neuropathic pain, diagnosis and management by Dr. Priya Rangari

1. Dr. Ashok Kumar Saxena,
Dr. Raman Azad
Indian J. Anaeshesia,2006;50(4), 249- 257
Trigeminal neuralgia
A review
Dr. Priti Shah , Dr Hetul Patel , Dr. Mona Shah , Dr.
Kevin Parikh; B U J O D, Vol. 4 Issue-1 January 2014

2. 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.”
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.

3.  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.

4.  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

5. 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

6. 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

7. 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 of
mechanical allodynia in patients with neuropathic pain. Neurology 2004;63:1838–46.

8.  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)

9. 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 of
mechanical allodynia in patients with neuropathic pain. Neurology 2004;63:1838–46.

10. 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.

11. 
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12.  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.

13.  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

14.  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.

15.  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.

16. 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.

18.  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.

19.  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.

20.  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.

21.  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.

23.  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.

24.  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.

25.  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

26.  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

27.  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

28. 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.).

29.  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

30. 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

31.  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

32.  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.

33.  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

34.  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

36. 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

37. 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

38.  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

39.  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.

40.  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.

41.  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

42.  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.

43.  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

44.  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

45.  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

46.  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

47.  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.

48.  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

49.  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

50.  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.

51. Peripheral denervation
 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.

52. Radiofrequency (RF) thermal lesions
 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.

53. Craniotomy procedures
 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

54. Thalamotomy and cortical leukotomy
 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.

55. Physiological inhibition of pain
 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.

56. Transcutaneous neural stimulation
 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.

57. Herbal treatment
 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.

58.  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

59.  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

60.  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.
Psychological approaches

61.  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

62. Pharmacological Analgesics Lidocaine patch 5%
Morphine- 50- to 100-mg/day
Tramadol- 50 -100 mg od or bid; upto 400 mg /d
Anticonvulsants Carbamazepine 100–1000 mg/d bid to qid
Gabapentin 900–3600 mg/d tid
Antidepressants Amitriptyline 10–200 mg/d qd
Imipramine 10–200 mg/d qd to bid
Corticosteroids Hydrocortisone- 0.5- 2ml intraarticular inj
Dexamethasone- (tab. & inj) 4-20mg/day oral or 4mg/ml(2ml)/day
Other Lidocaine 0.25–2 mg/kg/d IV
Ketamine 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