Vol 9 (1), 2008: S19-S30

Atypical odontalgia /idiopathic /phantom tooth pain

First reported by Mcelin And Horton in 1947.

3% to 6% of patients develop atypical odontalgia after endodontic treatment.

Clinical features-

Persistent toothache following pulp extirpations, apicoectomy, or tooth extraction.

Sometimes facial trauma and inferior alveolar nerve block.

Prolonged periods of constant throbbing or burning pain in teeth or the alveolar process.

Absence of any identifiable odontogenic etiology observed clinically or radiographically.

The pain is chronic; patient’s sleep is undisturbed, and there may be a brief symptom-

free period on waking.

Michael J. Matwychuk, Diagnostic Challenges of Neuropathic Tooth Pain J C Dent Asso 2004; 70(8):542–6

Difficulty in localizing the pain usually worst at the site of the original

trauma, but can spread to adjacent areas, unilaterally or bilaterally.

All ages can be affected except for children.

Fm>m

Molars and premolars in the maxilla are most often affected.

Local anesthetic block gives ambiguous results, and patients rarely find

relief with analgesics,

Including narcotics.

Atypical odontalgia is often mistaken for a normal post-treatment or post-

trauma complication.

Michael J. Matwychuk, Diagnostic Challenges of Neuropathic Tooth Pain J C Dent Asso 2004; 70(8):542–6

TRIGEMINAL NEURALGIA

Pain is characterized as unilateral,

paroxysmal and stabbing.

Trigger areas characterize pain.

May occur in the absence of obvious

trauma.

peaking in the 50s and 60s.

ATYPICAL ODONTALGIA

Pain is dull and continuous. More

common after 40 years of age More

frequent in women in their mid-40s.

Usually precipitated by a traumatic

event (RCT, extraction, etc.).

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Burning mouth syndrome Glossopyrosis, glossodynia

Unilateral or bilateral

Burning pain localized to tongue, palate, lips and gingiva

Pain that gets worsen over the day decreases on eating and sleep.

Absence of clinical findings.

Presence of abnormal or dysgeusic tastes, usually metallic, bitter or sour.

Complaint of dry mouth in presence of normal flows.

Sensory changes or paresthesia including complaints of areas of roughness or

irritation.

Prevalence rate of between 0.7–2.6% of all neuropathic pain

Miriam Grushkaa, Burning Mouth Syndrome; An Update, 2006, vol 63, pp 278–287

Etiology

Systemic causes

Nutritional deficiency: vitamin B, iron, zinc

Allergy: food or dental materials

Esophageal reflux disorder

Uncontrolled diabetes

Acoustic neuroma Central changes including multiple

sclerosis, Parkinson’s disease, trigeminal neuralgia

Autoimmune disorders: Sjögren’s syndrome

Local causes

Candidiasis, Poorly fitting dentures, restorations, Geographic, fissured tongue

Lichen planus other oral vesicullo-bullous conditions

Dry mouth: autoimmune disorders, medication

Viral infection: herpes simplex, herpes zoster

Trauma to lingual or mandibular nerve following dental surgery

History taking is the key to diagnosis of BMS.

The diagnosis is based on clinical characteristics, including either a sudden or intermittent onset of pain.

Bilateral presentation.

A progressive increase in pain during the day and the remission of pain with eating and sleeping.

Hummel T, Welge-Lüssen A: Taste and Smell. An Update, Adv Otorhinolaryngol, 2006, vol 63, pp 278–287

Lab Diagnosis

Haematological and biochemical investigations to assess if anaemic, low in iron, folate or vitamin B12, or if there is a raised level of glucose;

Microbiological tests for candidosis;

Salivary flows and taste function should be assessed.

Neurological imaging and consultation.

Allergy testing;

Immunological testing for conditions such as Sjögren’s syndrome or systemic lupus erythematosus.

A detailed drug history will highlight any drugs that may be associated with burning oral pain.

Complex regional pain syndrome

Formerly known as reflex sympathetic dystrophy, is a poorly understood chronic condition.

Unlike low back pain, postherpetic neuralgia, and diabetic neuropathy, the initial inciting event of complex regional pain syndrome may not be evident. Often, the inciting event is a seemingly innocuous injury to the soft tissue, but the injury then becomes transformed into an unrelenting, debilitating pain syndrome.

Also, dystrophic changes are not universal, and the transformation from an inciting event into chronic pain is not reflexive.

Complex regional pain syndrome is divided into Type I- no evidence of peripheral nerve injury and Type II- documented peripheral nerve injury.

Brian Hainline, Chronic Pain: Physiological, Diagnostic, and Management Considerations, Psychiatr Clin N Am 28 (2005) 713–735

Complex regional pain syndrome is diagnosed using the following four criteria.

1. There has been an initiating noxious event for a cause of immobilization.

2. There is continuing pain, allodynia, or hyperalgesia that is disproportionate to any inciting event.

3. There is evidence of edema, changes in skin blood flow, or abnormal pseudomotor activity in the region of the pain.

4. The condition is excluded by the existence of a condition that otherwise would account for the degree of pain and dysfunction.

Brian Hainline, Chronic Pain: Physiological, Diagnostic, and Management Considerations, Psychiatr Clin N Am 28 (2005) 713–735

MANAGEMENT

Pharmacologic Management

1. Assess and establish the diagnosis of neuropathic pain

• Establish and treat the cause of neuropathic pain

• Identify relevant co morbidities

• Explain diagnosis and treatment plan to patient

2. Initiate symptom treatment with 1 or more of the following:

• Selective serotonin nor epinephrine reuptake inhibitor or tricyclic

antidepressant

• Lidocaine patch 5%

• Opioid analgesic or tramadol— in selected clinical circumstances

• Evaluate for nonpharmacologic treatments

3. Reassess pain and health-related quality of life frequently

• If substantial pain relief and tolerable side effects, then continue same treatment

• If partial pain relief, titrate the initial medication or add another first-line medication

• If no or inadequate pain relief, switch to alternative first-line medication

4. If trial of first-line and second-line medications fails, consider third- line

medications or refer to a pain specialist

Dr. Ashok Kumar Saxena, Dr. Raman Azad2, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. Anaeshesia,2006;50(4), 249- 257

Pharmacological treatment Analgesics

The type of analgesic selected for pain control is determined by the severity and the nature of symptoms as well as the location of the neurological lesion.

Mild, chronic neuritis caused by inflammation in the skin, mucosa, and joints or when vasculitis and edema are best managed by mild analgesics, such as salicylates, propoxyphene, or para- aminophenols, for which the suspected site of action is in the peripheral tissue and paravascular receptors.

Because of the potential for addiction, chronic pain syndromes should not be managed solely by narcotic analgesics

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Topical Lidocaine patch 5% Maximum of 3 patches 3 weeks

Controlled trial evidence indicates that topical lidocaine patch is an effective treatment strategy for PHN through a direct effect of the LA and a “protective” effect of the patch vehicle on painfully sensitive skin. For lidocaine patch, blood levels are well below the minimum of systemic toxicity. Open label studies suggest that lidocaine patches may have utility for neuropathic pain disorders other than PHN.

Devers A, Galer BS. Topical lidocaine patch relieves a variety of neuropathic pain conditions: an open-label study. Clin J Pain 2000; 16: 205-08.

Morphine- DURAMOR 10- to 100-mg in div doses for 1-2 weeks

Tramadol- AMADOL, ANTRA 50 -100 mg once or twice daily ; Increase upto 400 mg daily

Lamotrigine- broadspectrum antiepileptic drug also used especially in TN caused by multiple sclerosis.

LAMITOR, LAMIDUS- 25, 50, 100mg tab Doses- 50mg/day initially increased upto 300 mg/day.

Leandri M. Lamotrigine in trigeminal neuralgia secondary to multiple sclerosis. J. Neurol. 2000, 247 : 556-558.

Anticonvulsants

Based on the concept that many paroxysmal pains are produced by the epileptiform mechanism, anticonvulsant agents have proved effective in the treatment of severe neuralgia.

For severe neuralgia, carbamazepine – MAZETOL, TEGTOL 200 once or twice daily increases to 400 mg 2-3 times daily Effective in controlling TN in 85% to 100% of cases.

This drug has also been useful in the control of multiple sclerosis, and post traumatic neuralgias.

However, it has been less than 50% effective in postherpetic neuralgia, phantom pain, and periodic migrainous neuralgia.

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Phenytoin – DILANTIN, EPILAN 100 mg 2-3 times daily, maximum dose 600mg daily controls the pain of idiopathic trigeminal neuralgia in approximately 50% of cases.

Gabapentina- DOBIN, GABAPIN 300 mg to 600 mg 3 times daily

Pregabalina-GABLIN-75, NEUGABA 75- 150mg bd increases upto 600 mg daily 4 weeks

Dworkin RH, Backonja M, Rowbotham MC et al. Advances in neuropathic pain: diagnosis, mechanisms and treatment recommendations. Arch Neurol 2003; 60: 1524-34.

Corticosteroids

Agents such as ACTH and adrenal corticosteroids are indicated when the neurological disorder is a result either directly or indirectly of inflammation.

They may be helpful in the early stages of facial nerve neuritis (Bell's palsy) to prevent degeneration of the nerve trunk within the facial canal.

Steroids may also be indirectly effective in preventing further degeneration when vasculitis is a factor, such as in connective tissue diseases, diabetic neuropathy, and temporal arthritis.

Hydrocortisone- DIZICART, H-CORT (inj) 0.5- 2ml intraarticular inj till the response

Dexamethasone- DEXONA, WYMESONE(tab. & inj) 4-20mg/day oral or 4mg/ml(2ml)/day till the response

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Antidepressant

Because of the association of chronic pain and emotional disorder, antidepressant and major tranquilizer drugs are necessary and effective.

Amitryptiline- AMIGEM, AMIPOX 10- 25 mg tds, can increase upto 200mg/day Imipramine- ANTIDEP, DEPSONIL, Dose ranges of 75 to 150 mg daily for 4 to 6 months.

Nortriptyline- PRIMOX, SENSIVAL 25 mg at Increase by 50- 150 mg daily 6-8 weeks

Venlafaxine DALIUM, FLAVIX, 75 mg/day in div doses increases by 225 mg daily 4-6 weeks

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Psychotropic drugs

In more severe forms of psychopathology, in which facial pain may represent a conversion hysteria or a "mask" for psychosis, major tranquilizers such as chlorpromazine or Duloxetine have been effective.

Chlorpromazine- CHLORPROMAZINE- CLOZINE, CPZ 10- 25 mg/day (use a bedtime 25 mg daily every level of active medication at

least 2 weeks

Duloxetine,- DELL, DIMOREX 30 mg once daily Increase to 60 mg twice daily 4 weeks 60 mg once daily after 1 week

Hempenstall K: Analgesic therapy in postherpetic neuralgia: A quantitative systematic review. P Med 2:e164, 2005

In a double-blinded, placebo-controlled RCT, the analgesic effect of a short-acting intravenous opioid, fentanyl, was compared with an active (diazepam) and inert (saline) placebo in 53 patients with various types of neuropathic pain including 3 with Post Herpetic Neuralgia.

Compared with the 2 control phases, patients had significantly superior average and maximum pain relief while receiving placebo, and the analgesic effect was independent of the degree of sedation.

Dellemijn PL, Vanneste JA: Randomised double-blind active-placebo-controlled crossover trial of intravenous fentanyl in neuropathic pain. Lancet 349:753-758, 1997

Surgical control

In the surgical control of maxillofacial pain, manipulations are made at

four main levels of the sensory nervous pathway:

(1) the peripheral nerves,

(2) the sensory ganglia and their roots,

(3) the brain stem, and

(4) the thalamus-cortex.

Surgery can be performed by using decompression, simple nerve section,

selective thermal lesions, cautery, cryosurgery, and mechanical and

chemical necrosis.

Treatment of nerve injuries

It is advisable to explore the injury site to decompress the nerve by evacuating hematoma, removing impinging bone fragments or foreign bodies, and resecting the neuroma segments and, finally, to rejoin the nerve segments using the suture techniques just described.

The prognosis is poor when motor nerves have been injured and when long segments of nerve have been lost.

Nerve grafting has been used to repair large nerve deficits.

In all cases of nerve damage, it is important to protect and maintain the nonneurological tissues that have been denervated to assure their maximum function when regeneration does occur

Mekhail NA, Cost benefit analysis of neurostimulation for chronic pain. Clin J Pain 2004; 20(6): 462-68

Therapeutic anesthetic blocks

Blocks of peripheral nerve, myofacial, or neurovascular trigger zones by anesthetic agents are of considerable value in managing pain syndromes. They have value as diagnostic aids as outlined previously.

They are also useful as a palliative procedure to achieve instant relief for a suffering patient and to "buy time” to establish more definitive therapy or to make a more thorough diagnosis.

Nerve blocks have prognostic value. Blocks may also be used in therapy, particularly for pain disorders of a cyclical

nature in which remissions are common such as the major neuralgias, posttraumatic pain, and certain myofascial pain syndromes. Using anesthetic blocks

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Palliative blocks with long-acting anesthetics such as 0.5% bupivacaine with epinephrine, may be given daily or at longer intervals to control acute triggered paroxysms of trigeminal neuralgia while effective levels of anticonvulsant drugs are being attained.

Blocks are given at 48-hour to weekly intervals into nerve distributions and particularly into zones of previous trauma and neural or muscular trigger foci.

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

The objectives is to give prompt and sustained relief from severe pain and also to attempt to block its regeneration.

It is indicated in old and debilitated patients, in cases in which the first and second divisions of the trigeminal system are involved, in neuralgias with multiple sclerosis and carcinoma, It is especially indicated for the patient with short life expectancy resulting from painful invasive cancers.

Interrutpion of the peripheral nerves may be brought about by injecting a 95% ethanol into the affected nerve branch or by surgical exposure and sectioning of the branch.

Nerve foramen should be obliterated with sterile wooden pegs, amalgam, or bone

plugs to block further nerve regeneration.

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Peripheral denervation

Radiofrequency (RF) thermal lesions performed most often at the level of the trigeminal ganglion and sensory root. Preliminary research had shown that RF thermal lesions of 60° to 70°C, when applied to peripheral nerves, have the effect of selectively destroying small nerve fibers but at the same time retaining the larger nerve fibers.

In the most common RF thermoganglionlysis technique a 22-gauge needle, insulated except at its tip, is inserted through the skin of the cheek, passed medial to the mandibular ramus and through the foramen ovale to come to rest at the ventral aspect of the trigeminal ganglion in Meckel's cavity.

A general anesthetic or deep sedative is given to the patient and one or two thermal lesions of 60° to 70°C are made for 30 seconds each. Results of these lesions have been very good, with a high control rate of pain, minimal complication, and a pain recurrence rate of approximately 20% per year.

Racz GB, Ruiz-Lopez R. Radiofrequency procedures. Pain Practice 2006; 6: 46-50.

Radiofrequency (RF) thermal lesions

With these techniques, a simple incision of the dural sleeve that surrounds the ganglia and sensory roots is made, followed by a gentle freeing and manipulation of the ganlgion and its roots. For unknown reasons, this manipulation alone has the surprising effect of pain elimination with retention of tactile and proprioceptive senses.

More recently, a major modification made in decompression procedures at the level of the trigeminal sensory root. In this operation, using a posterior fossa approach, the superior cerebellar arteries are elevated away from the sensory root and a Teflon sponge barrier is placed between root and vessels.

In spite of the apparent permanence of this procedure, there is a neuralgia recurrence rate of 13% to 15% that may be a result of either incomplete nerve lesion or the action of aberrant sensory fibers in the motor trigeminal root

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Craniotomy procedures

The known surgical treatments for most varieties of central pain such as phantom pain, thalamic syndrome, tabes dorsalis, and postherpetic facial neuralgia.

Lesions of the posterior medial thalamus are made by RF electrodes that are left implanted for a period of time to allow repetitive enlargement of the original lesion, thus adapting the lesion size to compensate for spreading of the pain disease.

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Current Opinions And Future Perspectives; Indian J. anaes,2006;50(4), 249- 257

Thalamotomy and cortical leukotomy

The use of physiological counterstimulation to inhibit chronic pathological pain grew out of the gate control concept of pain threshold. The earliest applications included the technique of dorsal column stimulation in which subcutaneous electrical transmitters have brought about pain relief .

Even peripheral nerve stimulations have shown promise by use of this technique. example, low-voltage RF waves have been passed through the surface and needle electrodes that were implanted into the infraorbital, lingual, and auriculotemporal nerves of patients with idiopathic trigeminal neuralgia.

Dr. Ashok Saxena, Dr. Raman Azad, Advances In The Mechanisms, Diagnosis And Management Of Neuropathic Pain : Indian J. anaes,2006;50(4), 249- 257

Gustav O Kruger ; Textbook of Oral and Maxillofacial Surgery, ch 26, 6th edi; 700-756

Physiological inhibition of pain

Gustav O Kruger ; Textbook of Oral and Maxillofacial Surgery, ch 26, 6th edi; 700-756

The most widely used and effective stimulation.

Cutaneous bipolar surface electrodes are placed in the painful body regions and low-voltage electrical currents are administered by the patient.

Best results have been obtained when intense stimulation is maintained for at least an hour daily for more than 3 weeks.

TNS portable units are in widespread use in pain clinics throughout the world, and TNS has proved most effective against neuropathic pain such as phantom limb pain and nerve injury pain.

It has been effective in a smaller percentage of patients with facial pain but, when successful, is an excellent noninvasive treatment.

Transcutaneous neural stimulation

Capsaicin. Derived from hot chille peppers, topical capsaicin may be useful for some people in relieving pain. "Capsaicin works by depleting substance P, a compound that conveys the pain sensation from the peripheral to the central nervous system. It takes a couple of days for pain relief,“

Topical capsaicin- RELAXYL- 0.05%, ALGIPAN-0.1% Cream Apply 3–4 times a day over affected region

Ginger. Though more studies are needed, ginger extract may help with joint and muscle pain because it contains phytochemicals, which help to stop inflammation.

David Kiefer, MD, Dr. Kiefer, professor of medicine at the Arizona Center for Integrative Medicine.

Herbal treatment

Feverfew- Feverfew has been used for centuries to treat headaches, stomachaches, and toothaches. Nowadays it's also used for migraines and rheumatoid arthritis.

Freeze dried capsules- 25mg/day.

Turmeric- This spice has been used to relieve arthritis pain and heartburn, and to reduce inflammation.

Turmeric oil is used for local application.

Kava Kava- (kavalactones) The roots of the plant are used to produce a drink with sedative, analgesic,

anticonvulsant,anxiolytic, hypnotic and anesthetic properties. It relieves tension headaches and neuropathic pain. Doses above 250mg are toxic.

Juhie Bhatia | Medically reviewed by Kevin O. Hwang, MD, MPHHerbal Remedies for Natural Pain Relief

Acupuncture Acupuncture involves stimulation of the body at certain points.

During a treatment, thin steel needles are inserted into the skin, then manipulated gently by hand or with light electrical stimulation.

Treatment is short and may be performed during dental treatment. About 6 week treatment is usually indicated.

Acupuncture needles stimulate the nervous system by releasing natural painkillers such as endorphins and serotonin.

Each patient responds to acupuncture differently. Some people notice an immediate improvement, while some need several treatments to experience the full effect.

The British Dental Acupuncture Association reported that about 70% of patients show some benefit.

Gustav O Kruger ; Textbook of Oral and Maxillofacial Surgery, ch 26, 6th edi; 700-756

Significant control over pain and other sensory complains may be gained through psychophysiological techniques such as yoga,meditation, biofeedback, hypnosis, and psychotherapy.

Many of the chronic pain like atypical burning mucosa are influenced by the patient's response to stress.

Hypnosis is another paraphysiological technique with primary action on pain tolerance thresholds for the control of chronic facial pain. Carefully selected patients may, with training in autosuggestion, come to effectively deny or accept their pain.

Counseling and psychotherapy can be included in the overall treatment.

Gustav O Kruger ; Textbook of Oral and Maxillofacial Surgery, ch 26, 6th edi; 700-756

Psychological approaches

Much of the psychological management of patients with neurological problems, especially pain, must be directed toward prevention.

Curable pain should be relieved promptly and not allowed to become chronic because pain that persists longer than 6 months in a neurotic individual often becomes too valuable in interpersonal relations to give up easily.

Because there is known to be a higher incidence of maxillofacial pain in paranoic and psychopathic deviates, the clinician should remain alert for signs of personality disorders.

Patients must not be allowed to become overly dependent on a given therapist. Demands for repetitive or irrelevant treatments should be tactfully opposed. It is often helpful to discuss openly with patients the nearly universal role of psychological components in neurological

Pharmacological

Analgesics Lidocaine patch 5% Morphine- 50- to 100-mg/dayTramadol- 50 -100 mg od or bid; upto 400 mg /d

Anticonvulsants Carbamazepine 100–1000 mg/d bid to qidGabapentin 900–3600 mg/d tid

Antidepressants Amitriptyline 10–200 mg/d qdImipramine 10–200 mg/d qd to bid

Corticosteroids Hydrocortisone- 0.5- 2ml intraarticular injDexamethasone- (tab. & inj) 4-20mg/day oral or 4mg/ml(2ml)/day

Other Lidocaine 0.25–2 mg/kg/d IVKetamine 0.25–0.5 mg/kg/day

Surgical Therapeutic anesthetic blocks 0.5% bupivacaine with epinephrine,

Peripheral denervation

Selective thermal lesions RF thermoganglionlysis technique for 60° to 70°C

Craniotomy procedures

Thalamotomy and cortical leukotomy

Physiologic inhibition of pain

Transcutaneous neural stimulation

nonsurgical herbal Capsacin, Ginger, termeric

Acupuncture & acupressure

Psychologic yoga,meditation, biofeedback, hypnosis, and psychotherapy.

Combination Medicinal+surgical medicinal+ nonsurgical

Thank you