Trigeminal neuralgia, herpetic neuralgia, myofascial pains

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TRIGEMINAL NEURALGIA, TRIGEMINAL NEURALGIA, HERPETIC NEURALGIA, HERPETIC NEURALGIA, MYOFASCIAL PAINS AND MYOFASCIAL PAINS AND MANAGEMENT MANAGEMENT DR. ARATI M. BADGANDI DR. ARATI M. BADGANDI

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Trigeminal neuralgia, herpetic neuralgia, myofascial pains

Transcript of Trigeminal neuralgia, herpetic neuralgia, myofascial pains

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TRIGEMINAL NEURALGIA, TRIGEMINAL NEURALGIA, HERPETIC NEURALGIA, HERPETIC NEURALGIA, MYOFASCIAL PAINS AND MYOFASCIAL PAINS AND

MANAGEMENTMANAGEMENT

DR. ARATI M. BADGANDIDR. ARATI M. BADGANDI

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TRIGEMINAL NEURALGIATRIGEMINAL NEURALGIA

BackgroundBackground Trigeminal neuralgia (TN) - Tic douloureux, common & potentially Trigeminal neuralgia (TN) - Tic douloureux, common & potentially

disabling pain syndrome, precise pathophysiology of which remains disabling 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 with Although 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 common Isolated involvement of ophthalmic division much less common (2.8%). (2.8%).

Typically, initial response to carbamazepine therapy is diagnostic Typically, initial response to carbamazepine therapy is diagnostic and successful. and successful.

Despite early relief with medication, pts may experience Despite early relief with medication, pts may experience breakthrough pain requiring additional drugs &/or 1+ of surgical breakthrough pain requiring additional drugs &/or 1+ of surgical interventions. interventions.

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Historical informationHistorical information clinical description of TN can be traced back >300 clinical description of TN can be traced back >300

years. years. Aretaeus of Cappadocia, known for 1 of earliest Aretaeus of Cappadocia, known for 1 of earliest

descriptions of migraine, is credited with 1st indication of descriptions 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 description John Fothergill was 1st to give full & accurate description

of this condition in paper titled "On a Painful Affliction of of this condition in paper titled "On a Painful Affliction of the Face," - presented to medical society of London in the Face," - presented to medical society of London in 1773. 1773.

Osler also described TN in great and accurate detail in Osler also described TN in great and accurate detail in his 1912 book his 1912 book The Principles and Practice of MedicineThe Principles and Practice of Medicine..

In 1900, in a landmark article, Cushing reported method In 1900, in a landmark article, Cushing reported method of total ablation of the gasserian ganglion to treat of total ablation of the gasserian ganglion to treat trigeminal neuralgia. trigeminal neuralgia.

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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 motor It 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, tensor motor 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 particularly motor root also contains sensory nerve fibers that particularly

mediate pain sensation. mediate pain sensation. gasserian ganglion is located in trigeminal fossa (Meckel cave) of gasserian 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 of peripheral 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.

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PathophysiologyPathophysiology exact pathophysiology remains controversial, etiology of exact 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%), although Usually, no structural lesion is present (85%), although

vascular compression, venous/arterial loops at trigeminal vascular compression, venous/arterial loops at trigeminal nerve entry into pons, critical to pathogenesis of nerve 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 as etiology is labeled idiopathic by default & categorized as

classic TN. classic TN. Neuropathic pain is cardinal sign of injury to small Neuropathic pain is cardinal sign of injury to small

unmyelinated & thinly myelinated primary afferent fibers unmyelinated & thinly myelinated primary afferent fibers that subserve nociception. that subserve nociception.

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Microanatomic small & large fiber damage in Microanatomic small & large fiber damage in nerve, essentially demyelination, commonly nerve, essentially demyelination, commonly observed at its root entry zone (REZ), leads to observed at its root entry zone (REZ), leads to ephaptic transmission, in which action potentials ephaptic transmission, in which action potentials jump from one fiber to another.jump from one fiber to another.

lack of inhibitory inputs from large myelinated lack of inhibitory inputs from large myelinated nerve fibers plays a role. nerve fibers plays a role.

Additionally, reentry mechanism causes Additionally, reentry mechanism causes amplification of sensory inputs. amplification of sensory inputs.

However, features also suggest additional However, features also suggest additional central mechanism (eg, delay between central mechanism (eg, delay between stimulation and pain, refractory period). stimulation and pain, refractory period).

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EtiologyEtiology questionable family clustering exists, but TN is most questionable family clustering exists, but TN is most

likely multifactorial.likely multifactorial. Most cases are idiopathic, but compression of trigeminal Most cases are idiopathic, but compression of trigeminal

roots by tumors/ vascular anomalies may cause similar roots by tumors/ vascular anomalies may cause similar pain.pain.

In one study, 64% of compressing vessels were In one study, 64% of compressing vessels were identified as an artery, most commonly superior identified 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), actually The classic form (considered idiopathic), actually

includes cases that are due to a normal artery present in includes cases that are due to a normal artery present in contact with nerve, such as superior cerebellar contact 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 lesions tumors, chronic meningeal inflammation, or other lesions may irritate trigeminal nerve roots along pons). may irritate trigeminal nerve roots along pons).

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Uncommonly, demyelination from multiple sclerosis may Uncommonly, demyelination from multiple sclerosis may be precipitant be 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 of Infrequently, adjacent dental fillings composed of

dissimilar metals may trigger attacks dissimilar metals may trigger attacks

Microscopic demonstration of demyelination in primary TN. Tortuous axon is surrounded by abnormally discontinuous myelin.

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EpidemiologyEpidemiology No geographic tendency or racial differences.No geographic tendency or racial differences. females are affected upto twice as often as females 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 after In 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 20-40 Pts who present with disease when aged 20-40

years more likely to suffer from demyelinating years 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 or younger 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.

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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 and Thus, 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 sensory Among best clinical predictors of symptomatic form are sensory

deficits upon examination & u/l distribution of symptoms (but deficits 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 poor Lack of therapeutic response and V1 distribution are poor predictors. predictors.

not associated with shortened life, morbidity associated can be not 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 from may 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, such Individuals 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.

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ComplicationsComplications chief complication - adverse effects & toxicity experienced routinely with chief 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 adverse requiring addition of 2nd anticonvulsant, causing more drug-related adverse reactions. reactions.

brainstem tumor/bone marrow aplasia as an idiosyncratic adverse effect of brainstem tumor/bone marrow aplasia as an idiosyncratic adverse effect of carbamazepine. carbamazepine.

Percutaneous neurosurgical procedures and microvascular decompression Percutaneous neurosurgical procedures and microvascular decompression procedures pose risks of long-term complications. Perioperative risks also procedures 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, and pts 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 a some 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 or Some 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 nerve Corneal 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)

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CHARACTERISTICSCHARACTERISTICS

TN is predominantly unilateral, has tactile "trigger“ areas, does TN is predominantly unilateral, has tactile "trigger“ areas, does not produce neurosensory/motor deficit, restricted to distribution not produce neurosensory/motor deficit, restricted to distribution of trigeminal nerve. of trigeminal nerve.

Pain attacks occur spontaneously/triggered by mechanical tactile Pain attacks occur spontaneously/triggered by mechanical tactile stimulus to skin, intraoral mucosa surrounding the teeth, or stimulus 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 head physical 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 special Cranial 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 trigeminal In 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.

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Note should be taken of any trigger areas Note should be taken of any trigger areas and they should be appropriately mapped and they should be appropriately mapped out. out.

In summary, the clinical criteria for a In 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 pain2. unilateral pain2. unilateral pain3. pain limited to the distribution of the 3. pain limited to the distribution of the

trigeminal nervetrigeminal nerve4. tactile trigger areas4. tactile trigger areas5. no neurosensory deficit5. no neurosensory deficit

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TREATMENTTREATMENT current treatment of idiopathic (primary) TN consists of current 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 surgical pharmacological approaches, while surgical management consists of numerous peripheral and management consists of numerous peripheral and intracranial neuroablative procedures. intracranial neuroablative procedures.

initial medical treatment is usually pharmacological initial medical treatment is usually pharmacological therapy with drugs such as carbamazepine (Tegretol), therapy with drugs such as carbamazepine (Tegretol), baclofen, gabapentin, topiramate, phenytoin or baclofen, gabapentin, topiramate, phenytoin or clonazepam in single or combination regimens.clonazepam in single or combination regimens.

however for some pts, these medications do not however for some pts, these medications do not relieve pain and/or produce intolerable side effects with relieve pain and/or produce intolerable side effects with significant medical and functional morbidity. significant medical and functional morbidity.

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Under surgical treatment for TN - several Under surgical treatment for TN - several procedures currently utilized: procedures currently utilized:

1.1. percutaneous stereotactic radiofrequency percutaneous stereotactic radiofrequency thermal rhizotomy (RTR), thermal rhizotomy (RTR),

2.2. glycerol rhizolysis (GR), glycerol rhizolysis (GR),

3.3. balloon compression of trigeminal ganglion balloon compression of trigeminal ganglion (BC), (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).

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RTR - best overall, long-term outcome dataRTR - best overall, long-term outcome data technique of controlled thermal ablation of nerve fibers in technique of controlled thermal ablation of nerve fibers in

trigeminal ganglion/nerve root, producing loss of pain trigeminal ganglion/nerve root, producing loss of pain with relative preservation of touch and more complex with relative preservation of touch and more complex facial sensationsfacial sensations

ability to allow for pre-lesion testing for localization in ability 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), in also affords the ability to test clinically after a lesion(s), in order to grade level of hypalgesia/paresthesia, avoid side order 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 less side effects and complications are less frequent and less

morbid.morbid.

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Glycerol rhizolysis - not division specific, very high recurrence Glycerol 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 during can produce significant bradycardia & hypotension during procedure, very high incidence of masticatory motor procedure, very high incidence of masticatory motor dysfunction, other cranial nerve abnormalities, does not have dysfunction, other cranial nerve abnormalities, does not have long follow up. long follow up.

Microvascular decompression (MVD) - long-term follow up Microvascular 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 of especially in non-life-threatening condition in addition to risk of long GA, there is risk of cerebellar dysfunction, hearing loss long GA, there is risk of cerebellar dysfunction, hearing loss and facial palsy. and facial palsy.

Recently, several reports have acknowledged Gamma Knife Recently, several reports have acknowledged Gamma Knife Radiosurgery, essentially non-invasive procedure, as having a Radiosurgery, essentially non-invasive procedure, as having a very high rate of pain relief, with no facial numbness & no side very high rate of pain relief, with no facial numbness & no side effects.effects.

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HERPETIC NEURALGIAHERPETIC NEURALGIAETIOLOGYETIOLOGY Herpes zoster results from reactivation of varicella-zoster Herpes zoster results from reactivation of varicella-zoster

virus. virus. Unlike varicella (chickenpox), HZ is sporadic, with Unlike varicella (chickenpox), HZ is sporadic, with

estimated lifetime incidence of 10- 20%. estimated lifetime incidence of 10- 20%. incidence increases sharply with advancing age, roughly incidence 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 immunity normal 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 therapy may Chronic CTS use, chemotherapy & radiation therapy may increase risk of developing HZ.increase risk of developing HZ.

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no evidence that HZ heralds onset of an underlying no evidence that HZ heralds onset of an underlying malignancy.malignancy.

Race may influence susceptibility. Blacks 1/4th as likely Race 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 varicella Although HZ is not as contagious as primary varicella infection, persons with reactivated infection can transmit infection, 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 be Household transmission rates have been noted to be approx 15%.approx 15%.

About 20% of pts with HZ develop postherpetic About 20% of pts with HZ develop postherpetic neuralgia. neuralgia.

most established risk factor is age; this complication most 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 are Other possible risk factors for postherpetic neuralgia are ophthalmic zoster, h/o prodromal pain before ophthalmic zoster, h/o prodromal pain before appearance of skin lesions, immunocompromised state.appearance of skin lesions, immunocompromised state.

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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 root During primary infection, virus gains entry into sensory dorsal root

ganglia. ganglia. How it does so & whether it resides in neurons or supporting cells How 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 of varicella-zoster virus genome identified in trigeminal ganglia of

nearly all seropositive patients.nearly all seropositive patients. remains latent for decades - virus specific cell-mediated immunity remains latent for decades - virus specific cell-mediated immunity

acquired during primary infection, & endogenous & exogenous acquired 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 - dermatomal reactivated 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 sensory However, pathologic studies demonstrated damage to sensory

nerves, sensory dorsal root ganglia & dorsal horns of spinal cord in nerves, sensory dorsal root ganglia & dorsal horns of spinal cord in pts with this condition.pts with this condition.

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CLINICAL PRESENTATIONCLINICAL PRESENTATION typically presents with prodrome consisting of typically presents with prodrome consisting of

hyperesthesia, paresthesias, burning hyperesthesia, paresthesias, burning dysesthesias/pruritus along affected dermatome(s). dysesthesias/pruritus along affected dermatome(s).

prodrome generally lasts 1-2 days, may precede prodrome 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 as During 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 without Some 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 of prodromal phase followed by development of characteristic skin lesions with characteristic type of characteristic skin lesions with characteristic type of pain.pain.

Pain - "burning“/ "stinging“, unrelenting. Pain - "burning“/ "stinging“, unrelenting. pts may have insomnia.pts may have insomnia.

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skin lesions begin as a skin lesions begin as a maculopapular rash - dermatomal maculopapular rash - dermatomal distribution, belt-like pattern.distribution, belt-like pattern.

evolves into vesicles with an evolves into vesicles with an erythematous baseerythematous base. .

vesicles painful, associated with the vesicles painful, associated with the occurrence of anxiety and flu-like occurrence of anxiety and flu-like symptoms.symptoms.

Although any vertebral dermatome Although any vertebral dermatome may be involved, T5 and T6 are may be involved, T5 and T6 are most commonly affected. most commonly affected.

most frequently involved cranial most frequently involved cranial nerve dermatome - ophthalmic nerve dermatome - ophthalmic division of trigeminal nerve. division of trigeminal nerve.

20+ lesions outside affected 20+ lesions outside affected dermatome reflect generalized dermatome reflect generalized viremia. Of which, approx 1/2 viremia. Of which, approx 1/2 manifest other neurologic/ visceral manifest other neurologic/ visceral involvement.involvement.

eventually become eventually become hemorrhagic/turbid - crust over hemorrhagic/turbid - crust over within 7-10 days. within 7-10 days.

scarring, pigmentary changes.scarring, pigmentary changes.

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COMPLICATIONSCOMPLICATIONS Ocular complications - approx 1/2 of pts with involvement of Ocular 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 as Pain that persists >1-3 mths after resolution of rash accepted as

postherpetic neuralgia.postherpetic neuralgia. Affected pts usually report constant burning, lancinating pain that Affected 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 stimuli -may 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.

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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-management Antiviral 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 these individualized 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 received However, 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 being Antiviral 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 more effectiveness of antiviral agents in preventing postherpetic neuralgia is more

controversial. controversial.

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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 frequency drawbacks of oral acyclovir - lower bioavailability, dosing frequency

(five times daily). (five times daily). IV acyclovir generally used only in severely IV 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 blood more 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, better advantages - 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.

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Oral Antiviral Medications for HZOral Antiviral Medications for HZMedicationMedication DosageDosage DurationDuration Adverse Adverse

EffectsEffects

Precautions/ Precautions/

contraindicationscontraindications

AcyclovirAcyclovir 800 mg 5 800 mg 5 times daily times daily (every 4–5 h) (every 4–5 h)

7-10days7-10days Nausea, Nausea, headacheheadache

Dose adjustment Dose adjustment for renal for renal insufficiency insufficiency

BrivudinBrivudin 125 mg once 125 mg once daily daily

7days7days Nausea, Nausea, headacheheadache

Drug interactions Drug interactions with 5-fluorouracil, with 5-fluorouracil, severe BM severe BM suppression suppression

FamciclovirFamciclovir 500 mg 3 500 mg 3 times daily times daily

7days7days Nausea, Nausea, headacheheadache

Dose adjustment Dose adjustment for renal for renal insufficiency insufficiency

ValacyclovirValacyclovir 1000 mg 3 1000 mg 3 times daily times daily

7days7days Nausea, Nausea, headacheheadache

Dose adjustment Dose adjustment for renal for renal insufficiency; insufficiency; TTP/HUS at TTP/HUS at doses >8000 mg doses >8000 mg daily in daily in immunocompromiimmunocompromised sed

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CorticosteroidsCorticosteroids

Oral CTS commonly used in HZ, even though clinical Oral 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 to Prednisone used in conjunction with acyclovir shown to reduce pain.reduce pain.

likely mechanism involves decreasing degree of neuritis likely mechanism involves decreasing degree of neuritis caused by active infection & decreasing residual damage caused 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 pts some 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.

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MedicationMedication Beginning Beginning dosedose

TitrationTitration Maximum Maximum dosedose

Adverse Adverse effectseffects

PrednisolonePrednisolone 60mg daily for 60mg daily for 7days7days

Decrease to Decrease to 30mg for 30mg for 7days, 7days,

then 15mg for then 15mg for 7 days,7 days,

then then discontinuediscontinue

60mg daily60mg daily GI distress, GI distress, nausea, mood nausea, mood changes, changes, oedemaoedema

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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 dosing When analgesics used, +/- narcotic, regular dosing

schedule results in better pain control & less anxiety than schedule results in better pain control & less anxiety than "as-needed" dosing."as-needed" dosing.

Lotions containing calamine (e.g., Caladryl) may be used Lotions 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 cream Once lesions have crusted over, capsaicin cream (Zostrix) may be applied. (Zostrix) may be applied.

Topically administered lidocaine (Xylocaine) & nerve Topically administered lidocaine (Xylocaine) & nerve blocks have also been reported to be effective in blocks have also been reported to be effective in reducing pain.reducing pain.

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MedicationMedication Beginning doseBeginning dose TitrationTitration Maximum doseMaximum dose Adverse effectsAdverse effects

OxycodoneOxycodone 5 mg every 4 h 5 mg every 4 h as needed; as needed; dosage can be dosage can be converted to converted to long-acting long-acting opioid analgesic opioid analgesic combined with combined with short-acting short-acting medication medication continued as continued as needed needed

Increase by 5 Increase by 5 mg 4 times mg 4 times daily every 2 daily every 2 days as days as tolerated tolerated

No maximum No maximum dosage with dosage with careful titration; careful titration; consider consider evaluation by a evaluation by a pain specialist pain specialist at dosages at dosages >120 mg daily >120 mg daily

Nausea/Nausea/vomiting, vomiting, constipation, constipation, sedation, sedation, dizziness dizziness

Tramadol1 Tramadol1 50 mg once or 50 mg once or twice daily twice daily

Increase by 50 Increase by 50 to 100 mg daily to 100 mg daily in divided doses in divided doses every 2 days as every 2 days as tolerated tolerated

400 mg daily 400 mg daily (100 mg 4 times (100 mg 4 times daily); for daily); for patients >75 patients >75 years of age, years of age, 300 mg daily in 300 mg daily in divided doses divided doses

Nausea/Nausea/vomiting, vomiting, constipation, constipation, sedation, sedation, dizziness, dizziness, seizures, seizures, postural postural hypotension hypotension

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MedicationMedication Beginning doseBeginning dose TitrationTitration Maximum doseMaximum dose Adverse effectsAdverse effects

Gabapentin 2Gabapentin 2 300 mg at 300 mg at bedtime or 100 bedtime or 100 to 300 mg 3 to 300 mg 3 times daily times daily

Increase by 100 Increase by 100 to 300 mg 3 to 300 mg 3 times daily times daily every 2 days as every 2 days as tolerated tolerated

3600 mg daily 3600 mg daily (1200 mg 3 (1200 mg 3 times daily); times daily); reduce if renal reduce if renal function is function is impaired impaired

Sedation, Sedation, dizziness, dizziness, peripheral peripheral edema edema

Pregabalin 2Pregabalin 2 75 mg at 75 mg at bedtime or 75 bedtime or 75 mg twice daily mg twice daily

Increase by 75 Increase by 75 mg twice daily mg twice daily every 3 days as every 3 days as tolerated tolerated

600 mg daily 600 mg daily (300 mg twice (300 mg twice daily); reduce if daily); reduce if renal function is renal function is impaired impaired

Sedation, Sedation, dizziness, dizziness, peripheral peripheral edema edema

TCAs TCAs (nortryptiline) 2(nortryptiline) 2

25 mg at 25 mg at bedtime bedtime

Increase by 25 Increase by 25 mg daily every mg daily every 2 to 3 days as 2 to 3 days as tolerated tolerated

150 mg daily 150 mg daily Sedation, dry Sedation, dry mouth, blurred mouth, blurred vision, weight vision, weight gain, urinary gain, urinary retention3 retention3

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.

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Ocular InvolvementOcular Involvement Ocular HZ treated with oral antiviral agents & CTS, same Ocular HZ treated with oral antiviral agents & CTS, same

as involvement elsewhere. as involvement elsewhere. most pts improve without lasting sequelae, some may most 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 & effective morbidity & mortality could be reduced if safe & effective

preventive treatment were available. preventive treatment were available. unusual to develop HZ > once, suggesting that 1st unusual to develop HZ > once, suggesting that 1st

reactivation of VZ provides future immunologic reactivation of VZ provides future immunologic protection. protection.

Studies are currently being conducted to evaluate the Studies are currently being conducted to evaluate the efficacy of the varicella-zoster vaccine in preventing or efficacy of the varicella-zoster vaccine in preventing or modifying herpes zoster in the elderly.modifying herpes zoster in the elderly.

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Treatment of Postherpetic NeuralgiaTreatment of Postherpetic Neuralgia

Although postherpetic neuralgia is generally a self-limited Although 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 the Treatment is directed at pain control while waiting for the condition to resolve. condition to resolve.

Pain therapy may include multiple interventions, such as Pain 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.

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AnalgesicsAnalgesics

CapsaicinCapsaicin – – extract from hot chili peppers, currently only drug labeled by FDA for extract from hot chili peppers, currently only drug labeled by FDA for

postherpetic neuralgia. Trials have shown it be more efficacious postherpetic neuralgia. Trials have shown it be more efficacious than placebo but not necessarily more than other conventional than 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 burning also released when capsaicin is applied to skin, producing a burning sensation. sensation.

Analgesia occurs when substance P is depleted from the nerve Analgesia occurs when substance P is depleted from the nerve fibers. fibers.

To achieve this response, capsaicin cream must be applied to the To 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 few Pts 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 capsaicin Pts 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.

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Patches containing lidocainePatches containing lidocaine – – 1 study found that compared with no treatment, lidocaine 1 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 each effect temporary, lasting only 4-12hrs with each

application.application.Over-the-counter analgesicsOver-the-counter analgesics – – Eg. acetaminophen (Tylenol), NSAIDs not been shown Eg. acetaminophen (Tylenol), NSAIDs not been shown

to be highly effective in treatment of postherpetic to be highly effective in treatment of postherpetic neuralgia. neuralgia.

However, often useful for potentiating the pain-relieving However, 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, their Because of the addictive properties of narcotics, their chronic use is discouraged except in the rare patient who chronic use is discouraged except in the rare patient who does not adequately respond to other modalities.does not adequately respond to other modalities.

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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 & norepinephrine most 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, postural TCAs 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; nortriptyline Nortriptyline 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 and potential 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 a As 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 by onset of pain relief using tricyclic antidepressants may be enhanced by

beginning treatment early in the course of herpes zoster infection in beginning treatment early in the course of herpes zoster infection in conjunction with antiviral medicationsconjunction with antiviral medications

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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 necessarily Lack 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 in dosages 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, memory associated with a variety of side effects, including sedation, memory

disturbances, electrolyte abnormalities, liver toxicity and disturbances, electrolyte abnormalities, liver toxicity and thrombocytopenia. thrombocytopenia.

Side effects may be reduced or eliminated by initiating treatment in Side 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 combination no specific contraindications to using anticonvulsants in combination with antidepressants or analgesics. However, the risk of side effects with 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 multiple Effective treatment of postherpetic neuralgia often requires multiple treatment approaches. treatment approaches.

In addition to medications, modalities to consider include In addition to medications, modalities to consider include transcutaneous electric nerve stimulation (TENS), biofeedback and transcutaneous electric nerve stimulation (TENS), biofeedback and nerve blocks.nerve blocks.

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MYOFASCIAL PAINS AND MYOFASCIAL PAINS AND MANAGEMENTMANAGEMENT

diagnosed in pts with chronic, non-malignant pain who lack clinical/lab evidence of diagnosed 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 of diagnosis 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

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hallmark is trigger point— tender area within contracted muscle hallmark is trigger point— tender area within contracted muscle bands that produces an involuntary contraction with stimulation bands that produces an involuntary contraction with stimulation

(1) (1) taut bands shown to have spontaneous electrical activity on EMG taut bands shown to have spontaneous electrical activity on EMG testing testing

(2)(2) important for diagnosis & also because they restrict normal muscle important for diagnosis & also because they restrict normal muscle stretch, reduce active range of motion & cause muscle weakness stretch, reduce active range of motion & cause muscle weakness (shortening). (shortening).

Taut bands produced involuntarily. Taut bands produced involuntarily.

Trigger points (Trigger points (distinguished from distinguished 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 localized most important distinction - myofascial pain represents localized

pain complaint (e.g., low-back or shoulder-girdle pain), whereas pain complaint (e.g., low-back or shoulder-girdle pain), whereas fibromyalgia produces widespread pain, covering most regions of fibromyalgia 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 additional activity, patients with fibromyalgia may develop additional myofascial pain complaints on the background of widespread myofascial pain complaints on the background of widespread fibromyalgia pain.fibromyalgia pain.

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Criteria for Distinguishing Between Myofascial Criteria for Distinguishing Between Myofascial Pain and FibromyalgiaPain and Fibromyalgia

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EPIDEMIOLOGYEPIDEMIOLOGYCommon myofascial syndromes include Common myofascial syndromes include 1.1. lateral epicondylitis (tennis elbow), lateral epicondylitis (tennis elbow), 2.2. quadratus lumborum syndrome (a common cause of quadratus lumborum syndrome (a common cause of

nonradicular low back pain), nonradicular low back pain), 3.3. piriformis syndrome (a common cause of buttock and piriformis 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 have Pts 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 to Active quadratus lumborum trigger points refer pain to

hip and buttock (Fig. 2). hip and buttock (Fig. 2).

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piriformis syndromepiriformis syndrome – – piriformis muscle attaches from inner ileum and sacrum to greater piriformis muscle attaches from inner ileum and sacrum to greater

trochanter (Fig. 3) & rotates hip externally, thereby contributing to trochanter (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, which When 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.

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Several muscle groups are commonly affected. Several muscle groups are commonly affected. These include the upper trapezius, scalene, rhomboids, levator These include the upper trapezius, scalene, rhomboids, levator

scapulae, serratus anterior muscles. scapulae, serratus anterior muscles. Areas of common trigger points & their referral patterns are shown Areas 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 the Identifying typical pain referral patterns in myofascial pain helps the

clinician recognize these common pain syndromes.clinician recognize these common pain syndromes.

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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 examiner Passive range of motion is evaluated by an examiner manipulating a joint through its full range in the relaxed manipulating a joint through its full range in the relaxed patient. patient.

Active range of motion, on the other hand, requires the patient Active range of motion, on the other hand, requires the patient to voluntarily activate muscles to move each joint through its to 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 with Greater restriction of active range of motion compared with passive range of motion suggests a myofascial restriction or passive range of motion suggests a myofascial restriction or reduced patient effort.reduced patient effort.

The presence of myofascial features can be identified by The 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 and which suggests a spasm, and by palpating for taut bands and trigger points. trigger points.

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Identification of taut bands is best performed by examining the Identification 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 the The taut band should feel like a tight cord or rope in the muscle. muscle.

In addition, palpation of taut bands demonstrates tenderness In addition, palpation of taut bands demonstrates tenderness and may cause involuntary muscle contraction locally (a local and 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 trigger This flinch response should occur exclusively when the trigger point is palpated and not as a response to palpation of other point is palpated and not as a response to palpation of other areas. areas.

Tenderness cannot be assessed in patients who do not permit Tenderness 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 these Myofascial 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 extreme If patients cannot cooperate with testing because of extreme pain, the clinician hould reschedule them for another visit pain, the clinician hould reschedule them for another visit when they may be more amenable to testing.when they may be more amenable to testing.

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No laboratory or radiographic abnormalities are No laboratory or radiographic abnormalities are associated with myofascial pain. associated with myofascial pain.

The diagnosis is generally based on a history of an The diagnosis is generally based on a history of an inciting event or injury, physical examination findings of inciting event or injury, physical examination findings of tight and tender muscles, and the absence of tight 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 suspected X-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 for Plain X-rays also provide a useful screening tool for patients with chronic pain over bony structures to rule patients with chronic pain over bony structures to rule out underlying bone disease. out underlying bone disease.

MRIs should be reserved for patients with evidence of MRIs should be reserved for patients with evidence of myelopathy, radiculopathy, or another specific type of myelopathy, radiculopathy, or another specific type of pathology that would beidentified with this testing.pathology that would beidentified with this testing.

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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 to exercise program needs to be tailor-made for each patient to

specifically address postural abnormalities and myofascial changes specifically address postural abnormalities and myofascial changes contributing to the pain complaints. Therapy must focus on active contributing 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 the supplemental 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 be Patients should be instructed in a home-exercise routine to be performed at least twice daily, in addition to their physical therapy performed at least twice daily, in addition to their physical therapy sessions. sessions.

Temporarily isolated muscle stretching during a 1-hour therapy Temporarily isolated muscle stretching during a 1-hour therapy session, with no additional exercise to maintain stretches between session, 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, or The addition of targeted trigger-point injections, medications, or other physical therapy modalities are all designed in improve the other 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

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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

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Physical TherapyPhysical Therapy

Although passive stretching (stretching performed by a therapist on a Although passive stretching (stretching performed by a therapist on a relaxed patient) may be soothing, myofascial pain is most likely to improve relaxed 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 targeted Patients 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 maximal Patients should not overstretch their muscles or attempt to achieve maximal

stretch. stretch. Stretching exercises help return shortened muscles to a more normal Stretching 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 start Several 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-motion The 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 included The 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 the both 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.

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Supplemental Treatment Modalities Used in ConjunctionSupplemental Treatment Modalities Used in ConjunctionWith 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 produces Force 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 before Hot 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 full Active 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 area Spray 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 20 TENS Electrodes placed around painful area and current applied for approximately 20

minutes.minutes.• • Interferential current therapy Electrodes placed around painful area and current applied Interferential current therapy Electrodes placed around painful area and current applied

for approximately 20 minutes. Minimal skin resistance with interferential current for 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 fail maximum amount of energy to penetrate to deeper tissues. Used in patients who fail TENS.TENS.

• • Myofascial release Passive stretching and traction techniques, applied by trained Myofascial release Passive stretching and traction techniques, applied by trained therapist.therapist.

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InjectionsInjections Trigger-point injections require infiltration of LA into myofascial trigger Trigger-point injections require infiltration of LA into myofascial trigger

points. points. 22- to 25-gauge needle is inserted into skin approximately 1 cm away from 22- 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 area needle 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/ muscle process is repeated until a local twitch response no longer elicited/ muscle

tautness is reduced/ 0.5-1.0 mL of anesthetic has been injected around tautness 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 hematoma Pressure 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 of It is not clear whether addition of steroids to injections lengthens duration of

relief.relief. Superficial dry needling involves insertion of a solid thin needle (resembling Superficial 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 in This 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 benefits benefits of dry needling are supported by studies showing similar benefits

after trigger point injections, regardless of the injected substance (including after trigger point injections, regardless of the injected substance (including saline).saline).

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Pharmacological TherapyPharmacological Therapy designed to supplement physical therapy. designed to supplement physical therapy. Patients who fail to benefit from stretching programs Patients who fail to benefit from stretching programs

alone may be treated with adjunctive tizanidine, a muscle alone may be treated with adjunctive tizanidine, a muscle relaxant with analgesic properties. relaxant with analgesic properties.

Unlike most muscle relaxants, which are ineffective in Unlike most muscle relaxants, which are ineffective in chronic pain, tizanidine effectively reduces chronic chronic pain, tizanidine effectively reduces chronic myofascial pain for many patients. myofascial pain for many patients.

Tizanidine is also mildly sedating and can improve sleep Tizanidine is also mildly sedating and can improve sleep disturbance in some patients when administered in low disturbance in some patients when administered in low doses at bedtime. doses at bedtime.

Analgesics may be used on an intermittent basis to treat Analgesics may be used on an intermittent basis to treat pain flares. pain flares.

Daily analgesics are rarely helpful and chronic use may Daily analgesics are rarely helpful and chronic use may produce significant gastric and renal toxicity.produce significant gastric and renal toxicity.

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SUMMARYSUMMARY Myofascial pain - unique pain syndrome, characterized by Myofascial pain - unique pain syndrome, characterized by

tight, tender muscles, with taut bands and tender trigger tight, tender muscles, with taut bands and tender trigger points. points.

distinguished from mechanical pain by absence of joint distinguished from mechanical pain by absence of joint pathology, from neuropathic pain by absence of neurological pathology, from neuropathic pain by absence of neurological dysfunction, and from fibromyalgia by absence of widespread dysfunction, 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) facilitates quadratus 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 and focus of treatment for myofascial pain is active stretching and range-of motion exercises. range-of motion exercises.

Passive physical therapy modalities, injections, and Passive physical therapy modalities, injections, and medications may be used adjunctively. medications may be used adjunctively.

Patients with long-standing myofascial pain may have Patients with long-standing myofascial pain may have additional psychological distress, disability, or both that will additional psychological distress, disability, or both that will require additional, targeted therapy, including psychological require additional, targeted therapy, including psychological interventions and occupational therapy.interventions and occupational therapy.

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