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Electrodiagnostics
NCSandneedleEMGaddcertaintytothelocationofnerveinjuryandelucidatethenatureand
severityofimpairment.ThecollectivedatafrombothNCSandEMGmayhelpdeterminethe
temporalcourseofinjury, differentiate neuropathyfrommyopathy, assess the severityofthe
axonaldamage,andrevealsignsofaxonalregeneration.Inaddition,electrodiagnosticstudies
providequantitativemeasurements,whichcanbefollowedovertime.
ImagingStudies
Standard radiographs and computed tomography have little role in the characterization of
neuropathies because of the inabilityto directlyvisualize nerves. Thetypical modalities to
imageperipheralnerveinjuryaremainlyultrasound(US)andMRI.
US hasgainedwide acceptanceasausefultoolinthe evaluationofthemusculoskeletal
system.High-resolutiontransducerscandepictindividualnerve fascicles.Theadvantagesof
this techniqueinclude dynamic, real-time examination,andquickassessmentofentire nerve
segments;USisalsononinvasive,welltolerated,andaffordableandcanbeperformedinthe
office;however,imagequalityisoperatordependent.64Inflamednervescanbeidentifiedby
increased caliber or internal signal changes, and focal thinning with proximal fusiform
swellingoccurswithnervecompression.65AnalogoustoEMGtesting,UScanyieldimportant
informationaboutmusclebydifferentiatingphasesofmusclecontraction.
MRprovidesresolutionuptothelevelofthenervefascicle.Thesignalcharacteristicsof
peripheral nerves using traditional MR pulse sequences are well described. Relative to
adjacentmuscletissue,T1-weightedimages ofnormalnerve fascicles are hypointense, with
hyperintense perineurialandepineurial fatsurrounding them. Roughly thereverseis seen in
T2-weightedimages.
66–69
Deviationfromthenormalsignalcharacteristicsofanerveindicates
pathology.T2hyperintensitywithinthenerveisthoughttoreflectdisruptionoftheblood–nerve
barrier,leading to endoneurial or perineurial edema.However,the underlying pathogenesis
remainsuncertain.
66,67
Changes innerve diameter shouldraise suspicionforpathology. The
fascicles in nerves distal to the common peroneal nerve are poorly visualized with MRI.
Neuropathyindistalnervesissuggestedbychangesconsistentwithdenervationmyopathy.
70,71
Denervatedmuscles areedematousinthesubacute phase andatrophicinthechronicphase.
T1-weightedimagesareusefulforvisualizingfattydepositsinchronicallydenervatedmuscle.
Denervationmyopathy is apparent onMRIup to4days after a traumatic nerve injury. The
abnormalsignalchangesarereversibleifthereisreinnervation.
IndividualNerveInjuries
CommonPeronealNerve
Table 6-4 lists common activities associated with injury of the peroneal nerve. Although
frequently asymptomatic, peroneal neuropathy is a common complication of ankle injuries.
Using electrodiagnostic studies, Nitz et al. found that 17% of patients with grade II ankle
sprainsand86% withgradeIIIsprainshad evidenceofsubclinical motorimpairmentinthe
peroneal nerve.72 Symptomatic ankle dorsiflexion and eversion weakness results from
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Table6-4.
plantarflexionandinversioninjuriesasseeninseveresprainsorfracturesofthedistaltibia
and fibula. The common peroneal nerve can be torn by sudden, extreme ankle inversion,
leadingtointernalhemorrhageandischemia.Aftersuchinjury,paralysisisusuallyimmediate,
butcanbe delayed forseveral days. Baccari etal. reported sixcases of delayed paralysis
because of peroneal nerve injury following ankle sprain by up to 3 days.73 Patients with
sensoryinjurytothecommonperonealnervemaycomplainofnumbnessorburningpainfrom
thekneetothetopofthefoot.
DeepPeronealNerve
Deepperonealnervecompressionmayresultfromanterior compartmentsyndrome,whichis
associatedwithapainful,tight,andswollenlowerleg.Intramuscularpressuremeasurements
facilitate diagnosis, and electrodiagnostic studies may document the extent of involvement.
Chroniccompartmentsyndromecanoccurinrunnersorotherathletesexperiencingrepetitive
lowerextremityimpact.Painthatincreasesonpassivestretchingandactivecontractionmaybe
present. Generally, symptoms disappear once the offending activity is stopped. The deep
peroneal nerve can also be compressed against the talonavicular joint in crush injuries, in
postsurgicalinflammation,andbytightlytiedshoes.Compressionoccursovertheheadofthe
taluswhentheankleisplantarflexedandinverted.74Chroniccompressionbeneaththeextensor
retinaculum has been referred to as the “anterior tarsal tunnel syndrome.”63 Patients with
lateralbranchcompressiontypicallycomplainofpainradiatingtothelateraltarsometatarsal
joints,whereasmedial nervecompressioncausessymptomswithin thefirstwebspace. The
precisesiteofcompressioncanbeconfirmedwithafocalnerveblock.
ActivitiesAssociatedwithInjurytothePeronealNerve
Activity AssociatedNerveInjury
Running Entrapmentatthefibularneck;anteriortibialcompartmentsyndrome;compressionat
thecapitulumperoneibyamucouscyst
Dancing Footwearcompression
Martialarts Impactnervecontusion
Football Kneedislocationand/orligamentousinjurywithsubsequentnervetrauma(incidence
of24%)
Soccer Entrapmentatthefibularneck
Autoracing Compressionwithinsmallcockpit
Surfing Chronicnervetrauma
Rollerskating Entrapmentsecondarytofootwear
SuperficialPeronealNerve
The superficial peroneal nerve cansustain traction injury during inversion ankle sprain or
become entrapped as it exits the deep fascia. Entrapment can be seen in dancers with a
techniqueflawreferredtoas“sickling”inwhichthefootiseitherinvertedorevertedduring
dancing. Hypertrophiedperonealmuscles mayalso leadtoentrapmentby causingincreased
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Table6-5.
compartment pressure. In dancers with lateral ligament deficiency or ankle instability, the
superficialperonealnervemaybetetheredandstretched.Painatthedistalthirdofthelateral
leg is precipitated by dancing and relieved by rest. The examiner may reproduce sensory
symptomsoverthedorsumandlateralaspectofthefootbydorsiflexingandevertingtheankle.
Nervepercussioncanalsoreproducesymptoms.
TibialNerve
Table6-5listscommonactivitiesassociatedwithinjuryofthetibialnerve.Entrapmentofthe
tibialnervewithinthetarsaltunnelhasbeenfrequentlydescribedinathletes.Anyswellingof
structures in or adjacent to the tunnel can lead to the so-called tarsal tunnel syndrome.
Inflammatorytenosynovitis,edemarelatedtotrauma,andgangliaofadjacentjointsortendon
sheathsarepotentialcauses.The classicsymptomsare paininthe heelandsoleofthefoot
withaccompanyingsensorychanges.
Morton’s neuroma is a well-known cause of impingement of the interdigital nerves.
Although the name implies a nerve tumor, histologic analysis reveals fibrosis and
demyelination instead. It is suspected that repetitive dorsiflexion of the toes against the
transversemetatarsal ligamentcauses nervetrauma andsubsequentfibrosis. Inflammationof
theintermetatarsalbursaisanotherpotentialcause.Morton’sneuromacanbefoundbetween
any of the metatarsals, but most commonly occurs in the third followed by the second
interdigital space.
75,76
Although the exact incidence is unknown, it is considered to be a
common cause of forefoot pain. Symptoms are exacerbated by running and tight-fitting
footwear. Female predominancemaybe duetofootwear differences.MRIis 90% sensitive
and100%specificfordetectingMorton’sneuroma.Thediameterofthemassisusually5mm
orlargerwithT1andT2hypointensityandoccasionalenhancement.Afluidcollectionmaybe
seenwithintheintermetatarsalbursa.Greaterthan3mmoffluidisconsideredabnormal.77US
isalsocommonlyusedtoimageneuromas,withreportedsensitivity>90%.
78
ActivitiesAssociatedwithInjurytotheTibialNerve
Activity AssociatedNerveInjury
Running Chronictraumawithinthetarsaltunnelcausedbyrepetitiveankledorsiflexion;Morton
neuroma;entrapmentatthecalcanealnerve;injuryoflateralandmedialbranches
Dancing Mortonneuroma
Martialarts Mortonneuroma
Hiking Chronictraumawithinthetarsaltunnelcausedbyrepetitiveankledorsiflexion
Hockey Footwearcompressionatthetarsaltunnel
Treatment
Once the diagnosis is established, intervention should focus on minimizing further injury,
treating symptoms, and accelerating recovery. Acute ankle and foot trauma may require
surgery. Anti-inflammatory drugs can be used acutely as adjuvant or primary therapy to
decreaseedemaandinflammation.
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Table6-6.
Theapproachtochronic injuriesisdifferent,andlikewisedependsonthemechanismof
injury.Interventionsforcompressiveneuropathymaybeassimpleasappareladjustment,asin
deep peroneal nerve compression from tight footwear. In other cases, decompression may
require surgery. Pain canbe a disablingresult ofperipheral nerve injury. Itis important to
identifyandtreatneuropathicpaintopreventmorbidity,giventhehighprevalenceofcomorbid
depression in chronic pain patients.79 Gabapentin, carbamazepine, and pregabalin are
anticonvulsants used to treat neuropathic pain.Gabapentin is used most frequently, and has
proven efficacy.80 Carbamazepine is an older drug. It was the initial anticonvulsant
investigatedinthetreatmentoftrigeminalneuralgiaandisstill considered first-linetherapy.
Tricyclic antidepressants such as amitriptyline or nortriptyline are also very effective. NmethylD-aspartatereceptorantagonists,opioidanalgesics,andtopicalagentsarealsouseful
treatmentoptions.Combinationtherapymaybenecessarytoachieveadequatepaincontrol.
Recovery from peripheral nerve injury is variable. Currently, physical medicine and
rehabilitation offer the best options. Rigorous rehabilitation programs produced improved
outcomeswithimprovedstrength,agility,andbalance.
Surgicaltreatmentcontinues tobeinvestigated.Neurotizationisatechniquebywhichan
autologousnerveoflittlefunctionalsignificanceistransplantedtothesiteofdisablingnerve
injury. Thistechniquehasbeenusedextensivelyinpatientswithbrachialplexus injuries. In
patientswithtibialisanteriordenervation,Schwanncelltransplanthasbeenshowntoenhance
reinnervationafterneurotization.81Theseapproachesarecurrentlyexperimentalandshouldbe
consideredonlyonacase-to-casebasis.
PERIPHERALNEUROPATHIES
PeripheralNerveAnatomy
Peripheralsensorynervesoriginateatthedorsalrootgangliaandexitdorsallyfromthespinal
cord.Theperipheralmotornervesemergefromtheanterolateralhorncellsinthespinalcord
and brain stem motor nuclei. They exit the spinal cord via the ventral roots. Finally, the
peripheralpreganglionicautonomicnervefibersexitthespinalinteromedialcolumn,alsovia
the ventralroots.Allthese fibersexitthroughthe intervertebral foramina.Peripheralnerves
arecategorizedintothreetypes(A,B,C)bysizeandmyelinthickness(Table6-6).
NerveFiberTypesandTheirFunction
Type FiberType Function
A Largemyelinated Motor,proprioception,vibratory,touch,pressuresensation
B Smallmyelinated Autonomic(preganglionicfibers)
C Smallunmyelinated Pain/temperaturesensation,autonomic(postganglionicfibers)
Myelinated axons are individually enveloped by a myelin sheath and Schwann cell
membrane, whereas unmyelinated nerve fibers are bundled together and are covered by a
singleSchwanncellmembrane.Ingeneral,nervefibersareadditionallyenvelopedbymultiple
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connectivetissuesheathsrichinvascularsupply:endoneurium,whichcoversindividualnerve
fibers;perineurium,whichsurroundseachfascicleorbundleofnervefibers;andepineurium,
whichenvelopesallthefasciclesofanerve.
DiagnosingPeripheralNeuropathy
Symptoms
Peripheralneuropathyorpolyneuropathyreferstoadiseaseprocessinvolvingthe cellbody,
axon, and/or myelin of sensory, motor, or autonomic peripheral nerves. It is distinct from
mononeuropathy(injury toasinglenerve) andmononeuropathymultiplex(disease oftwo or
morenoncontiguousnervetrunks).Asaresult,itsclinicalpresentationislargelysymmetricin
thelimbsortrunk.Themaincategoriesofperipheralneuropathyinvolvedamagetoeitherthe
axonormyelin,andtheirclinicalpresentationsdiffer(Table6-7).Manytimes,boththeaxon
andmyelinareaffected,althoughusuallyonemoresothantheother.Electrodiagnostictesting
can indicate whether the pathologic process is predominately axonal or demyelinating, or
revealasubclinicalprocess.
Electrodiagnostics
NCScanindicatewhetheraperipheralneuropathyispredominatelyaxonalordemyelinating
andcanruleoutradiculopathyandmyopathy.Demyelinationimpliesdecreasedconductionthat
manifests as temporal dispersion of compound action potentials, conduction block, partial
conduction block at noncompressible nerve sites, prolonged distal latencies, prolonged or
absent F waves, andprolongedor absentH waves. In contrast,axonalinjurydecreases the
totalamountofchargecarriedviathenerveandresultsindecreasedareaunderthecurveof
theactionpotential.Specificallyformotorneuropathies,themuscleitselfcanbeaffected.The
EMGcandemonstratefibrillations,fasciculations,decreased recruitmentofmotorunits,and
motorunitrecruitmentthatislongindurationandpolyphasic.
Biopsy
A nerve biopsy can be helpful in cases of inconclusive EMG/NCS. Nerve biopsy is also
informativewhencertainconditionsaresuspected,forexample,infiltrativediseasessuchas
amyloidorsarcoidosis.82Biopsycanalsoaidindiagnosingsuspectedcasesofautonomicor
small fiber neuropathywhere EMG/NCStesting will be normal or impractical.83 Thesural
nerveismostcommonlybiopsied.
LaboratoryStudies
High-yield serology tests prior to EMG/CNS include B12, fasting glucose, methylmalonic
acid,andserumelectrophoresis.82The clinicianshouldotherwiserefrainfromsending most
testsuntilafter EMG/NCSis done.If axonal neuropathy, screening forsystemic diseasesis
indicated.If demyelinating, screeningfor an inflammatoryprocess usinglumbar puncture is
oftennecessary(Table6-8).
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Table6-7.
Table6-8.
Table6-9.
CommonEtiologiesofPeripheralNeuropathy
Manyetiologiesofperipheralneuropathyhavebeenidentifiedovertheyears(seeTable6-9
for a comprehensive list by etiology). Despite this, up to 25% of peripheral neuropathies,
mostlyaxonalneuropathies,remainidiopathic.
GeneralSymptomsofPeripheralNeuropathies
Symptoms Axonal Demyelinating
Motor Symmetricweakness Symmetricweaknessisthetypicalpresenting
complaint
Sensory Symmetricsensoryloss/numbness,
burning/pain,mildgaitdisturbancespriorto
weakness
Distaldysesthesias,impairedproprioception
andvibratorysensation,handclumsiness
andgaitdisturbance
Duration Bothchronicoveryearsbutcanhaveacute
fulminantsymptoms
Weekstoyears
Examfindings Intrinsichandandfootmusclewasting;distal
sensationlosstoallsensationmodalities;
hypoactiveorabsentreflexes,usuallyankle
reflexesaffectedfirst
Generalizedweakness(distalmorethan
proximal),sensoryloss(vibratoryand
proprioceptivelossmorethanpainand
temperature),globallydecreasedreflexes,
autonomicinstability
ScreeningTestsforPeripheralNeuropathies
ScreeningTestsifEMG/NCSShowPredominatelyAxonalNeuropathy
TSH,HbA1c Cellcountandcompletemetabolicpanel
B12,folate,B1,methylmalonicacid+/−homocysteine Lyme,HIV,RPR,hepatitisscreen
Serumandurineelectrophoresis ANA,ESR,RF,Anti-Ro/La
Heavymetals Porphyrins
ScreeningTestsifEMG/NCSShowPredominatelyDemyelinatingNeuropathy
Serumandurineelectrophoresis Hepatitisscreen,HIV
LumbarpunctureforelevatedCSFprotein Anti-myelin-associatedglycoprotein(MAG)(if
predominatelysensorysymptoms)
GenetictestingforCharcot–Marie–Toothdisease(if“inverted
champagnebottle”phenotypeobservedinlegs)
Anti-GM1(ifpredominatelymotorsymptoms,
indicativeofAIDP)
EtiologiesofPeripheralNeuropathies
SystemicDisease
Diabetesmellitus Criticalillness/sepsis Carcinoma Uremia
Vitamindeficiency B12deficiency Chronicliverdisease Malabsorption(sprue,
celiac)
HIV Lyme Lymphoma Multiplemyeloma
Benignmonoclonal
gammopathy(IgA,IgG,
Porphyria Hypoglycemia Primarybiliarycholangitis
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IgM)
Primarysystemic
amyloidosis
Hypothyroidism Chronicobstructivelung
disease
Acromegaly
Polycythemiavera Cryoglobulinemia Sjögrensyndrome Rheumatoidarthritis
Systemiclupus
erythematosus
Systemicsclerosis Mixedconnectivetissue
disease
Sarcoidosis
Hypereosinophilicsyndrome Celiacdisease Inflammatoryboweldisease Leprosy
Herpesvaricella-zoster
virus
Hepatitis Paraneoplastic
Drugs/Medications
Amiodarone Aurothioglucose Cisplatin Dapsone
Disulfiram Hydralazine Isoniazid Leflunomide
Linezolid Metronidazole Misonidazole Nitrofurantoin
Nucleosideanalogues Oxaliplatin Phenytoin Pyridoxine
Suramin Taxol Vincristine Cytarabine
Etoposide Bortezomib Hydroxychloroquine Colchicine
Podophyllin Thalidomide Ethambutol Lithium
Toxins
Acrylamide Arsenic Diphtheriatoxin Gamma-diketone
hexacarbons
Lead Organophosphates Thallium Carbondisulfide
Ethyleneoxide Mercury Gold
Genetic
CMTtype1 CMTtype2 CMT1,X-linked CMTtype4a
Porphyricneuropathy Hereditaryliabilityto
pressurepalsy
Fabrydisease Adrenomyeloneuropathy
Hereditarysensoryand
autonomicneuropathy
typeI
Hereditarysensoryand
autonomicneuropathy
typeII
Dejerine–Sottassyndrome Hereditaryamyloid
polyneuropathies
Refsumdisease Ataxia-telangiectasia Abetalipoproteinemia Giantaxonalneuropathy
Metachromatic
leukodystrophy
Friedrichataxia Hereditaryneuralgic
amyotrophy
Tangier
AxonalPredominantNeuropathies
Axonal polyneuropathies are predominately manifestations of systemic disease. The most
commonisdiabetesmellitus,characterizedbydistalsymmetricsensoryloss,paresthesias,and
autonomic dysfunction (commonly postural hypotension or gastroparesis). Critical illness
polyneuropathy is common in critically ill patients, frequently presenting as weakness and
inability to wean from the ventilator. Autoimmune and inflammatory conditions can also
produceaxonalneuropathies.ExamplesincludeSjögrendisease,scleroderma,variousmixed
connective tissuedisorders, sarcoidosis, and inflammatory bowel disease (IBD). Infectious
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causesinclude leprosy, Lyme disease, diphtheria, andHIV.84 Other systemic conditionsthat
lead to axonal peripheral neuropathy include lymphoproliferative disorders (multiple
myeloma, Waldenström macroglobulinemia, lymphoma, other plasmacytomas) and
endocrinopathiessuchashypothyroidism,whichpresentsascarpaltunnelsyndromeorsensory
neuropathywithpainfulparesthesias.
Toxinexposurecanalsoleadtoaxonalneuropathy.Themostcommonexampleisalcohol.
Othersincludemercury,lead,arsenic,thallium,andhexa-carbons.Taxane,platinum,orvinca
alkaloid–basedchemotherapyhasantimicrotubuleeffectsthatareparticularlytoxictoaxons.
85
Onsetandtime course vary depending on intensityand duration of exposure. Mostpatients
present with sensory and motor symptoms, but some toxins lead to primarily sensory
neuropathies (pyridoxine, oxaliplatin, cisplatin), whereas others are primarily motor
neuropathies (dapsone). Some toxins affect both the axon and myelin, including
aurothioglucose,suramin,paclitaxel,amiodarone,andvincristine.
Othercausesofaxonal neuropathyinclude vitaminor nutritional deficiencies (B12, B6,
B1,E,niacin,copper),environmentalexposures(coldandhypoxemia),andraremitochondrial
disorders (Charcot–Marie–Tooth [CMT] type 2A and syndrome of neuropathy, ataxia, and
retinitispigmentosa).
86
Axonal peripheral neuropathies have predominantly sensorimotor involvement, though
primarysensoryaxonalperipheralneuropathiescanbeseeninB12deficiency,primarybiliary
cholangitis, hypothyroidism, acromegaly, and polycythemia vera. Hypoglycemia has been
linkedtomotor-onlyneuropathy,andsystemicdiseasessuchasdiabetesandprimarysystemic
amyloidosisofteninjuretheperipheralautonomicnervoussystemaswell.
DemyelinatingPredominantNeuropathies
Demyelinatingpolyneuropathiesarebroadlyclassifiedintotwocategories,acuteandchronic
inflammatory demyelinating polyneuropathies (AIDP andCIDP, respectively), dependingon
whethersymptomspersist>2months.AIDPisotherwiseknownasGuillain–Barrésyndrome
(GBS).Thereisusually,thoughnotalways,aprecedinginfectionweeksprior(Campylobacter
jejuniisawell-knownoffender), followedbysymmetricascendingnumbnessandweakness
affectingthelegsandthenarmsaswellaslossofdistalreflexes.TheMillerFishervariantof
GBSpreferentiallyaffectscranialnervesfirst.
Diagnosis is made based on history andsupportive diagnostic studies including lumbar
puncture(albuminocytologicdissociation—normalCSFcellcountwithelevatedprotein)and
NCS/EMG(absentFwavesarean earlysign).Notethatduringthe firstweek,thesestudies
maybenormal.FortheMillerFishervariantofGBS,apositivegangliosideantibodypanelis
diagnostic. Gangliosides specific to cranial nerve myelin are thought to be the antigen
mistakenlytargetedbytheimmunesystem.
TreatmentforGBSisprimarilysupportive,includingintubationifthedisease ascendsto
the diaphragm. Intravenous immunoglobulin(IVIG) andplasma exchange (PLEX) temporize
symptoms. Steroids are nothelpful. With physical therapy, mostpatients havefull recovery
after2months.
CIDPischaracterizedbyprogressiveweakness(symmetricproximalanddistal,although
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1.
2.
3.
4.
5.
6.
thereareatypicalforms)withorwithoutsensorylossovermorethana2-monthperiod.CSF
typicallydemonstratesalbuminocytologicdissociation.NCSandnervebiopsycanadditionally
be helpful in the diagnosis of CIDP. When CIDP is suspected, paraproteinemia and other
alternativeetiologiesshouldbeexcluded.
Chronic demyelinating neuropathies are commonly a manifestation of systemic disease.
These diseases include monoclonal gammopathies, paraneoplastic syndromes (anti-CV2),
celiac disease, andIBD.87 Notably, anadditional demyelinating component can be seen in
diabetes. Certain toxin exposures can cause demyelinating neuropathy, including n-hexane,
thalidomide,andarsenic.
85
Multiplegeneticdiseasesproducedemyelinatingpolyneuropathies.CMTdiseaseisamore
commonexample.CMTtype1presentsduringchildhoodorearlyadulthood,withprogressive
distalsensorylossandweakness.ItisanautosomaldominantduplicationofthePMP-22gene
onchromosome17.CMT type3isalso autosomal dominant,butpresentsininfancy,andis
characterized by severe motor weakness. Common metabolic diseases of childhood can
present with a demyelinating neuropathy, including Krabbe disease, metachromatic
leukodystrophy,andadrenoleukodystrophy.
Treatments
For axonal polyneuropathies, treatment is focused on the underlying disease, that is, tight
glucose control in diabetes or avoiding toxins in exposure cases. For demyelinating
polyneuropathy,inautoimmunecases,IVIGorPLEXisusuallyhelpful,butitisalsocrucialto
treattheunderlyingdiseaseifpossible.InCIDP,steroidscanalsobeofhelp.Forrefractory
CIDP, alternative immunomodulatory agentscanbe used such asazathioprine,cyclosporine,
mycophenolatemofetil,methotrexate,andrituximab.
There are many waystotreatneuropathic pain.Gammaaminobutyricacid (GABA)ergic
agentssuchasgabapentinorpregabalin(notethattheydonotactdirectlyonGABAreceptors
but rather on voltage-gated calcium channels) and tricyclic antidepressants are first line.
Second-lineagentsincludecertainantiepileptics(carbamazepine,lamotrigine) andserotonin
norepinephrine reuptake inhibitors. Third-line agents are a mix of nonsteroidal antiinflammatories, capsaicin,baclofen,andlow-dosenarcotics.Manypatientsrequiremultiple
agents of various drug classes. In these cases, referral to a pain management specialist is
recommended.
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