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DRUG THERAPY OF NEURALGIAS
DR.V.SATHYANARAYANAN MBBS., M.D., ACME.,
PROFESSOR OF PHARMACOLOGY,
SRM MCH & RC, CHENNAI, INDIA
 Definition
 Neuralgia vs Neuropathy
 Classification, Characteristics and clinical course of neuralgias
 Types of neuralgias
 Drugs for neuralgias
 Trigeminal neuralgia
 Glossopharyngeal neuralgia
 Occipital neuralgia
 Post herpetic neuralgia
 Conclusion
OUTLINE
WHAT IS NEURALGIA ?
 neuralgia refers to pain in the distribution of a nerve
 Neuropathy implies neuronal injury.
 Patients with neuralgia may or may not have a
secondary cause.
NEURALGIA VS NEUROPATHY
 primary (classical) or
 secondary (symptomatic)
 Distinguishing between the 2 is critical for
 developing an appropriate diagnostic and therapeutic
plan
CLASSIFICATION
 The neuralgias are characterized by
 paroxysmal, brief, and intense pains
 described as
 sharp,
 lancinating,
 stabbing, or
lightning-like
 within the distribution of a particular nerve.
CHARACTERISTICS
 They are often associated with triggers that may take the
form of trivial stimuli,
 such as brushing teeth or shaving.
 generally followed by pain-free periods known as refractory
periods.
 Tenderness over the involved nerve is typical
 as is abolishment of pain by local anaesthetic blockade
CHARACTERISTICS
 monophasic,
 relapsing and remitting,
 or chronic in nature..
Clinical course
 The most commonly encountered neuralgias are
 Trigeminal neuralgia
 Post herpetic neuralgia
 Glossopharyngeal neuralgia
 Occipital neuralgia
TYPES
 Carbamazepine 200 mg/day , 400–800 mg/d
 Oxcarbazepine 150 mg/d, 150 mg/3d, 750–1800 mg/d
 Gabapentin 300 mg/d, 300 mg/3–7 d, 900–2400 mg/d
 Pregabalin 150 mg/d, 150 mg/wk, 600–1200 mg/d
 Lamotrigine 25 mg/d, 25 mg/wk, 100–400 mg/d
 Topiramate 25 mg/d , 25 mg/wk , 100–400 mg/d
 Baclofen 5–10 mg/d, 5 mg/3d, 50–75 mg TID
 Amitriptyline
DRUGS FOR NEURALGIAS
CARBAMAZEPINE
 Chemically related to imipramine
 MOA – Prolongs the inactivated state of neuronal
voltage dependent sodium channels and stabilize
neuronal membrane
 75% protein bound
 Long half life
 Autoinduction occur
Sodium channels
ADVERSE EFFECTS
 Hypersensitivity
 Dose related neurotoxicity- drowsiness, ataxia,
vertigo
 Hypersensitivity reactions- Hepatitis, lupus like
syndrome
 Enhance ADH action
 Aplastic anemia
 Minor fetal malformations
USES IN NEURALGIA
1st choice in Trigeminal neuralgia ,
post herpetic neuralgia
and other neuropathic pain
OXCARBAZEPINE
 Less toxic than carbamazepine
 Mild enzyme inducer – less drug interactions
 Less side effects
 Cause hyponatremia
GABAPENTIN
 GABA derivative
 Increases GABA release
 Add on drug in SPS, CPS
 Pain due to diabetic neuropathy, post herpetic neuralgia
 Migraine
 Manic depression
 ADR- sedation, tiredness
PREGABALIN
LAMOTRIGENE
 Broad spectrum action
 Blocks Na channels  stabilizes presynaptic
membrane
 blocks high voltage dependent Ca channels
 Prevents release of excitatory neurotransmitters
ADVERSE EFFECTS
 Sedation,
 ataxia,
 diplopia,
 RASH –sometimes life threatening
 Negative effect on cognitive function not reported
TOPIRAMATE
 Weak Carbonic anhydrase inhibitor
 Broad spectrum anticonvulsant
 Act by antagonizing glutamate, GABA potentiation, prolonging
Na channel prolongation
 ADR – sedation, ataxia, psychiatric symptoms
BACLOFEN
 Selective GABAB receptor agonist
 Act at spinal cord
 Depress both poysynaptic, monosynaptic reflexes
 Less sedative
 Reduces spasticity in many neurological disorders
 S/E – mental confusion, ataxia, weakness
 Tricyclic antidepressant
 Acts by inhibiting NE and serotonin reuptake by
presynaptic neurons  increased NE in the synapse
 takes 3 to 4 weeks time for full benefit
 Widely used in neuropathic pain in low doses
 Side effects  dizziness, drowsiness, dry mouth, nausea
and constipation
AMITRIPTYLINE
OTHER DRUGS
 Clonidine is an α2-adrenergic agonist  provides potent
analgesia.
 In neuropathic pain, α2 adrenoreceptors are upregulated and
are sensitive to norepinephrine.
 Activation of α2 adrenoreceptors therefore inhibits the
release of calcitonin gene-related peptide and glutamate
role in nociception as neurotransmitters.
 Clonidine may be compounded into a cream and applied
topically to provide pain relief.
 Systemic side effects include sedation and hypotension
requiring close monitoring.
CLONIDINE
 5% lidocaine plasters comprised of 700 mg of
lidocaine mixed with a polyethylene terephthalate
backing.
 used 12 hours per day for 4 weeks for TN
 a lidocaine 5% patch  post-herpetic neuralgia and
other peripheral neuropathic conditions.
 Adverse effects are minimal and include erythema
and rash.
LIDOCAINE
 Capsaicin is a component of chili peppers.
 It binds to the nociceptor, TRPV1, which is located on
polymodal C-fibers.
 Initially capsaicin works by increasing the production of
inflammatory mediators, causing hyperalgesia.
 However, repeated application may cause prolonged
activation of the TRPV1 receptor, rendering it dysfunctional.
 Capsaicin is available at low concentrations in ove rthe-
counter creams.
 0.025% capsaicin for 3 minutes twice a day, after local
anesthetic application to the painful site
CAPSAICIN
 nausea, dyspepsia, and initial increase in pain when applied
topically.
 Pain relief is dose dependent and
 may last for several weeks.
 Capsaicin preparations at higher doses, (capsaicin patch 8% )
have shown to be more efficacious.
 treatment is challenged by low adherence to this medication
 due to its side effects, particularly the burning pain .
CAPSAICIN PREPARATIONS
 carbamazepine 4% (a sodium channel blocker)
 lidocaine 1%
 ketoprofen 4% (a non-steroidal anti-inflammatory drug, or
NSAID)
 ketamine 4% (an NMDA-receptor antagonist)
 gabapentin 4%
 These medications were mixed with anhydrous gels and
bio-adhesive copolymers
COMPOUNDED FORMULAS
 Cannabinoids have been identified as potential adjuvant
analgesics and are currently under investigation
 The natural cannabis plant (Cannabis Sativa L) contains more than
60 cannabinoids
 Tetrahydrocannabinol (THC)/Cannabinol(CBD) oromucosal spray
 Formulated from plant-based extracts
 treatment of central neuropathic pain in patients with multiple
sclerosis (MS),
Tetrahydrocannabinol and Cannabinol
as a Spray
 Brief, intense, electrical pain
 characteristically triggered by
 chewing,
 talking,
 and light touch (eg, wind).
Trigeminal Neuralgia
 Trigeminal neuralgia may mimic tooth pain,
 and some patients report an intraoral trigger zone.
TRIGEMINAL NEURALGIA
 involves the trigeminal nerve in the head.
 It has three branches that send signals from the
brain to the face, mouth, teeth, and nose.
Trigeminal neuralgia (TN)
 TYPE 1 AND TYPE 2
 Type 1 TN  causes a painful burning or electric shock-
like sensation in parts of the face
 irregular episodes that come on suddenly
 duration of these episodes varies
 can last up to 2 minutes.
 Type 2 TN - produces a constant, dull aching sensation
in the face.
TYPES
 The initial treatment of TN always involves
pharmacotherapy with carbamazepine
 (target=400–800 mg/d)
 the first-line treatment of choice.
TREATMENT
 Oxcarbazepine (target=900–1800 mg/d)
 is equally efficacious
 with a better side effect profile
TREATMENT
 often as add-on therapies, include
 phenytoin (target=300–500 mg/d),
 baclofen (target=40–80 mg/d),
 clonazepam (target=1.5–8 mg/d),
 lamotrigine (target=150–400 mg/d),
 gabapentin (target=900–2400 mg/d),
 and pimozide (target=4–12 mg/d)
OTHER DRUGS
 Pimozide is not widely used
due to potential cardiac and neurologic toxicity
 The clinical utility of certain agents, especially lamotrigine,
is limited by
 the requirement for a slow titration
LIMITATIONS
 botulinum toxin type A (BTX) INJECTION 
generally effective treatment without major adverse
events
 The optimal injection strategy is yet to be
determined
REFRACTORY CASES
 Opioids are sometimes used during acute
exacerbations
 rescue intravenous infusion of either fosphenytoin
or lidocaine may provide transient relief while
awaiting interventional procedures
OTHER DRUGS
 20% benzocaine,
 capsaicin,
 or a compounded formula of anticonvulsants,
tricyclic antidepressants, serotonin and
norepinephrine reuptake inhibitors
 applied over an intraoral trigger zone
TOPICAL MEDICATIONS
 reduced systemic side effects
 lessened potential for drug-drug interactions
 the ability to provide direct, local analgesia;
 and improved patient compliance
ADVANTAGES OF TOPICAL
MEDICATIONS
for refractory TN
 ablative (destructive)
 (eg, peripheral neurectomy,
 glycerol rhizolysis,
 sensory rhizotomy, and
 gamma-knife radiosurgery)
 and nonablative (nondestructive) (eg, microvascular
decompression (MVD)) interventions
Neurosurgical interventions
 The severity of pain associated with TN and its devastating
psychological effects  prompt diagnosis and
treatment essential.
 Without a proper understanding of its clinical features and
medical course  TN may go undiagnosed for years.
 With a proper diagnosis and early treatment, however,
 patients may achieve pain relief, and
 resume a healthy life.
TRIGEMINAL NEURALGIA
 GN ( vagoglossopharyngeal neuralgia) is less Common
 relatively less severe attacks
 The 2 disorders may occasionally co-exist.
 most common in females and patients over 50
 Most cases of GN are idiopathic,
 neurovascular compression may also be seen.
Glossopharyngeal Neuralgia
 GN is characterized by severe, transient, stabbing,
unilateral pain
 in the ear,
 tongue base,
 tonsillar fossa and/or
 beneath the angle of the jaw
CHARACTERISTICS
 include talking, yawning, coughing, and
Swallowing  may be severe enough to cause weight loss.
 also be triggered by touching the external auditory canal,
 the side of the neck,
 and the skin anterior to the ear
Common triggers
 GN may involve branches of the vagal nerve
 leading to bradycardia and syncope
 that may necessitate pacemaker placement
COMPLICATION
 Management of GN mirrors that of TN.
 Pharmacotherapy should be tried initially with the
preferred agents being the same as those used in TN
TREATMENT
 ON is a neuralgia with pathology related to cervical rather
than cranial nerves.
 The characteristic clinical presentation consists of
 brief, sharp shooting pain
 in the distribution of the occipital nerves,
 which is often associated with dysesthesia and allodynia
Occipital Neuralgia
 Nerve block with a local anesthetic
 and corticosteroid may provide temporary relief
 while a neuropathic pain medication (eg,
gabapentin) and physical therapy are initiated
TREATMENT
 pulsed radiofrequency ablation,
 occipital nerve stimulation,
 or a trial of BTX may be considered
REFRACTORY CASES
 PHN is the most common complication of
herpes zoster (also known as shingles),
 which results from reactivation of latent varicella
zoster virus
Postherpetic Neuralgia
 pain persisting more than 4 months after the
onset of rash in the area affected by herpes
zoster.
DEFINITION
 first line therapies for PHN include
 Carbamazepine
 tricyclic antidepressants (target=25–150 mg/d),
 Gabapentin (target=1800–3600 mg/d),
 pregabalin (target=150–600 mg/ d),
 topical lidocaine 5 % patch,
 Divalproex sodium 1000 mg per day
DRUG THERAPY
 In refractory cases or in patients intolerant of first
line agents,
 opioids and capsaicin may be considered.
 Combining the lidocaine patch with other agents has
also proven effective.
 Intravenous acyclovir for 2 weeks followed by
 oral valacyclovir ( latent ganglionitis is present and
may contribute to pain)
REFRACTORY CASES
 The neuralgias represent painful conditions of the head occurring
in a specific nerve dermatome.
 These disorders may be recognized by their characteristic clinical
presentations, including pain in a restricted topography.
 Although many cases are classical (primary), secondary etiologies
are not uncommon.
 Pharmacologic agents remain the first line treatment for many of
the neuralgias,
 but nerve blocks, surgery, and other procedures may be necessary
in refractory cases.
 Topical medications, in particular, may offer several advantages
CONCLUSION
THANK YOU...

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Drug therapy of neuralgias prof satyanarayan

  • 1.
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  • 11.
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  • 14.
  • 15. DRUG THERAPY OF NEURALGIAS DR.V.SATHYANARAYANAN MBBS., M.D., ACME., PROFESSOR OF PHARMACOLOGY, SRM MCH & RC, CHENNAI, INDIA
  • 16.  Definition  Neuralgia vs Neuropathy  Classification, Characteristics and clinical course of neuralgias  Types of neuralgias  Drugs for neuralgias  Trigeminal neuralgia  Glossopharyngeal neuralgia  Occipital neuralgia  Post herpetic neuralgia  Conclusion OUTLINE
  • 18.
  • 19.  neuralgia refers to pain in the distribution of a nerve  Neuropathy implies neuronal injury.  Patients with neuralgia may or may not have a secondary cause. NEURALGIA VS NEUROPATHY
  • 20.  primary (classical) or  secondary (symptomatic)  Distinguishing between the 2 is critical for  developing an appropriate diagnostic and therapeutic plan CLASSIFICATION
  • 21.  The neuralgias are characterized by  paroxysmal, brief, and intense pains  described as  sharp,  lancinating,  stabbing, or lightning-like  within the distribution of a particular nerve. CHARACTERISTICS
  • 22.  They are often associated with triggers that may take the form of trivial stimuli,  such as brushing teeth or shaving.  generally followed by pain-free periods known as refractory periods.  Tenderness over the involved nerve is typical  as is abolishment of pain by local anaesthetic blockade CHARACTERISTICS
  • 23.
  • 24.  monophasic,  relapsing and remitting,  or chronic in nature.. Clinical course
  • 25.  The most commonly encountered neuralgias are  Trigeminal neuralgia  Post herpetic neuralgia  Glossopharyngeal neuralgia  Occipital neuralgia TYPES
  • 26.
  • 27.  Carbamazepine 200 mg/day , 400–800 mg/d  Oxcarbazepine 150 mg/d, 150 mg/3d, 750–1800 mg/d  Gabapentin 300 mg/d, 300 mg/3–7 d, 900–2400 mg/d  Pregabalin 150 mg/d, 150 mg/wk, 600–1200 mg/d  Lamotrigine 25 mg/d, 25 mg/wk, 100–400 mg/d  Topiramate 25 mg/d , 25 mg/wk , 100–400 mg/d  Baclofen 5–10 mg/d, 5 mg/3d, 50–75 mg TID  Amitriptyline DRUGS FOR NEURALGIAS
  • 28.
  • 29. CARBAMAZEPINE  Chemically related to imipramine  MOA – Prolongs the inactivated state of neuronal voltage dependent sodium channels and stabilize neuronal membrane  75% protein bound  Long half life  Autoinduction occur
  • 31. ADVERSE EFFECTS  Hypersensitivity  Dose related neurotoxicity- drowsiness, ataxia, vertigo  Hypersensitivity reactions- Hepatitis, lupus like syndrome  Enhance ADH action  Aplastic anemia  Minor fetal malformations
  • 32.
  • 33.
  • 34.
  • 35.
  • 36.
  • 37. USES IN NEURALGIA 1st choice in Trigeminal neuralgia , post herpetic neuralgia and other neuropathic pain
  • 38.
  • 39.
  • 40. OXCARBAZEPINE  Less toxic than carbamazepine  Mild enzyme inducer – less drug interactions  Less side effects  Cause hyponatremia
  • 41.
  • 42. GABAPENTIN  GABA derivative  Increases GABA release  Add on drug in SPS, CPS  Pain due to diabetic neuropathy, post herpetic neuralgia  Migraine  Manic depression  ADR- sedation, tiredness
  • 43.
  • 44.
  • 45.
  • 47.
  • 48.
  • 49.
  • 50. LAMOTRIGENE  Broad spectrum action  Blocks Na channels  stabilizes presynaptic membrane  blocks high voltage dependent Ca channels  Prevents release of excitatory neurotransmitters
  • 51.
  • 52. ADVERSE EFFECTS  Sedation,  ataxia,  diplopia,  RASH –sometimes life threatening  Negative effect on cognitive function not reported
  • 53.
  • 54.
  • 55.
  • 56. TOPIRAMATE  Weak Carbonic anhydrase inhibitor  Broad spectrum anticonvulsant  Act by antagonizing glutamate, GABA potentiation, prolonging Na channel prolongation  ADR – sedation, ataxia, psychiatric symptoms
  • 57.
  • 58. BACLOFEN  Selective GABAB receptor agonist  Act at spinal cord  Depress both poysynaptic, monosynaptic reflexes  Less sedative  Reduces spasticity in many neurological disorders  S/E – mental confusion, ataxia, weakness
  • 59.
  • 60.  Tricyclic antidepressant  Acts by inhibiting NE and serotonin reuptake by presynaptic neurons  increased NE in the synapse  takes 3 to 4 weeks time for full benefit  Widely used in neuropathic pain in low doses  Side effects  dizziness, drowsiness, dry mouth, nausea and constipation AMITRIPTYLINE
  • 61.
  • 62.
  • 63.
  • 65.  Clonidine is an α2-adrenergic agonist  provides potent analgesia.  In neuropathic pain, α2 adrenoreceptors are upregulated and are sensitive to norepinephrine.  Activation of α2 adrenoreceptors therefore inhibits the release of calcitonin gene-related peptide and glutamate role in nociception as neurotransmitters.  Clonidine may be compounded into a cream and applied topically to provide pain relief.  Systemic side effects include sedation and hypotension requiring close monitoring. CLONIDINE
  • 66.
  • 67.  5% lidocaine plasters comprised of 700 mg of lidocaine mixed with a polyethylene terephthalate backing.  used 12 hours per day for 4 weeks for TN  a lidocaine 5% patch  post-herpetic neuralgia and other peripheral neuropathic conditions.  Adverse effects are minimal and include erythema and rash. LIDOCAINE
  • 68.
  • 69.
  • 70.
  • 71.  Capsaicin is a component of chili peppers.  It binds to the nociceptor, TRPV1, which is located on polymodal C-fibers.  Initially capsaicin works by increasing the production of inflammatory mediators, causing hyperalgesia.  However, repeated application may cause prolonged activation of the TRPV1 receptor, rendering it dysfunctional.  Capsaicin is available at low concentrations in ove rthe- counter creams.  0.025% capsaicin for 3 minutes twice a day, after local anesthetic application to the painful site CAPSAICIN
  • 72.
  • 73.
  • 74.  nausea, dyspepsia, and initial increase in pain when applied topically.  Pain relief is dose dependent and  may last for several weeks.  Capsaicin preparations at higher doses, (capsaicin patch 8% ) have shown to be more efficacious.  treatment is challenged by low adherence to this medication  due to its side effects, particularly the burning pain . CAPSAICIN PREPARATIONS
  • 75.
  • 76.
  • 77.  carbamazepine 4% (a sodium channel blocker)  lidocaine 1%  ketoprofen 4% (a non-steroidal anti-inflammatory drug, or NSAID)  ketamine 4% (an NMDA-receptor antagonist)  gabapentin 4%  These medications were mixed with anhydrous gels and bio-adhesive copolymers COMPOUNDED FORMULAS
  • 78.  Cannabinoids have been identified as potential adjuvant analgesics and are currently under investigation  The natural cannabis plant (Cannabis Sativa L) contains more than 60 cannabinoids  Tetrahydrocannabinol (THC)/Cannabinol(CBD) oromucosal spray  Formulated from plant-based extracts  treatment of central neuropathic pain in patients with multiple sclerosis (MS), Tetrahydrocannabinol and Cannabinol as a Spray
  • 79.
  • 80.
  • 81.
  • 82.
  • 83.
  • 84.  Brief, intense, electrical pain  characteristically triggered by  chewing,  talking,  and light touch (eg, wind). Trigeminal Neuralgia
  • 85.
  • 86.  Trigeminal neuralgia may mimic tooth pain,  and some patients report an intraoral trigger zone. TRIGEMINAL NEURALGIA
  • 87.
  • 88.
  • 89.
  • 90.  involves the trigeminal nerve in the head.  It has three branches that send signals from the brain to the face, mouth, teeth, and nose. Trigeminal neuralgia (TN)
  • 91.
  • 92.
  • 93.
  • 94.  TYPE 1 AND TYPE 2  Type 1 TN  causes a painful burning or electric shock- like sensation in parts of the face  irregular episodes that come on suddenly  duration of these episodes varies  can last up to 2 minutes.  Type 2 TN - produces a constant, dull aching sensation in the face. TYPES
  • 95.
  • 96.
  • 97.  The initial treatment of TN always involves pharmacotherapy with carbamazepine  (target=400–800 mg/d)  the first-line treatment of choice. TREATMENT
  • 98.
  • 99.  Oxcarbazepine (target=900–1800 mg/d)  is equally efficacious  with a better side effect profile TREATMENT
  • 100.
  • 101.
  • 102.  often as add-on therapies, include  phenytoin (target=300–500 mg/d),  baclofen (target=40–80 mg/d),  clonazepam (target=1.5–8 mg/d),  lamotrigine (target=150–400 mg/d),  gabapentin (target=900–2400 mg/d),  and pimozide (target=4–12 mg/d) OTHER DRUGS
  • 103.  Pimozide is not widely used due to potential cardiac and neurologic toxicity  The clinical utility of certain agents, especially lamotrigine, is limited by  the requirement for a slow titration LIMITATIONS
  • 104.  botulinum toxin type A (BTX) INJECTION  generally effective treatment without major adverse events  The optimal injection strategy is yet to be determined REFRACTORY CASES
  • 105.
  • 106.
  • 107.
  • 108.  Opioids are sometimes used during acute exacerbations  rescue intravenous infusion of either fosphenytoin or lidocaine may provide transient relief while awaiting interventional procedures OTHER DRUGS
  • 109.
  • 110.
  • 111.
  • 112.  20% benzocaine,  capsaicin,  or a compounded formula of anticonvulsants, tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors  applied over an intraoral trigger zone TOPICAL MEDICATIONS
  • 113.
  • 114.
  • 115.
  • 116.  reduced systemic side effects  lessened potential for drug-drug interactions  the ability to provide direct, local analgesia;  and improved patient compliance ADVANTAGES OF TOPICAL MEDICATIONS
  • 117. for refractory TN  ablative (destructive)  (eg, peripheral neurectomy,  glycerol rhizolysis,  sensory rhizotomy, and  gamma-knife radiosurgery)  and nonablative (nondestructive) (eg, microvascular decompression (MVD)) interventions Neurosurgical interventions
  • 118.
  • 119.
  • 120.  The severity of pain associated with TN and its devastating psychological effects  prompt diagnosis and treatment essential.  Without a proper understanding of its clinical features and medical course  TN may go undiagnosed for years.  With a proper diagnosis and early treatment, however,  patients may achieve pain relief, and  resume a healthy life. TRIGEMINAL NEURALGIA
  • 121.
  • 122.
  • 123.
  • 124.
  • 125.
  • 126.  GN ( vagoglossopharyngeal neuralgia) is less Common  relatively less severe attacks  The 2 disorders may occasionally co-exist.  most common in females and patients over 50  Most cases of GN are idiopathic,  neurovascular compression may also be seen. Glossopharyngeal Neuralgia
  • 127.  GN is characterized by severe, transient, stabbing, unilateral pain  in the ear,  tongue base,  tonsillar fossa and/or  beneath the angle of the jaw CHARACTERISTICS
  • 128.
  • 129.
  • 130.
  • 131.  include talking, yawning, coughing, and Swallowing  may be severe enough to cause weight loss.  also be triggered by touching the external auditory canal,  the side of the neck,  and the skin anterior to the ear Common triggers
  • 132.
  • 133.
  • 134.  GN may involve branches of the vagal nerve  leading to bradycardia and syncope  that may necessitate pacemaker placement COMPLICATION
  • 135.  Management of GN mirrors that of TN.  Pharmacotherapy should be tried initially with the preferred agents being the same as those used in TN TREATMENT
  • 136.
  • 137.
  • 138.
  • 139.
  • 140.  ON is a neuralgia with pathology related to cervical rather than cranial nerves.  The characteristic clinical presentation consists of  brief, sharp shooting pain  in the distribution of the occipital nerves,  which is often associated with dysesthesia and allodynia Occipital Neuralgia
  • 141.
  • 142.
  • 143.
  • 144.
  • 145.
  • 146.
  • 147.  Nerve block with a local anesthetic  and corticosteroid may provide temporary relief  while a neuropathic pain medication (eg, gabapentin) and physical therapy are initiated TREATMENT
  • 148.
  • 149.
  • 150.
  • 151.  pulsed radiofrequency ablation,  occipital nerve stimulation,  or a trial of BTX may be considered REFRACTORY CASES
  • 152.
  • 153.
  • 154.  PHN is the most common complication of herpes zoster (also known as shingles),  which results from reactivation of latent varicella zoster virus Postherpetic Neuralgia
  • 155.
  • 156.
  • 157.
  • 158.  pain persisting more than 4 months after the onset of rash in the area affected by herpes zoster. DEFINITION
  • 159.
  • 160.
  • 161.  first line therapies for PHN include  Carbamazepine  tricyclic antidepressants (target=25–150 mg/d),  Gabapentin (target=1800–3600 mg/d),  pregabalin (target=150–600 mg/ d),  topical lidocaine 5 % patch,  Divalproex sodium 1000 mg per day DRUG THERAPY
  • 162.
  • 163.  In refractory cases or in patients intolerant of first line agents,  opioids and capsaicin may be considered.  Combining the lidocaine patch with other agents has also proven effective.  Intravenous acyclovir for 2 weeks followed by  oral valacyclovir ( latent ganglionitis is present and may contribute to pain) REFRACTORY CASES
  • 164.
  • 165.
  • 166.
  • 167.
  • 168.
  • 169.
  • 170.
  • 171.  The neuralgias represent painful conditions of the head occurring in a specific nerve dermatome.  These disorders may be recognized by their characteristic clinical presentations, including pain in a restricted topography.  Although many cases are classical (primary), secondary etiologies are not uncommon.  Pharmacologic agents remain the first line treatment for many of the neuralgias,  but nerve blocks, surgery, and other procedures may be necessary in refractory cases.  Topical medications, in particular, may offer several advantages CONCLUSION
  • 172.
  • 173.
  • 174.
  • 175.

Notes de l'éditeur

  1. Carbamazepine allergy. Extensive rash over the back and arms of a 74-year-old woman due to an allergic reaction to carbamazepine. Carbamazepine is an anticonvulsant drug used in the long term treatment of epilepsy and to relieve neuralgia. A reaction to the drug has caused a rash consisting of numerous circular or irregular red spots which may be itchy. The rash may be accompanied by fever, sore throat, headache or diarrhoea. Treatment of such allergic reactions involves withdrawal of the causative drug. Corticosteroid drugs can be given to reduce inflammation and irritation.