Trigeminal neuralgia, herpetic neuralgia, myofascial pains

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Trigeminal neuralgia, herpetic neuralgia, myofascial pains

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Trigeminal neuralgia, herpetic neuralgia, myofascial pains

  1. 1. TRIGEMINAL NEURALGIA,TRIGEMINAL NEURALGIA, HERPETIC NEURALGIA,HERPETIC NEURALGIA, MYOFASCIAL PAINS ANDMYOFASCIAL PAINS AND MANAGEMENTMANAGEMENT DR. ARATI M. BADGANDIDR. ARATI M. BADGANDI
  2. 2. TRIGEMINAL NEURALGIATRIGEMINAL NEURALGIA BackgroundBackground  Trigeminal neuralgia (TN) - Tic douloureux, common & potentiallyTrigeminal neuralgia (TN) - Tic douloureux, common & potentially disabling pain syndrome, precise pathophysiology of which remainsdisabling pain syndrome, precise pathophysiology of which remains obscure.obscure.  known to drive pts to the brink of suicide.known to drive pts to the brink of suicide.  Although neurologic examination findings are normal in pts withAlthough neurologic examination findings are normal in pts with idiopathic variety (most common type), clinical history is distinctive.idiopathic variety (most common type), clinical history is distinctive.  characterized by unilateral pain (paroxysms of severe, lancinating,characterized by unilateral pain (paroxysms of severe, lancinating, "electric-like" bouts) following sensory distribution of cranial nerve V"electric-like" bouts) following sensory distribution of cranial nerve V —typically radiating to maxillary (V2) or mandibular (V3) area in—typically radiating to maxillary (V2) or mandibular (V3) area in 35%, often accompanied by brief facial spasm or tic.35%, often accompanied by brief facial spasm or tic.  Isolated involvement of ophthalmic division much less commonIsolated involvement of ophthalmic division much less common (2.8%).(2.8%).  Typically, initial response to carbamazepine therapy is diagnosticTypically, initial response to carbamazepine therapy is diagnostic and successful.and successful.  Despite early relief with medication, pts may experienceDespite early relief with medication, pts may experience breakthrough pain requiring additional drugs &/or 1+ of surgicalbreakthrough pain requiring additional drugs &/or 1+ of surgical interventions.interventions.
  3. 3. Historical informationHistorical information  clinical description of TN can be traced back >300clinical description of TN can be traced back >300 years.years.  Aretaeus of Cappadocia, known for 1 of earliestAretaeus of Cappadocia, known for 1 of earliest descriptions of migraine, is credited with 1st indication ofdescriptions of migraine, is credited with 1st indication of TN.TN.  Nicholaus Andre coined term tic douloureux in 1756.Nicholaus Andre coined term tic douloureux in 1756.  John Fothergill was 1st to give full & accurate descriptionJohn Fothergill was 1st to give full & accurate description of this condition in paper titled "On a Painful Affliction ofof this condition in paper titled "On a Painful Affliction of the Face," - presented to medical society of London inthe Face," - presented to medical society of London in 1773.1773.  Osler also described TN in great and accurate detail inOsler also described TN in great and accurate detail in his 1912 bookhis 1912 book The Principles and Practice of MedicineThe Principles and Practice of Medicine..  In 1900, in a landmark article, Cushing reported methodIn 1900, in a landmark article, Cushing reported method of total ablation of the gasserian ganglion to treatof total ablation of the gasserian ganglion to treat trigeminal neuralgia.trigeminal neuralgia.
  4. 4. AnatomyAnatomy  trigeminal nerve - largest of all cranial nerves.trigeminal nerve - largest of all cranial nerves.  It exits laterally at mid-pons level & has 2 divisions— smaller motorIt exits laterally at mid-pons level & has 2 divisions— smaller motor root (portion minor) & larger sensory root (portion major).root (portion minor) & larger sensory root (portion major).  motor root supplies temporalis, pterygoid, tensor tympani, tensormotor root supplies temporalis, pterygoid, tensor tympani, tensor palati, mylohyoid, & anterior belly of digastric.palati, mylohyoid, & anterior belly of digastric.  motor root also contains sensory nerve fibers that particularlymotor root also contains sensory nerve fibers that particularly mediate pain sensation.mediate pain sensation.  gasserian ganglion is located in trigeminal fossa (Meckel cave) ofgasserian ganglion is located in trigeminal fossa (Meckel cave) of petrous bone in middle cranial fossa.petrous bone in middle cranial fossa.  It contains 1st-order general somatic sensory fibers that carry pain,It contains 1st-order general somatic sensory fibers that carry pain, temperature, touch.temperature, touch.  peripheral processes of neurons in ganglion form 3 divisions ofperipheral processes of neurons in ganglion form 3 divisions of trigeminal nerve (ie, ophthalmic, maxillary, and mandibular).trigeminal nerve (ie, ophthalmic, maxillary, and mandibular).  ophthalmic division exits cranium via superior orbital fissure;ophthalmic division exits cranium via superior orbital fissure; maxillary & mandibular divisions exit via foramen rotundum &maxillary & mandibular divisions exit via foramen rotundum & foramen ovale.foramen ovale.  proprioceptive afferent fibers travel with efferent & afferent roots.proprioceptive afferent fibers travel with efferent & afferent roots.
  5. 5. PathophysiologyPathophysiology  exact pathophysiology remains controversial, etiology ofexact pathophysiology remains controversial, etiology of TN may be central/ peripheral/ both.TN may be central/ peripheral/ both.  trigeminal nerve (cranial nerve V) can cause pain,trigeminal nerve (cranial nerve V) can cause pain, because its major function is sensory.because its major function is sensory.  Usually, no structural lesion is present (85%), althoughUsually, no structural lesion is present (85%), although vascular compression, venous/arterial loops at trigeminalvascular compression, venous/arterial loops at trigeminal nerve entry into pons, critical to pathogenesis ofnerve entry into pons, critical to pathogenesis of idiopathic variety.idiopathic variety.  compression results in focal demyelination.compression results in focal demyelination.  etiology is labeled idiopathic by default & categorized asetiology is labeled idiopathic by default & categorized as classic TN.classic TN.  Neuropathic pain is cardinal sign of injury to smallNeuropathic pain is cardinal sign of injury to small unmyelinated & thinly myelinated primary afferent fibersunmyelinated & thinly myelinated primary afferent fibers that subserve nociception.that subserve nociception.
  6. 6.  Microanatomic small & large fiber damage inMicroanatomic small & large fiber damage in nerve, essentially demyelination, commonlynerve, essentially demyelination, commonly observed at its root entry zone (REZ), leads toobserved at its root entry zone (REZ), leads to ephaptic transmission, in which action potentialsephaptic transmission, in which action potentials jump from one fiber to another.jump from one fiber to another.  lack of inhibitory inputs from large myelinatedlack of inhibitory inputs from large myelinated nerve fibers plays a role.nerve fibers plays a role.  Additionally, reentry mechanism causesAdditionally, reentry mechanism causes amplification of sensory inputs.amplification of sensory inputs.  However, features also suggest additionalHowever, features also suggest additional central mechanism (eg, delay betweencentral mechanism (eg, delay between stimulation and pain, refractory period).stimulation and pain, refractory period).
  7. 7. EtiologyEtiology  questionable family clustering exists, but TN is mostquestionable family clustering exists, but TN is most likely multifactorial.likely multifactorial.  Most cases are idiopathic, but compression of trigeminalMost cases are idiopathic, but compression of trigeminal roots by tumors/ vascular anomalies may cause similarroots by tumors/ vascular anomalies may cause similar pain.pain.  In one study, 64% of compressing vessels wereIn one study, 64% of compressing vessels were identified as an artery, most commonly superioridentified as an artery, most commonly superior cerebellar (81%). Venous compression identified in 36%cerebellar (81%). Venous compression identified in 36% of cases.of cases.  TN divided into 2 categories, classic and symptomatic.TN divided into 2 categories, classic and symptomatic.  The classic form (considered idiopathic), actuallyThe classic form (considered idiopathic), actually includes cases that are due to a normal artery present inincludes cases that are due to a normal artery present in contact with nerve, such as superior cerebellarcontact with nerve, such as superior cerebellar artery/primitive trigeminal artery.artery/primitive trigeminal artery.  Symptomatic forms - multiple origins. (Aneurysms,Symptomatic forms - multiple origins. (Aneurysms, tumors, chronic meningeal inflammation, or other lesionstumors, chronic meningeal inflammation, or other lesions may irritate trigeminal nerve roots along pons).may irritate trigeminal nerve roots along pons).
  8. 8.  Uncommonly, demyelination from multiple sclerosis mayUncommonly, demyelination from multiple sclerosis may be precipitantbe precipitant  Tumor-related causes (most commonly in CP angle)Tumor-related causes (most commonly in CP angle) include acoustic neurinoma, chordoma at level of clivus,include acoustic neurinoma, chordoma at level of clivus, pontine glioma/glioblastoma, epidermoid, metastases, &pontine glioma/glioblastoma, epidermoid, metastases, & lymphoma.lymphoma.  may result from paraneoplastic etiologies.may result from paraneoplastic etiologies.  Vascular causes - pontine infarct/ AV malformation /Vascular causes - pontine infarct/ AV malformation / aneurysm in the vicinity.aneurysm in the vicinity.  Inflammatory causes - multiple sclerosis, sarcoidosis,Inflammatory causes - multiple sclerosis, sarcoidosis, Lyme disease neuropathy.Lyme disease neuropathy.  Infrequently, adjacent dental fillings composed ofInfrequently, adjacent dental fillings composed of dissimilar metals may trigger attacksdissimilar metals may trigger attacks Microscopic demonstration of demyelination in primary TN. Tortuous axon is surrounded by abnormally discontinuous myelin.
  9. 9. EpidemiologyEpidemiology  No geographic tendency or racial differences.No geographic tendency or racial differences.  females are affected upto twice as often asfemales are affected upto twice as often as males (range, 3:2 to 2:1).males (range, 3:2 to 2:1).  In addition, in 90% of pts, disease begins afterIn addition, in 90% of pts, disease begins after age 40 years, with typical onset of 60-70 years.age 40 years, with typical onset of 60-70 years.  Pts who present with disease when aged 20-40Pts who present with disease when aged 20-40 years more likely to suffer from demyelinatingyears more likely to suffer from demyelinating lesion in pons secondary to multiple sclerosislesion in pons secondary to multiple sclerosis  younger pts also tend to have symptomatic oryounger pts also tend to have symptomatic or secondary TN.secondary TN.  occasional reports of pediatric cases.occasional reports of pediatric cases.  Another risk factor for this syndrome is HTN.Another risk factor for this syndrome is HTN.
  10. 10. PrognosisPrognosis  After an initial attack, TN may remit for mths/yrs.After an initial attack, TN may remit for mths/yrs.  Thereafter attacks may become more frequent, easily triggered,Thereafter attacks may become more frequent, easily triggered, disabling, requiring long-term medication.disabling, requiring long-term medication.  Thus, disease course is typically of clusters of attacks that wax andThus, disease course is typically of clusters of attacks that wax and wane in frequency.wane in frequency.  Exacerbations most commonly occur in the fall and spring.Exacerbations most commonly occur in the fall and spring.  Among best clinical predictors of symptomatic form are sensoryAmong best clinical predictors of symptomatic form are sensory deficits upon examination & u/l distribution of symptoms (butdeficits upon examination & u/l distribution of symptoms (but absence is not a negative predictor).absence is not a negative predictor).  Lack of therapeutic response and V1 distribution are poorLack of therapeutic response and V1 distribution are poor predictors.predictors.  not associated with shortened life, morbidity associated can benot associated with shortened life, morbidity associated can be considerable if not controlled adequately.considerable if not controlled adequately.  may evolve into a chronic pain syndrome, pts may suffer frommay evolve into a chronic pain syndrome, pts may suffer from depression & related loss of daily functioning.depression & related loss of daily functioning.  Individuals may choose to limit activities that precipitate pain, suchIndividuals may choose to limit activities that precipitate pain, such as chewing, possibly losing weight in extreme circumstances.as chewing, possibly losing weight in extreme circumstances. 
  11. 11. ComplicationsComplications  chief complication - adverse effects & toxicity experienced routinely withchief complication - adverse effects & toxicity experienced routinely with long-term use of anticonvulsant agents.long-term use of anticonvulsant agents.  Another complication is waning efficacy over several yrs of these drugs,Another complication is waning efficacy over several yrs of these drugs, requiring addition of 2nd anticonvulsant, causing more drug-related adverserequiring addition of 2nd anticonvulsant, causing more drug-related adverse reactions.reactions.  brainstem tumor/bone marrow aplasia as an idiosyncratic adverse effect ofbrainstem tumor/bone marrow aplasia as an idiosyncratic adverse effect of carbamazepine.carbamazepine.  Percutaneous neurosurgical procedures and microvascular decompressionPercutaneous neurosurgical procedures and microvascular decompression procedures pose risks of long-term complications. Perioperative risks alsoprocedures pose risks of long-term complications. Perioperative risks also exist.exist.  pts may have to wait for weeks or months after the operation for relief, andpts may have to wait for weeks or months after the operation for relief, and some find relief only for 1-2 years and then must weigh the option of asome find relief only for 1-2 years and then must weigh the option of a second operation.second operation.  Some patients permanently lose sensation over portion of the face orSome patients permanently lose sensation over portion of the face or mouth.mouth.  Occasionally, patients may suffer jaw weakness and/or corneal anesthesia.Occasionally, patients may suffer jaw weakness and/or corneal anesthesia.  Corneal ulceration can result because of trophic disturbances from nerveCorneal ulceration can result because of trophic disturbances from nerve deafferentation.deafferentation.  worst complication is anesthesia dolorosa, an intractable facial dysesthesia,worst complication is anesthesia dolorosa, an intractable facial dysesthesia, more disabling than original TN. (may be caused by procedures/surgery)more disabling than original TN. (may be caused by procedures/surgery)
  12. 12. CHARACTERISTICSCHARACTERISTICS  TN is predominantly unilateral, has tactile "trigger“ areas, doesTN is predominantly unilateral, has tactile "trigger“ areas, does not produce neurosensory/motor deficit, restricted to distributionnot produce neurosensory/motor deficit, restricted to distribution of trigeminal nerve.of trigeminal nerve.  Pain attacks occur spontaneously/triggered by mechanical tactilePain attacks occur spontaneously/triggered by mechanical tactile stimulus to skin, intraoral mucosa surrounding the teeth, orstimulus to skin, intraoral mucosa surrounding the teeth, or tongue.tongue.  usually lasts only secs- mins, may be repetitive at short intervals.usually lasts only secs- mins, may be repetitive at short intervals.  more common on right side of face, over age of 40, & in females.more common on right side of face, over age of 40, & in females.  physical examination entails a thorough evaluation of the headphysical examination entails a thorough evaluation of the head and neck with special emphasis on neurological examination.and neck with special emphasis on neurological examination.  Cranial nerve examination should be performed with specialCranial nerve examination should be performed with special attention to hearing abnormalities and facial nerve abnormalities.attention to hearing abnormalities and facial nerve abnormalities.  In addition, standard neurosensory testing of the trigeminalIn addition, standard neurosensory testing of the trigeminal system should include light touch, sharp touch, temperature,system should include light touch, sharp touch, temperature, contact detection and two-point discrimination.contact detection and two-point discrimination.
  13. 13.  Note should be taken of any trigger areasNote should be taken of any trigger areas and they should be appropriately mappedand they should be appropriately mapped out.out.  In summary, the clinical criteria for aIn summary, the clinical criteria for a diagnosis of idiopathic (primary) TN are:diagnosis of idiopathic (primary) TN are: 1. severe, lancinating paroxysmal pain1. severe, lancinating paroxysmal pain 2. unilateral pain2. unilateral pain 3. pain limited to the distribution of the3. pain limited to the distribution of the trigeminal nervetrigeminal nerve 4. tactile trigger areas4. tactile trigger areas 5. no neurosensory deficit5. no neurosensory deficit
  14. 14. TREATMENTTREATMENT  current treatment of idiopathic (primary) TN consists ofcurrent treatment of idiopathic (primary) TN consists of medical and surgical therapies.medical and surgical therapies.  Medical management - pharmacological and non-Medical management - pharmacological and non- pharmacological approaches, while surgicalpharmacological approaches, while surgical management consists of numerous peripheral andmanagement consists of numerous peripheral and intracranial neuroablative procedures.intracranial neuroablative procedures.  initial medical treatment is usually pharmacologicalinitial medical treatment is usually pharmacological therapy with drugs such as carbamazepine (Tegretol),therapy with drugs such as carbamazepine (Tegretol), baclofen, gabapentin, topiramate, phenytoin orbaclofen, gabapentin, topiramate, phenytoin or clonazepam in single or combination regimens.clonazepam in single or combination regimens.  however for some pts, these medications do nothowever for some pts, these medications do not relieve pain and/or produce intolerable side effects withrelieve pain and/or produce intolerable side effects with significant medical and functional morbidity.significant medical and functional morbidity.
  15. 15.  Under surgical treatment for TN - severalUnder surgical treatment for TN - several procedures currently utilized:procedures currently utilized: 1.1. percutaneous stereotactic radiofrequencypercutaneous stereotactic radiofrequency thermal rhizotomy (RTR),thermal rhizotomy (RTR), 2.2. glycerol rhizolysis (GR),glycerol rhizolysis (GR), 3.3. balloon compression of trigeminalballoon compression of trigeminal ganglion (BC),ganglion (BC), 4.4. posterior fossa exploration,posterior fossa exploration, 5.5. microvascular decompression (MVD)microvascular decompression (MVD) 6.6. gamma knife radiosurgery (GKR).gamma knife radiosurgery (GKR).
  16. 16.  RTR - best overall, long-term outcome dataRTR - best overall, long-term outcome data  technique of controlled thermal ablation of nerve fibers intechnique of controlled thermal ablation of nerve fibers in trigeminal ganglion/nerve root, producing loss of paintrigeminal ganglion/nerve root, producing loss of pain with relative preservation of touch and more complexwith relative preservation of touch and more complex facial sensationsfacial sensations  ability to allow for pre-lesion testing for localization inability to allow for pre-lesion testing for localization in order to produce a lesion in only division(s) involved.order to produce a lesion in only division(s) involved.  also affords the ability to test clinically after a lesion(s), inalso affords the ability to test clinically after a lesion(s), in order to grade level of hypalgesia/paresthesia, avoid sideorder to grade level of hypalgesia/paresthesia, avoid side effects, while still providing pain relief.effects, while still providing pain relief.  initial pain relief is equal to/ better than other proceduresinitial pain relief is equal to/ better than other procedures  recurrence rate is lessrecurrence rate is less  side effects and complications are less frequent and lessside effects and complications are less frequent and less morbid.morbid.
  17. 17.  Glycerol rhizolysis - not division specific, very high recurrenceGlycerol rhizolysis - not division specific, very high recurrence rate (approx 50%), equally high incidence of dysesthesia.rate (approx 50%), equally high incidence of dysesthesia.  Balloon compression of ganglion - also not division specific,Balloon compression of ganglion - also not division specific, can produce significant bradycardia & hypotension duringcan produce significant bradycardia & hypotension during procedure, very high incidence of masticatory motorprocedure, very high incidence of masticatory motor dysfunction, other cranial nerve abnormalities, does not havedysfunction, other cranial nerve abnormalities, does not have long follow up.long follow up.  Microvascular decompression (MVD) - long-term follow upMicrovascular decompression (MVD) - long-term follow up data, very effective, typically does not produce sensory deficit,data, very effective, typically does not produce sensory deficit, several significant disadvantages when compared to RTR.several significant disadvantages when compared to RTR.  MVD requires a craniotomy with retraction of cerebellum &MVD requires a craniotomy with retraction of cerebellum & brainstem.brainstem.  Certain potential complications in performing craniotomy,Certain potential complications in performing craniotomy, especially in non-life-threatening condition in addition to risk ofespecially in non-life-threatening condition in addition to risk of long GA, there is risk of cerebellar dysfunction, hearing losslong GA, there is risk of cerebellar dysfunction, hearing loss and facial palsy.and facial palsy.  Recently, several reports have acknowledged Gamma KnifeRecently, several reports have acknowledged Gamma Knife Radiosurgery, essentially non-invasive procedure, as having aRadiosurgery, essentially non-invasive procedure, as having a very high rate of pain relief, with no facial numbness & no sidevery high rate of pain relief, with no facial numbness & no side effects.effects.
  18. 18. HERPETIC NEURALGIAHERPETIC NEURALGIA ETIOLOGYETIOLOGY  Herpes zoster results from reactivation of varicella-zosterHerpes zoster results from reactivation of varicella-zoster virus.virus.  Unlike varicella (chickenpox), HZ is sporadic, withUnlike varicella (chickenpox), HZ is sporadic, with estimated lifetime incidence of 10- 20%.estimated lifetime incidence of 10- 20%.  incidence increases sharply with advancing age, roughlyincidence increases sharply with advancing age, roughly doubling in each decade >50 yrs.doubling in each decade >50 yrs.  uncommon in persons <15 yrs old.uncommon in persons <15 yrs old.  normal age-related decrease in cell-mediated immunitynormal age-related decrease in cell-mediated immunity thought to account for increased incidence of varicella-thought to account for increased incidence of varicella- zoster virus reactivation.zoster virus reactivation.  Pts with disease states affecting cell-mediated immunity,Pts with disease states affecting cell-mediated immunity, eg. HIV, certain malignancies, at increased risk.eg. HIV, certain malignancies, at increased risk.  Chronic CTS use, chemotherapy & radiation therapyChronic CTS use, chemotherapy & radiation therapy may increase risk of developing HZ.may increase risk of developing HZ.
  19. 19.  no evidence that HZ heralds onset of an underlyingno evidence that HZ heralds onset of an underlying malignancy.malignancy.  Race may influence susceptibility. Blacks 1/4th as likelyRace may influence susceptibility. Blacks 1/4th as likely as whites to develop this condition.as whites to develop this condition.  Although HZ is not as contagious as primary varicellaAlthough HZ is not as contagious as primary varicella infection, persons with reactivated infection can transmitinfection, persons with reactivated infection can transmit varicella-zoster virus to nonimmune contacts.varicella-zoster virus to nonimmune contacts.  Household transmission rates have been noted to beHousehold transmission rates have been noted to be approx 15%.approx 15%.  About 20% of pts with HZ develop postherpeticAbout 20% of pts with HZ develop postherpetic neuralgia.neuralgia.  most established risk factor is age; this complicationmost established risk factor is age; this complication occurs nearly 15 times more often >50 yrs.occurs nearly 15 times more often >50 yrs.  Other possible risk factors for postherpetic neuralgia areOther possible risk factors for postherpetic neuralgia are ophthalmic zoster, h/o prodromal pain beforeophthalmic zoster, h/o prodromal pain before appearance of skin lesions, immunocompromised state.appearance of skin lesions, immunocompromised state.
  20. 20. PATHOPHYSIOLOGYPATHOPHYSIOLOGY  Varicella-zoster virus is highly contagious DNA virus.Varicella-zoster virus is highly contagious DNA virus.  Varicella represents primary infection in non/incompletely immune.Varicella represents primary infection in non/incompletely immune.  During primary infection, virus gains entry into sensory dorsal rootDuring primary infection, virus gains entry into sensory dorsal root ganglia.ganglia.  How it does so & whether it resides in neurons or supporting cellsHow it does so & whether it resides in neurons or supporting cells not completely understood.not completely understood.  varicella-zoster virus genome identified in trigeminal ganglia ofvaricella-zoster virus genome identified in trigeminal ganglia of nearly all seropositive patients.nearly all seropositive patients.  remains latent for decades - virus-specific cell-mediated immunityremains latent for decades - virus-specific cell-mediated immunity acquired during primary infection, & endogenous & exogenousacquired during primary infection, & endogenous & exogenous boosting of immune system periodically throughout life.boosting of immune system periodically throughout life.  Reactivation occurs following decrease in virus-specific cell-Reactivation occurs following decrease in virus-specific cell- mediated immunity.mediated immunity.  reactivated virus travels down sensory nerve - dermatomalreactivated virus travels down sensory nerve - dermatomal distribution of pain and skin lesions.distribution of pain and skin lesions.  pathophysiology of postherpetic neuralgia remains unclear.pathophysiology of postherpetic neuralgia remains unclear.  However, pathologic studies demonstrated damage to sensoryHowever, pathologic studies demonstrated damage to sensory nerves, sensory dorsal root ganglia & dorsal horns of spinal cord innerves, sensory dorsal root ganglia & dorsal horns of spinal cord in pts with this condition.pts with this condition.
  21. 21. CLINICAL PRESENTATIONCLINICAL PRESENTATION  typically presents with prodrome consisting oftypically presents with prodrome consisting of hyperesthesia, paresthesias, burninghyperesthesia, paresthesias, burning dysesthesias/pruritus along affected dermatome(s).dysesthesias/pruritus along affected dermatome(s).  prodrome generally lasts 1-2 days, may precedeprodrome generally lasts 1-2 days, may precede appearance of skin lesions by upto 3 wks.appearance of skin lesions by upto 3 wks.  During prodromal phase, may be misdiagnosed asDuring prodromal phase, may be misdiagnosed as cardiac disease, pleurisy, herniated nucleus pulposus,cardiac disease, pleurisy, herniated nucleus pulposus, various GI or gynecologic disorders.various GI or gynecologic disorders.  Some pts may have prodromal symptoms withoutSome pts may have prodromal symptoms without developing characteristic rash. ("zoster sine herpete,"developing characteristic rash. ("zoster sine herpete," further complicates diagnosis)further complicates diagnosis)  prodromal phase followed by development ofprodromal phase followed by development of characteristic skin lesions with characteristic type ofcharacteristic skin lesions with characteristic type of pain.pain.  Pain - "burning“/ "stinging“, unrelenting.Pain - "burning“/ "stinging“, unrelenting.  pts may have insomnia.pts may have insomnia.
  22. 22.  skin lesions begin as askin lesions begin as a maculopapular rash - dermatomalmaculopapular rash - dermatomal distribution, belt-like pattern.distribution, belt-like pattern.  evolves into vesicles with anevolves into vesicles with an erythematous baseerythematous base..  vesicles painful, associated with thevesicles painful, associated with the occurrence of anxiety and flu-likeoccurrence of anxiety and flu-like symptoms.symptoms.  Although any vertebral dermatomeAlthough any vertebral dermatome may be involved, T5 and T6 aremay be involved, T5 and T6 are most commonly affected.most commonly affected.  most frequently involved cranialmost frequently involved cranial nerve dermatome - ophthalmicnerve dermatome - ophthalmic division of trigeminal nerve.division of trigeminal nerve.  20+ lesions outside affected20+ lesions outside affected dermatome reflect generalizeddermatome reflect generalized viremia. Of which, approx 1/2viremia. Of which, approx 1/2 manifest other neurologic/ visceralmanifest other neurologic/ visceral involvement.involvement.  eventually becomeeventually become hemorrhagic/turbid - crust overhemorrhagic/turbid - crust over within 7-10 days.within 7-10 days.  scarring, pigmentary changes.scarring, pigmentary changes.
  23. 23. COMPLICATIONSCOMPLICATIONS  Ocular complications - approx 1/2 of pts with involvement ofOcular complications - approx 1/2 of pts with involvement of ophthalmic division of trigeminal nerve.ophthalmic division of trigeminal nerve.  Ocular complications - include mucopurulent conjunctivitis,Ocular complications - include mucopurulent conjunctivitis, episcleritis, keratitis & anterior uveitis.episcleritis, keratitis & anterior uveitis.  Cranial nerve palsies of 3rd, 4th & 6th cranial nerves may occur,Cranial nerve palsies of 3rd, 4th & 6th cranial nerves may occur, affecting extraocular motility.affecting extraocular motility.  most common chronic complication - postherpetic neuralgia.most common chronic complication - postherpetic neuralgia.  Pain that persists >1-3 mths after resolution of rash accepted asPain that persists >1-3 mths after resolution of rash accepted as postherpetic neuralgia.postherpetic neuralgia.  Affected pts usually report constant burning, lancinating pain thatAffected pts usually report constant burning, lancinating pain that may be radicular in nature.may be radicular in nature.  may also complain of pain in response to non-noxious stimulimay also complain of pain in response to non-noxious stimuli -slightest pressure from clothing, bedsheets or wind may elicit pain.-slightest pressure from clothing, bedsheets or wind may elicit pain.  Postherpetic neuralgia is generally self-limited disease.Postherpetic neuralgia is generally self-limited disease.  Symptoms tend to abate over time.Symptoms tend to abate over time.  <1/4 pts still experience pain at 6mths after HZ, <1 in 20 has pain at<1/4 pts still experience pain at 6mths after HZ, <1 in 20 has pain at 1 yr.1 yr.
  24. 24. Treatment of Herpes ZosterTreatment of Herpes Zoster  3 major objectives:3 major objectives: (1)(1) treatment of acute viral infection,treatment of acute viral infection, (2) treatment of acute pain(2) treatment of acute pain (3) prevention of postherpetic neuralgia.(3) prevention of postherpetic neuralgia.  Antiviral agents, oral CTS & adjunctive individualized pain-managementAntiviral agents, oral CTS & adjunctive individualized pain-management modalities are used to achieve these objectives.modalities are used to achieve these objectives.  individualized pain-management modalities are used to achieve theseindividualized pain-management modalities are used to achieve these objectives.objectives. Antiviral AgentsAntiviral Agents  shown to decrease duration of rash & severity of painshown to decrease duration of rash & severity of pain  However, these benefits have only been demonstrated in pts who receivedHowever, these benefits have only been demonstrated in pts who received antiviral agents within 72 hours after onset of rash.antiviral agents within 72 hours after onset of rash.  Antiviral agents may be beneficial as long as new lesions are actively beingAntiviral agents may be beneficial as long as new lesions are actively being formed, unlikely to be helpful after lesions have crusted.formed, unlikely to be helpful after lesions have crusted.  effectiveness of antiviral agents in preventing postherpetic neuralgia is moreeffectiveness of antiviral agents in preventing postherpetic neuralgia is more controversial.controversial.
  25. 25. AcyclovirAcyclovir - prototype antiviral drug, DNA polymerase inhibitor.- prototype antiviral drug, DNA polymerase inhibitor.  may be given orally/IV.may be given orally/IV.  drawbacks of oral acyclovir - lower bioavailability, dosing frequencydrawbacks of oral acyclovir - lower bioavailability, dosing frequency (five times daily).(five times daily).  IV acyclovir generally used only in severelyIV acyclovir generally used only in severely immunocompromised/unable to take medications orally.immunocompromised/unable to take medications orally. ValacyclovirValacyclovir - prodrug of acyclovir- prodrug of acyclovir  administered TID.administered TID.  slightly better at decreasing severity of pain & duration of neuralgia.slightly better at decreasing severity of pain & duration of neuralgia.  more bioavailable than acyclovir, oral administration produces bloodmore bioavailable than acyclovir, oral administration produces blood drug levels comparable to IV acyclovir.drug levels comparable to IV acyclovir. FamciclovirFamciclovir - DNA polymerase inhibitor.- DNA polymerase inhibitor.  advantages - dosing schedule (TID), longer intracellular t1/2, betteradvantages - dosing schedule (TID), longer intracellular t1/2, better bioavailability (compared with acyclovir and valacyclovir).bioavailability (compared with acyclovir and valacyclovir).  All 3 antiviral agents are generally well tolerated.All 3 antiviral agents are generally well tolerated.  most common adverse effects are nausea, headache, vomiting,most common adverse effects are nausea, headache, vomiting, dizziness and abdominal pain.dizziness and abdominal pain.
  26. 26. Oral Antiviral Medications for HZOral Antiviral Medications for HZ MedicationMedication DosageDosage DurationDuration AdverseAdverse EffectsEffects Precautions/Precautions/ contraindicationscontraindications AcyclovirAcyclovir 800 mg 5800 mg 5 times dailytimes daily (every 4–5 h)(every 4–5 h) 7-10days7-10days Nausea,Nausea, headacheheadache Dose adjustmentDose adjustment for renalfor renal insufficiencyinsufficiency BrivudinBrivudin 125 mg once125 mg once dailydaily 7days7days Nausea,Nausea, headacheheadache Drug interactionsDrug interactions with 5-fluorouracil,with 5-fluorouracil, severe BMsevere BM suppressionsuppression FamciclovirFamciclovir 500 mg 3500 mg 3 times dailytimes daily 7days7days Nausea,Nausea, headacheheadache Dose adjustmentDose adjustment for renalfor renal insufficiencyinsufficiency ValacyclovirValacyclovir 1000 mg 31000 mg 3 times dailytimes daily 7days7days Nausea,Nausea, headacheheadache Dose adjustmentDose adjustment for renalfor renal insufficiency;insufficiency; TTP/HUS atTTP/HUS at doses >8000 mgdoses >8000 mg daily indaily in immunocompromiimmunocompromi sedsed
  27. 27. CorticosteroidsCorticosteroids  Oral CTS commonly used in HZ, even though clinicalOral CTS commonly used in HZ, even though clinical trials have shown variable results.trials have shown variable results.  Prednisone used in conjunction with acyclovir shown toPrednisone used in conjunction with acyclovir shown to reduce pain.reduce pain.  likely mechanism involves decreasing degree of neuritislikely mechanism involves decreasing degree of neuritis caused by active infection & decreasing residual damagecaused by active infection & decreasing residual damage to affected nerves.to affected nerves.  Given theoretic risk of immunosuppression with CTS,Given theoretic risk of immunosuppression with CTS, some investigators believe should be used only in ptssome investigators believe should be used only in pts >50 yrs as at greater risk of developing postherpetic>50 yrs as at greater risk of developing postherpetic neuralgia.neuralgia.
  28. 28. MedicationMedication BeginningBeginning dosedose TitrationTitration MaximumMaximum dosedose AdverseAdverse effectseffects PrednisolonePrednisolone 60mg daily for60mg daily for 7days7days Decrease toDecrease to 30mg for30mg for 7days,7days, then 15mg forthen 15mg for 7 days,7 days, thenthen discontinuediscontinue 60mg daily60mg daily GI distress,GI distress, nausea, moodnausea, mood changes,changes, oedemaoedema
  29. 29. AnalgesicsAnalgesics  pain ranges from mild to excruciating.pain ranges from mild to excruciating.  Pts with mild-moderate pain may respond to over-the-Pts with mild-moderate pain may respond to over-the- counter analgesics.counter analgesics.  Pts with more severe pain may require narcotics.Pts with more severe pain may require narcotics.  When analgesics used, +/- narcotic, regular dosingWhen analgesics used, +/- narcotic, regular dosing schedule results in better pain control & less anxiety thanschedule results in better pain control & less anxiety than "as-needed" dosing."as-needed" dosing.  Lotions containing calamine (e.g., Caladryl) may be usedLotions containing calamine (e.g., Caladryl) may be used on open lesions to reduce pain and pruritus.on open lesions to reduce pain and pruritus.  Once lesions have crusted over, capsaicin creamOnce lesions have crusted over, capsaicin cream (Zostrix) may be applied.(Zostrix) may be applied.  Topically administered lidocaine (Xylocaine) & nerveTopically administered lidocaine (Xylocaine) & nerve blocks have also been reported to be effective inblocks have also been reported to be effective in reducing pain.reducing pain.
  30. 30. MedicationMedication Beginning doseBeginning dose TitrationTitration Maximum doseMaximum dose Adverse effectsAdverse effects OxycodoneOxycodone 5 mg every 4 h5 mg every 4 h as needed;as needed; dosage can bedosage can be converted toconverted to long-actinglong-acting opioid analgesicopioid analgesic combined withcombined with short-actingshort-acting medicationmedication continued ascontinued as neededneeded Increase by 5Increase by 5 mg 4 timesmg 4 times daily every 2daily every 2 days asdays as toleratedtolerated No maximumNo maximum dosage withdosage with careful titration;careful titration; considerconsider evaluation by aevaluation by a pain specialistpain specialist at dosagesat dosages >120 mg daily>120 mg daily Nausea/vomitinNausea/vomitin g, constipation,g, constipation, sedation,sedation, dizzinessdizziness Tramadol1Tramadol1 50 mg once or50 mg once or twice dailytwice daily Increase by 50Increase by 50 to 100 mg dailyto 100 mg daily in divided dosesin divided doses every 2 days asevery 2 days as toleratedtolerated 400 mg daily400 mg daily (100 mg 4 times(100 mg 4 times daily); fordaily); for patients >75patients >75 years of age,years of age, 300 mg daily in300 mg daily in divided dosesdivided doses Nausea/vomitinNausea/vomitin g, constipation,g, constipation, sedation,sedation, dizziness,dizziness, seizures,seizures, posturalpostural hypotensionhypotension
  31. 31. MedicationMedication Beginning doseBeginning dose TitrationTitration Maximum doseMaximum dose Adverse effectsAdverse effects Gabapentin 2Gabapentin 2 300 mg at300 mg at bedtime or 100bedtime or 100 to 300 mg 3to 300 mg 3 times dailytimes daily Increase by 100Increase by 100 to 300 mg 3to 300 mg 3 times dailytimes daily every 2 days asevery 2 days as toleratedtolerated 3600 mg daily3600 mg daily (1200 mg 3(1200 mg 3 times daily);times daily); reduce if renalreduce if renal function isfunction is impairedimpaired Sedation,Sedation, dizziness,dizziness, peripheralperipheral edemaedema Pregabalin 2Pregabalin 2 75 mg at75 mg at bedtime or 75bedtime or 75 mg twice dailymg twice daily Increase by 75Increase by 75 mg twice dailymg twice daily every 3 days asevery 3 days as toleratedtolerated 600 mg daily600 mg daily (300 mg twice(300 mg twice daily); reduce ifdaily); reduce if renal function isrenal function is impairedimpaired Sedation,Sedation, dizziness,dizziness, peripheralperipheral edemaedema TCAsTCAs (nortryptiline) 2(nortryptiline) 2 25 mg at25 mg at bedtimebedtime Increase by 25Increase by 25 mg daily everymg daily every 2 to 3 days as2 to 3 days as toleratedtolerated 150 mg daily150 mg daily Sedation, drySedation, dry mouth, blurredmouth, blurred vision, weightvision, weight gain, urinarygain, urinary retention3retention3 1 Consider lower starting dosages, slower titration for frail, elderly patients ( 5 mg twice bd oxycodone) 2 Consider lower starting dosages, slower titration for frail, elderly patients (10 mg HS for TCAs). 3 Consider a screening electrocardiogram for patients >40 years of age. 4 (all) Should be initiated only in combination with antiviral therapy.
  32. 32. Ocular InvolvementOcular Involvement  Ocular HZ treated with oral antiviral agents & CTS, sameOcular HZ treated with oral antiviral agents & CTS, same as involvement elsewhere.as involvement elsewhere.  most pts improve without lasting sequelae, some maymost pts improve without lasting sequelae, some may develop severe complications, including loss of vision.develop severe complications, including loss of vision.  ophthalmologic consultation is usually recommended.ophthalmologic consultation is usually recommended. Preventive TreatmentPreventive Treatment  morbidity & mortality could be reduced if safe & effectivemorbidity & mortality could be reduced if safe & effective preventive treatment were available.preventive treatment were available.  unusual to develop HZ > once, suggesting that 1stunusual to develop HZ > once, suggesting that 1st reactivation of VZ provides future immunologicreactivation of VZ provides future immunologic protection.protection.  Studies are currently being conducted to evaluate theStudies are currently being conducted to evaluate the efficacy of the varicella-zoster vaccine in preventing orefficacy of the varicella-zoster vaccine in preventing or modifying herpes zoster in the elderly.modifying herpes zoster in the elderly.
  33. 33. Treatment of Postherpetic NeuralgiaTreatment of Postherpetic Neuralgia  Although postherpetic neuralgia is generally a self-limitedAlthough postherpetic neuralgia is generally a self-limited condition, it can last indefinitely.condition, it can last indefinitely.  Treatment is directed at pain control while waiting for theTreatment is directed at pain control while waiting for the condition to resolve.condition to resolve.  Pain therapy may include multiple interventions, such asPain therapy may include multiple interventions, such as topical medications, over-the-counter analgesics, TCAs,topical medications, over-the-counter analgesics, TCAs, anticonvulsants & nonmedical modalities.anticonvulsants & nonmedical modalities.  Occasionally, narcotics may be required.Occasionally, narcotics may be required.
  34. 34. AnalgesicsAnalgesics CapsaicinCapsaicin ––  extract from hot chili peppers, currently only drug labeled by FDA forextract from hot chili peppers, currently only drug labeled by FDA for postherpetic neuralgia. Trials have shown it be more efficaciouspostherpetic neuralgia. Trials have shown it be more efficacious than placebo but not necessarily more than other conventionalthan placebo but not necessarily more than other conventional treatments.treatments.  Substance P (neuropeptide from pain fibers in response to trauma)Substance P (neuropeptide from pain fibers in response to trauma) also released when capsaicin is applied to skin, producing a burningalso released when capsaicin is applied to skin, producing a burning sensation.sensation.  Analgesia occurs when substance P is depleted from the nerveAnalgesia occurs when substance P is depleted from the nerve fibers.fibers.  To achieve this response, capsaicin cream must be applied to theTo achieve this response, capsaicin cream must be applied to the affected area 3-5 times daily.affected area 3-5 times daily.  Pts need to be counseled that pain will likely increase during 1st fewPts need to be counseled that pain will likely increase during 1st few days - 1wk after therapy is initiated.days - 1wk after therapy is initiated.  Pts should wash their hands thoroughly after applying capsaicinPts should wash their hands thoroughly after applying capsaicin cream in order to prevent inadvertent contact with other areas.cream in order to prevent inadvertent contact with other areas.
  35. 35. Patches containing lidocainePatches containing lidocaine ––  1 study found that compared with no treatment, lidocaine1 study found that compared with no treatment, lidocaine patches reduced pain intensity.patches reduced pain intensity.  minimal systemic absorption.minimal systemic absorption.  effect temporary, lasting only 4-12hrs with eacheffect temporary, lasting only 4-12hrs with each application.application. Over-the-counter analgesicsOver-the-counter analgesics ––  Eg. acetaminophen (Tylenol), NSAIDs not been shownEg. acetaminophen (Tylenol), NSAIDs not been shown to be highly effective in treatment of postherpeticto be highly effective in treatment of postherpetic neuralgia.neuralgia.  However, often useful for potentiating the pain-relievingHowever, often useful for potentiating the pain-relieving effects of narcotics in patients with severe pain.effects of narcotics in patients with severe pain.  Because of the addictive properties of narcotics, theirBecause of the addictive properties of narcotics, their chronic use is discouraged except in the rare patient whochronic use is discouraged except in the rare patient who does not adequately respond to other modalities.does not adequately respond to other modalities.
  36. 36. Tricyclic AntidepressantsTricyclic Antidepressants  effective adjuncts in reducing neuropathic pain of postherpetic neuralgia.effective adjuncts in reducing neuropathic pain of postherpetic neuralgia.  most likely lessen pain by inhibiting reuptake of serotonin & norepinephrinemost likely lessen pain by inhibiting reuptake of serotonin & norepinephrine neurotransmitters.neurotransmitters.  amitriptyline, nortriptyline, imipramine & desipramine.amitriptyline, nortriptyline, imipramine & desipramine.  best tolerated when they are started in a low dosage and given at bedtime.best tolerated when they are started in a low dosage and given at bedtime.  dosage is increased every 2-4 wks to achieve an effective dose.dosage is increased every 2-4 wks to achieve an effective dose.  TCAs share common side effects, such as sedation, dry mouth, posturalTCAs share common side effects, such as sedation, dry mouth, postural hypotension, blurred vision and urinary retention.hypotension, blurred vision and urinary retention.  Nortriptyline and amitriptyline appear to have equal efficacy; nortriptylineNortriptyline and amitriptyline appear to have equal efficacy; nortriptyline tends to produce fewer anticholinergic effects & better tolerated.tends to produce fewer anticholinergic effects & better tolerated.  can occasionally lead to cardiac conduction abnormalities or liver toxicity.can occasionally lead to cardiac conduction abnormalities or liver toxicity.  potential for these problems should be considered in elderly patients andpotential for these problems should be considered in elderly patients and patients with cardiac or liver disease.patients with cardiac or liver disease.  As TCAs do not act quickly, trial of at least 3 mths required to judge aAs TCAs do not act quickly, trial of at least 3 mths required to judge a patient's response.patient's response.  onset of pain relief using tricyclic antidepressants may be enhanced byonset of pain relief using tricyclic antidepressants may be enhanced by beginning treatment early in the course of herpes zoster infection inbeginning treatment early in the course of herpes zoster infection in conjunction with antiviral medicationsconjunction with antiviral medications
  37. 37. AnticonvulsantsAnticonvulsants  Phenytoin, carbamazepine & gabapentin often used.Phenytoin, carbamazepine & gabapentin often used.  drug selection often involves trial and error.drug selection often involves trial and error.  Lack of response to one of these medications does not necessarilyLack of response to one of these medications does not necessarily portend a poor response to another.portend a poor response to another.  dosages required for analgesia are often lower than those used indosages required for analgesia are often lower than those used in the treatment of epilepsy.the treatment of epilepsy.  associated with a variety of side effects, including sedation, memoryassociated with a variety of side effects, including sedation, memory disturbances, electrolyte abnormalities, liver toxicity anddisturbances, electrolyte abnormalities, liver toxicity and thrombocytopenia.thrombocytopenia.  Side effects may be reduced or eliminated by initiating treatment inSide effects may be reduced or eliminated by initiating treatment in a low dosage, which can then be slowly titrated upward.a low dosage, which can then be slowly titrated upward.  no specific contraindications to using anticonvulsants in combinationno specific contraindications to using anticonvulsants in combination with antidepressants or analgesics. However, the risk of side effectswith antidepressants or analgesics. However, the risk of side effects increases when multiple medications are used.increases when multiple medications are used.  Effective treatment of postherpetic neuralgia often requires multipleEffective treatment of postherpetic neuralgia often requires multiple treatment approaches.treatment approaches.  In addition to medications, modalities to consider includeIn addition to medications, modalities to consider include transcutaneous electric nerve stimulation (TENS), biofeedback andtranscutaneous electric nerve stimulation (TENS), biofeedback and nerve blocks.nerve blocks.
  38. 38. MYOFASCIAL PAINS ANDMYOFASCIAL PAINS AND MANAGEMENTMANAGEMENT  diagnosed in pts with chronic, non-malignant pain who lack clinical/lab evidence ofdiagnosed in pts with chronic, non-malignant pain who lack clinical/lab evidence of radiculopathy, neuropathy, or joint disease.radiculopathy, neuropathy, or joint disease.  believed to be caused by chronic changes in muscles and surrounding soft tissues.believed to be caused by chronic changes in muscles and surrounding soft tissues.  diagnosis of myofascial pain not a diagnosis of exclusion, but requires presence ofdiagnosis of myofascial pain not a diagnosis of exclusion, but requires presence of specific abnormalities.specific abnormalities.  Myofascial pain is characterized by localized shortened (contracted), tender muscles.Myofascial pain is characterized by localized shortened (contracted), tender muscles. Diagnostic Criteria for Trigger PointsDiagnostic Criteria for Trigger Points •• Taut bandTaut band _ Palpable contracted cord-like group of muscle fibers_ Palpable contracted cord-like group of muscle fibers _ Point tenderness over taut band_ Point tenderness over taut band •• Local twitch responseLocal twitch response _ Involuntary contraction of taut band after physically plucking or inserting a needle into it_ Involuntary contraction of taut band after physically plucking or inserting a needle into it •• Trigger pointsTrigger points _ Active if palpation results in pain referred to chronic pain area_ Active if palpation results in pain referred to chronic pain area _ Latent if locally tender, but without referred pain_ Latent if locally tender, but without referred pain
  39. 39.  hallmark is trigger point— tender area within contracted musclehallmark is trigger point— tender area within contracted muscle bands that produces an involuntary contraction with stimulationbands that produces an involuntary contraction with stimulation (1)(1) taut bands shown to have spontaneous electrical activity on EMGtaut bands shown to have spontaneous electrical activity on EMG testingtesting (2)(2) important for diagnosis & also because they restrict normal muscleimportant for diagnosis & also because they restrict normal muscle stretch, reduce active range of motion & cause muscle weaknessstretch, reduce active range of motion & cause muscle weakness (shortening).(shortening).  Taut bands produced involuntarily.Taut bands produced involuntarily.  Trigger points (Trigger points (distinguished fromdistinguished from tender points)tender points), which represent, which represent areas of increased sensitivity to stimulation.areas of increased sensitivity to stimulation.  myofascial pain & fibromyalgia, have specific diagnostic criteria.myofascial pain & fibromyalgia, have specific diagnostic criteria.  most important distinction - myofascial pain represents localizedmost important distinction - myofascial pain represents localized pain complaint (e.g., low-back or shoulder-girdle pain), whereaspain complaint (e.g., low-back or shoulder-girdle pain), whereas fibromyalgia produces widespread pain, covering most regions offibromyalgia produces widespread pain, covering most regions of the body.the body.  Because fibromyalgia may result in modification of posture, gait,Because fibromyalgia may result in modification of posture, gait, activity, patients with fibromyalgia may develop additionalactivity, patients with fibromyalgia may develop additional myofascial pain complaints on the background of widespreadmyofascial pain complaints on the background of widespread fibromyalgia pain.fibromyalgia pain.
  40. 40. Criteria for Distinguishing Between MyofascialCriteria for Distinguishing Between Myofascial Pain and FibromyalgiaPain and Fibromyalgia
  41. 41. EPIDEMIOLOGYEPIDEMIOLOGY Common myofascial syndromes includeCommon myofascial syndromes include 1.1. lateral epicondylitis (tennis elbow),lateral epicondylitis (tennis elbow), 2.2. quadratus lumborum syndrome (a common cause ofquadratus lumborum syndrome (a common cause of nonradicular low back pain),nonradicular low back pain), 3.3. piriformis syndrome (a common cause of buttock andpiriformis syndrome (a common cause of buttock and hip pain).hip pain). Quadratus lumborum syndromeQuadratus lumborum syndrome ––  one of most common causes of low back pain.one of most common causes of low back pain.  quadratus lumborum muscle connects at the 12th rib,quadratus lumborum muscle connects at the 12th rib, iliac crest, and lumbar vertebrae (Fig. 1).iliac crest, and lumbar vertebrae (Fig. 1).  responsible for lateral bending of lumbar spine.responsible for lateral bending of lumbar spine.  Pts with quadratus lumborum syndrome often havePts with quadratus lumborum syndrome often have unilateral hip elevation because of muscle shortening.unilateral hip elevation because of muscle shortening.  Active quadratus lumborum trigger points refer pain toActive quadratus lumborum trigger points refer pain to hip and buttock (Fig. 2).hip and buttock (Fig. 2).
  42. 42. piriformis syndromepiriformis syndrome ––  piriformis muscle attaches from inner ileum and sacrum to greaterpiriformis muscle attaches from inner ileum and sacrum to greater trochanter (Fig. 3) & rotates hip externally, thereby contributing totrochanter (Fig. 3) & rotates hip externally, thereby contributing to stability of hip & back.stability of hip & back.  Active piriformis trigger points also refer to hip & buttock (Fig. 4).Active piriformis trigger points also refer to hip & buttock (Fig. 4).  When hypertrophied, piriformis may compress sciatic nerve, whichWhen hypertrophied, piriformis may compress sciatic nerve, which usually travels beneath it, resulting in additional leg pain or sciatica.usually travels beneath it, resulting in additional leg pain or sciatica.
  43. 43.  Several muscle groups are commonly affected.Several muscle groups are commonly affected.  These include the upper trapezius, scalene, rhomboids, levatorThese include the upper trapezius, scalene, rhomboids, levator scapulae, serratus anterior muscles.scapulae, serratus anterior muscles.  Areas of common trigger points & their referral patterns are shownAreas of common trigger points & their referral patterns are shown in Figs. 5–9.in Figs. 5–9.  Identifying typical pain referral patterns in myofascial pain helps theIdentifying typical pain referral patterns in myofascial pain helps the clinician recognize these common pain syndromes.clinician recognize these common pain syndromes.
  44. 44. EVALUATIONEVALUATION  detailed musculoskeletal examination to assess posture,detailed musculoskeletal examination to assess posture, range of motion, muscle tone and tenderness, joint motion,range of motion, muscle tone and tenderness, joint motion, and neurological function.and neurological function.  Passive range of motion is evaluated by an examinerPassive range of motion is evaluated by an examiner manipulating a joint through its full range in the relaxedmanipulating a joint through its full range in the relaxed patient.patient.  Active range of motion, on the other hand, requires the patientActive range of motion, on the other hand, requires the patient to voluntarily activate muscles to move each joint through itsto voluntarily activate muscles to move each joint through its range of motion.range of motion.  An examiner can record the extent of active range of motion,An examiner can record the extent of active range of motion, as observed through patient performance.as observed through patient performance.  Greater restriction of active range of motion compared withGreater restriction of active range of motion compared with passive range of motion suggests a myofascial restriction orpassive range of motion suggests a myofascial restriction or reduced patient effort.reduced patient effort.  The presence of myofascial features can be identified byThe presence of myofascial features can be identified by directly visualizing painful areas for increased muscle bulk,directly visualizing painful areas for increased muscle bulk, which suggests a spasm, and by palpating for taut bands andwhich suggests a spasm, and by palpating for taut bands and trigger points.trigger points.
  45. 45.  Identification of taut bands is best performed by examining theIdentification of taut bands is best performed by examining the stretched muscle with the fingertips.stretched muscle with the fingertips.  The taut band should feel like a tight cord or rope in theThe taut band should feel like a tight cord or rope in the muscle.muscle.  In addition, palpation of taut bands demonstrates tendernessIn addition, palpation of taut bands demonstrates tenderness and may cause involuntary muscle contraction locally (a localand may cause involuntary muscle contraction locally (a local twitch response), flinching and vocalizing pain, or both.twitch response), flinching and vocalizing pain, or both.  This flinch response should occur exclusively when the triggerThis flinch response should occur exclusively when the trigger point is palpated and not as a response to palpation of otherpoint is palpated and not as a response to palpation of other areas.areas.  Tenderness cannot be assessed in patients who do not permitTenderness cannot be assessed in patients who do not permit even the gentlest touch of areas distant to the painful area.even the gentlest touch of areas distant to the painful area.  Myofascial pain should not be diagnosed unless theseMyofascial pain should not be diagnosed unless these abnormal clinical examination findings are identified.abnormal clinical examination findings are identified.  If patients cannot cooperate with testing because of extremeIf patients cannot cooperate with testing because of extreme pain, the clinician hould reschedule them for another visitpain, the clinician hould reschedule them for another visit when they may be more amenable to testing.when they may be more amenable to testing.
  46. 46.  No laboratory or radiographic abnormalities areNo laboratory or radiographic abnormalities are associated with myofascial pain.associated with myofascial pain.  The diagnosis is generally based on a history of anThe diagnosis is generally based on a history of an inciting event or injury, physical examination findings ofinciting event or injury, physical examination findings of tight and tender muscles, and the absence oftight and tender muscles, and the absence of mechanical instability or neurological deficits.mechanical instability or neurological deficits.  X-rays should be performed in patients with suspectedX-rays should be performed in patients with suspected joint abnormality, inflammation, or instability.joint abnormality, inflammation, or instability.  Plain X-rays also provide a useful screening tool forPlain X-rays also provide a useful screening tool for patients with chronic pain over bony structures to rulepatients with chronic pain over bony structures to rule out underlying bone disease.out underlying bone disease.  MRIs should be reserved for patients with evidence ofMRIs should be reserved for patients with evidence of myelopathy, radiculopathy, or another specific type ofmyelopathy, radiculopathy, or another specific type of pathology that would beidentified with this testing.pathology that would beidentified with this testing.
  47. 47. TREATMENTTREATMENT  Physical therapy is the cornerstone of myofascial pain therapy.Physical therapy is the cornerstone of myofascial pain therapy.  exercise program needs to be tailor-made for each patient toexercise program needs to be tailor-made for each patient to specifically address postural abnormalities and myofascial changesspecifically address postural abnormalities and myofascial changes contributing to the pain complaints. Therapy must focus on activecontributing to the pain complaints. Therapy must focus on active stretching and range-of-motion exercises, althoughstretching and range-of-motion exercises, although  supplemental passive treatment modalities (administered by thesupplemental passive treatment modalities (administered by the therapist) may also be utilized.therapist) may also be utilized.  Patients should be instructed in a home-exercise routine to bePatients should be instructed in a home-exercise routine to be performed at least twice daily, in addition to their physical therapyperformed at least twice daily, in addition to their physical therapy sessions.sessions.  Temporarily isolated muscle stretching during a 1-hour therapyTemporarily isolated muscle stretching during a 1-hour therapy session, with no additional exercise to maintain stretches betweensession, with no additional exercise to maintain stretches between appointments, will not be effective for most patients.appointments, will not be effective for most patients.  The addition of targeted trigger-point injections, medications, orThe addition of targeted trigger-point injections, medications, or other physical therapy modalities are all designed in improve theother physical therapy modalities are all designed in improve the ability to achieve an effective muscle stretch during active exerciseability to achieve an effective muscle stretch during active exercise
  48. 48. Treatment of Myofascial PainTreatment of Myofascial Pain •• Primary treatmentPrimary treatment _ Physical therapy_ Physical therapy _ Posture correction_ Posture correction _ Stretching exercises_ Stretching exercises _ Active range of motion exercises_ Active range of motion exercises •• Secondary treatmentSecondary treatment (a) Pharmacological therapy(a) Pharmacological therapy _ Analgesics for pain flares_ Analgesics for pain flares _ Acetaminophen_ Acetaminophen _ Nonsteroidal anti-inflammatory drugs_ Nonsteroidal anti-inflammatory drugs _ Tramadol_ Tramadol _ Tizanidine_ Tizanidine Initially 1–2 mg at bedtime. May increase slowly to 24 mg/day in divided dosesInitially 1–2 mg at bedtime. May increase slowly to 24 mg/day in divided doses _ Trigger point injections_ Trigger point injections (b) Nonpharmacological therapy(b) Nonpharmacological therapy _ Occupational therapy_ Occupational therapy __ Work simplification/modificationWork simplification/modification _ Pain management psychology_ Pain management psychology _ Relaxation techniques_ Relaxation techniques _ Stress management_ Stress management _ Coping skills_ Coping skills
  49. 49. Physical TherapyPhysical Therapy  Although passive stretching (stretching performed by a therapist on aAlthough passive stretching (stretching performed by a therapist on a relaxed patient) may be soothing, myofascial pain is most likely to improverelaxed patient) may be soothing, myofascial pain is most likely to improve in patients who perform active exercise.in patients who perform active exercise.  Patients should perform both whole-body stretches and stretches targetedPatients should perform both whole-body stretches and stretches targeted to the painful area twice daily.to the painful area twice daily.  Muscles should be stretched until a stretched sensation is first felt.Muscles should be stretched until a stretched sensation is first felt.  Patients should not overstretch their muscles or attempt to achieve maximalPatients should not overstretch their muscles or attempt to achieve maximal stretch.stretch.  Stretching exercises help return shortened muscles to a more normalStretching exercises help return shortened muscles to a more normal length, inactivating the taut band and trigger points.length, inactivating the taut band and trigger points.  Several weeks after beginning a stretching program, patients should startSeveral weeks after beginning a stretching program, patients should start using light weights to incorporate strengthening into the exercise routine.using light weights to incorporate strengthening into the exercise routine.  The addition of any therapy to hot packs plus active range-of-motionThe addition of any therapy to hot packs plus active range-of-motion exercises resulted in significantly better pain reduction.exercises resulted in significantly better pain reduction.  The most effective forms of therapy were those that includedThe most effective forms of therapy were those that included transcutaneous electrical nerve stimulation or interferential current therapy.transcutaneous electrical nerve stimulation or interferential current therapy.  both therapies were appropriately used as adjunctive therapy to improve theboth therapies were appropriately used as adjunctive therapy to improve the benefit that could be achieved from active range-ofmotion exercises.benefit that could be achieved from active range-ofmotion exercises.
  50. 50. Supplemental Treatment Modalities Used in ConjunctionSupplemental Treatment Modalities Used in Conjunction With a Physical Therapy Stretching Exercise ProgramWith a Physical Therapy Stretching Exercise Program InjectionsInjections •• Trigger-point injections Local anesthetic (e.g., 0.5–1% lidocaine or 0.25–0.5%Trigger-point injections Local anesthetic (e.g., 0.5–1% lidocaine or 0.25–0.5% bupivacaine) injected into trigger point.bupivacaine) injected into trigger point. •• Dry needling Insertion of a solid, acupuncture-type needle intotrigger point.Dry needling Insertion of a solid, acupuncture-type needle intotrigger point. Physical therapy modalitiesPhysical therapy modalities •• Ischemic compression Application of pressure to trigger points for 90 seconds.Ischemic compression Application of pressure to trigger points for 90 seconds. Force is halfway between that which producesany pain and that which producesForce is halfway between that which producesany pain and that which produces intolerable pain.intolerable pain. •• Hot packs Moist heating pads placed over the painful area for 20 minutes beforeHot packs Moist heating pads placed over the painful area for 20 minutes before exercise.exercise. •• Active range-of-motion Five repetitions of actively moving painful area through fullActive range-of-motion Five repetitions of actively moving painful area through full range-of-motion.range-of-motion. •• Spray and stretch Vasocoolant fluorimethane spray is applied to the entire painful areaSpray and stretch Vasocoolant fluorimethane spray is applied to the entire painful area (not just the trigger point) prior to stretching.(not just the trigger point) prior to stretching. •• TENS Electrodes placed around painful area and current applied for approximately 20TENS Electrodes placed around painful area and current applied for approximately 20 minutes.minutes. •• Interferential current therapy Electrodes placed around painful area and current appliedInterferential current therapy Electrodes placed around painful area and current applied for approximately 20 minutes. Minimal skin resistance with interferential currentfor approximately 20 minutes. Minimal skin resistance with interferential current therapy allows atherapy allows a maximum amount of energy to penetrate to deeper tissues. Used in patients who failmaximum amount of energy to penetrate to deeper tissues. Used in patients who fail TENS.TENS. •• Myofascial release Passive stretching and traction techniques, applied by trainedMyofascial release Passive stretching and traction techniques, applied by trained therapist.therapist.
  51. 51. InjectionsInjections  Trigger-point injections require infiltration of LA into myofascial triggerTrigger-point injections require infiltration of LA into myofascial trigger points.points.  22- to 25-gauge needle is inserted into skin approximately 1 cm away from22- to 25-gauge needle is inserted into skin approximately 1 cm away from trigger point, then advanced to trigger point.trigger point, then advanced to trigger point.  After withdrawing, 0.1 to 0.2 mL of anesthetic is injected.After withdrawing, 0.1 to 0.2 mL of anesthetic is injected.  needle is partially withdrawn, redirected, & advanced toward another areaneedle is partially withdrawn, redirected, & advanced toward another area within trigger point.within trigger point.  process is repeated until a local twitch response no longer elicited/ muscleprocess is repeated until a local twitch response no longer elicited/ muscle tautness is reduced/ 0.5-1.0 mL of anesthetic has been injected aroundtautness is reduced/ 0.5-1.0 mL of anesthetic has been injected around trigger point.trigger point.  Pressure is maintained over area after injection to minimize hematomaPressure is maintained over area after injection to minimize hematoma development.development.  Trigger-point injections are contraindicated in coagulopathy.Trigger-point injections are contraindicated in coagulopathy.  It is not clear whether addition of steroids to injections lengthens duration ofIt is not clear whether addition of steroids to injections lengthens duration of relief.relief.  Superficial dry needling involves insertion of a solid thin needle (resemblingSuperficial dry needling involves insertion of a solid thin needle (resembling acupuncture needle) into trigger points.acupuncture needle) into trigger points.  This method can also help deactivate myofascial trigger points when used inThis method can also help deactivate myofascial trigger points when used in conjunction with stretching exercises.conjunction with stretching exercises.  benefits of dry needling are supported by studies showing similar benefitsbenefits of dry needling are supported by studies showing similar benefits after trigger point injections, regardless of the injected substance (includingafter trigger point injections, regardless of the injected substance (including saline).saline).
  52. 52. Pharmacological TherapyPharmacological Therapy  designed to supplement physical therapy.designed to supplement physical therapy.  Patients who fail to benefit from stretching programsPatients who fail to benefit from stretching programs alone may be treated with adjunctive tizanidine, aalone may be treated with adjunctive tizanidine, a muscle relaxant with analgesic properties.muscle relaxant with analgesic properties.  Unlike most muscle relaxants, which are ineffective inUnlike most muscle relaxants, which are ineffective in chronic pain, tizanidine effectively reduces chronicchronic pain, tizanidine effectively reduces chronic myofascial pain for many patients.myofascial pain for many patients.  Tizanidine is also mildly sedating and can improve sleepTizanidine is also mildly sedating and can improve sleep disturbance in some patients when administered in lowdisturbance in some patients when administered in low doses at bedtime.doses at bedtime.  Analgesics may be used on an intermittent basis to treatAnalgesics may be used on an intermittent basis to treat pain flares.pain flares.  Daily analgesics are rarely helpful and chronic use mayDaily analgesics are rarely helpful and chronic use may produce significant gastric and renal toxicity.produce significant gastric and renal toxicity.
  53. 53. SUMMARYSUMMARY  Myofascial pain - unique pain syndrome, characterized byMyofascial pain - unique pain syndrome, characterized by tight, tender muscles, with taut bands and tender triggertight, tender muscles, with taut bands and tender trigger points.points.  distinguished from mechanical pain by absence of jointdistinguished from mechanical pain by absence of joint pathology, from neuropathic pain by absence of neurologicalpathology, from neuropathic pain by absence of neurological dysfunction, and from fibromyalgia by absence of widespreaddysfunction, and from fibromyalgia by absence of widespread body pain.body pain.  Knowledge of typical myofascial pain referral patterns (e.g.,Knowledge of typical myofascial pain referral patterns (e.g., quadratus lumborum and piriformis syndromes) facilitatesquadratus lumborum and piriformis syndromes) facilitates identification of these common pain syndromes.identification of these common pain syndromes.  focus of treatment for myofascial pain is active stretching andfocus of treatment for myofascial pain is active stretching and range-of motion exercises.range-of motion exercises.  Passive physical therapy modalities, injections, andPassive physical therapy modalities, injections, and medications may be used adjunctively.medications may be used adjunctively.  Patients with long-standing myofascial pain may havePatients with long-standing myofascial pain may have additional psychological distress, disability, or both that willadditional psychological distress, disability, or both that will require additional, targeted therapy, including psychologicalrequire additional, targeted therapy, including psychological interventions and occupational therapy.interventions and occupational therapy.

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