Peripheral Neuropathy Peripheral Neuropathy

Rebecca Meyerson, MDRebecca Meyerson, MD

NeurologyNeurology

SMDCSMDC

Peripheral Nervous SystemPeripheral Nervous System

Motor peripheral nerves: neuron Motor peripheral nerves: neuron in the anterior horn of the spinal in the anterior horn of the spinal cord, axon extends peripherally cord, axon extends peripherally to the skinto the skin

Sensory peripheral nerves: Sensory peripheral nerves: neuron in the dorsal root ganglia, neuron in the dorsal root ganglia, axon extending peripherally to axon extending peripherally to the skin surfacethe skin surface

Pathology of the peripheral nerve Pathology of the peripheral nerve may take place at any place along may take place at any place along its pathway, and any peripheral its pathway, and any peripheral nerve lesion must first be nerve lesion must first be localized.localized.• Anterior horn cellAnterior horn cell• Spinal nerve rootSpinal nerve root• Nerve plexusNerve plexus• Nerve (certain places are prone to Nerve (certain places are prone to

compression or injury)compression or injury)• Neuromuscular junctionNeuromuscular junction• MuscleMuscle

Differentiating upper motor neuron Differentiating upper motor neuron and lower motor neuron lesionsand lower motor neuron lesions

UMN lesionUMN lesion LMN lesionLMN lesion

Muscle bulkMuscle bulk PreservedPreserved AtrophyAtrophy

Muscle toneMuscle tone SpasticSpastic FlaccidFlaccid

Spontaneous Spontaneous movementsmovements

NoneNone FasciculationFasciculation's's

ReflexesReflexes IncreasedIncreased AbsentAbsent

Babinski Babinski reflexreflex

PresentPresent AbsentAbsent

Peripheral Nerves Contain:Peripheral Nerves Contain:

Motor nerve fibersMotor nerve fibers Sensory nerve fibersSensory nerve fibers

• Large myelinated fibers: vibration, Large myelinated fibers: vibration, proprioception, light touchproprioception, light touch

• Small unmyelinated fibers: pain and Small unmyelinated fibers: pain and temperaturetemperature

Autonomic nerve fibersAutonomic nerve fibers

Nerve injuryNerve injury

Compressive injuryCompressive injury Vascular insultVascular insult Axonal damageAxonal damage

• Metabolic disruption of axonal transportMetabolic disruption of axonal transport• Ion channel dysfunctionIon channel dysfunction

DemyelinationDemyelination Infiltrative processInfiltrative process

Differentiating Clinical FeaturesDifferentiating Clinical Features RadiculopathyRadiculopathy

• Radiating pain in a nerve Radiating pain in a nerve root distributionroot distribution

• WeaknessWeakness• Decreased DTRDecreased DTR• Decreased sensationDecreased sensation• Often associated with back Often associated with back

and neck pain, and muscle and neck pain, and muscle stiffnessstiffness

• Aggravated by sneeze, Aggravated by sneeze, cough, valsalva maneuver, cough, valsalva maneuver, neck/trunk movementneck/trunk movement

PlexopathyPlexopathy• Does not fit nicely into a Does not fit nicely into a

root or nerve patternroot or nerve pattern• Is typically unilateralIs typically unilateral

MononeuropathyMononeuropathy• Single nerve involvedSingle nerve involved

Mononeuropathy Mononeuropathy multiplexmultiplex• Multiple single nerves Multiple single nerves

involvedinvolved PolyneuropathyPolyneuropathy

• Chronic and insidious Chronic and insidious onsetonset

• Length dependent Length dependent patternpattern

Cervical RadiculopathiesCervical Radiculopathies

Lumbar RadiculopathiesLumbar Radiculopathies

L5 and S1 L5 and S1 nerve root nerve root compression compression most commonmost common

Pain radiates Pain radiates in the in the distribution of distribution of the nerve rootthe nerve root

Mononeuropathies of the upper Mononeuropathies of the upper extremitiesextremities

Median neuropathyMedian neuropathy Ulnar neuropathyUlnar neuropathy Radial neuropathyRadial neuropathy

Median neuropathyMedian neuropathy Vulnerable at the Vulnerable at the

carpal tunnelcarpal tunnel Most common, most Most common, most

common neuro prob in common neuro prob in pregnancypregnancy

Pain severe at nightPain severe at night Pain thumb, index and Pain thumb, index and

middle finger, split middle finger, split sensory loss 4sensory loss 4thth digit digit

Motor usually confined Motor usually confined to abductor pollicis to abductor pollicis brevisbrevis

Ulnar neuropathyUlnar neuropathy Injury usually occurs at the Injury usually occurs at the

elbowelbow May occur from repeated May occur from repeated

and trivial trauma (resting and trivial trauma (resting elbow)elbow)

Tardy ulnar palsy occurs Tardy ulnar palsy occurs after a childhood fracture after a childhood fracture of the supracondylar of the supracondylar humerushumerus

Sensory loss medial aspect Sensory loss medial aspect hand and forearm, medial hand and forearm, medial 2 fingers2 fingers

Weakness of intrinsic hand Weakness of intrinsic hand musclesmuscles

Radial neuropathyRadial neuropathy

Radial neuropathyRadial neuropathy Damaged in the axilla by incorrect use of a Damaged in the axilla by incorrect use of a

crutch, causing weakness of all the radial nerve crutch, causing weakness of all the radial nerve innervated muscles – triceps, wrist extensors, innervated muscles – triceps, wrist extensors, finger extensors and brachoradialis.finger extensors and brachoradialis.

Classic appearance – wrist drop and finger Classic appearance – wrist drop and finger extension weakness. Sensory loss occurs on the extension weakness. Sensory loss occurs on the dorsum of the handdorsum of the hand

Injury of the radial nerve in the medial aspect of Injury of the radial nerve in the medial aspect of the arm results in the Saturday night palsy. the arm results in the Saturday night palsy. Occurs when inebriated or heavily sedated Occurs when inebriated or heavily sedated patients go to sleep with their arm hanging over patients go to sleep with their arm hanging over the back of a chair or over the edge of the bed.the back of a chair or over the edge of the bed.

Peroneal neuropathyPeroneal neuropathy

Nerve in leg most often Nerve in leg most often damaged, usually by damaged, usually by compression at the fibular compression at the fibular neck where protected only neck where protected only by skin and fasciaby skin and fascia

Weakness of dorsiflexion Weakness of dorsiflexion (foot drop) and eversion of (foot drop) and eversion of the foot. (Distinction the foot. (Distinction between peroneal and L5 between peroneal and L5 root lesion – L5 affects root lesion – L5 affects dorsiflexion and inversion)dorsiflexion and inversion)

Sensory loss occurs in the Sensory loss occurs in the lower anterolateral leg and lower anterolateral leg and on to the dorsum of the foot on to the dorsum of the foot in a triangular area.in a triangular area.

Assessment of UE strengthAssessment of UE strength

Assessment of UE StrengthAssessment of UE Strength

UE RadiculopathiesUE Radiculopathies

Sensory deficit in UE MononeuropathiesSensory deficit in UE Mononeuropathies

Assessment of LE StrengthAssessment of LE Strength

LE RadiculopathiesLE Radiculopathies

Electrodiagnostic studiesElectrodiagnostic studies

Electrodiagnostic studiesElectrodiagnostic studies

Clinical features of Clinical features of polyneuropathiespolyneuropathies

Motor symptoms – weak, atrophy, diminished Motor symptoms – weak, atrophy, diminished reflexesreflexes

Sensory symptoms – Sensory symptoms – • loss of small fiber (pain temperature), loss of large fiber loss of small fiber (pain temperature), loss of large fiber

(vibration, propriception, light touch)(vibration, propriception, light touch)• Gain of abnormal sensation: allodynia, hyperalgesia, Gain of abnormal sensation: allodynia, hyperalgesia,

paresthesiasparesthesias Autonomic symptoms – orthostatic hypotension, Autonomic symptoms – orthostatic hypotension,

impotence, gastroparesis, altered sweating impotence, gastroparesis, altered sweating responseresponse

Orthopedic abnormalities – high arched feet and Orthopedic abnormalities – high arched feet and hammer toes suggests a long standing conditionhammer toes suggests a long standing condition

Neurological clinical evaluation of Neurological clinical evaluation of polyneuropathypolyneuropathy

SensorySensory: evaluate at least one test of : evaluate at least one test of both large and small fiber modalities ie: both large and small fiber modalities ie: vibration and painvibration and pain

MotorMotor: assess muscle tone, visual : assess muscle tone, visual inspection for fasciculations and atrophy, inspection for fasciculations and atrophy, in addition to muscle srengthin addition to muscle srength

ReflexesReflexes GaitGait: inability to walk on heels early sign : inability to walk on heels early sign

of distal weaknessof distal weakness RombergRomberg: evaluates distal large fiber : evaluates distal large fiber

sensationsensation

Clinical evaluation contClinical evaluation cont

Electrodiagnostic studies (NCS/EMG)Electrodiagnostic studies (NCS/EMG)• Extablish extent and involvement of Extablish extent and involvement of

nerve pathologynerve pathology• Distinguish primary axonal or Distinguish primary axonal or

demyelinating processdemyelinating process• Will not tell you anything about small Will not tell you anything about small

fiber dysfunctionfiber dysfunction Nerve biopsyNerve biopsy

Causes of polyneuropathyCauses of polyneuropathy

Diabetes, alcohol, hypothyroidism, uremia, Diabetes, alcohol, hypothyroidism, uremia, amyloidosis, medications, B 12 deficiency, amyloidosis, medications, B 12 deficiency, B1 deficiency, B6 deficiency or toxicity, B1 deficiency, B6 deficiency or toxicity, arsenic, lead, HIV, hepatitis, leprosy, lyme, arsenic, lead, HIV, hepatitis, leprosy, lyme, polyarteritis nodosum, lupus, sjogrens, polyarteritis nodosum, lupus, sjogrens, chronic inflammatory demyelinating chronic inflammatory demyelinating polyneuropathy, guillian barre syndrome, polyneuropathy, guillian barre syndrome, paraneoplastic, charcot marie tooth, paraneoplastic, charcot marie tooth, diptheria, thallium, porphyoria, diptheria, thallium, porphyoria, acrylamide, gold salts, methotrexae, acrylamide, gold salts, methotrexae, nitrofurantoin………………………nitrofurantoin………………………

Schema to tease out etiology of Schema to tease out etiology of polyneuropathiespolyneuropathies

Timing: chronic vs acuteTiming: chronic vs acute Modalities affected (large fiber, small Modalities affected (large fiber, small

fiber, motor, sensory)fiber, motor, sensory) Distribution (symmetric, asymmetric, Distribution (symmetric, asymmetric,

focal, multiple focal nerves)focal, multiple focal nerves) Nature of primary pathology (axonal Nature of primary pathology (axonal

vs demyelinatingvs demyelinating

Metabolic causes of Metabolic causes of polyneuropathypolyneuropathy

DiabetesDiabetes: most common cause of : most common cause of neuropathyneuropathy

Occurs from a combination of metabolic Occurs from a combination of metabolic and vascular abnormalities due to and vascular abnormalities due to hyperglycemiahyperglycemia• Severity of diabetic neuropathy correlates with Severity of diabetic neuropathy correlates with

the severity of hyperlipidemia and the severity of hyperlipidemia and hypertensionhypertension

No treatment to reverse pathologyNo treatment to reverse pathology Management: optimize blood glucose Management: optimize blood glucose

control, foot care, and symptomatic control, foot care, and symptomatic treatment of neuropathic paintreatment of neuropathic pain

Metabolic etiologiesMetabolic etiologies Diabetes: Diabetes:

• typically cause symmetric sensorimotor axonal neuropathytypically cause symmetric sensorimotor axonal neuropathy• Other presentations:Other presentations:

sensorimotor demyelination sensorimotor demyelination prominent autonomic involvement prominent autonomic involvement mononeuropathy-especially carpal tunnel syndrome, truncal mononeuropathy-especially carpal tunnel syndrome, truncal

radiculopathies, cranial neuropathies (CN3)radiculopathies, cranial neuropathies (CN3) Mononeuropathy multiplex: results in simultaneous dysfunction of Mononeuropathy multiplex: results in simultaneous dysfunction of

several peripheral nerves, due to ischemic infarction of the vasa several peripheral nerves, due to ischemic infarction of the vasa nervorumnervorum

Diabetic amyotrophy (ischemic infarction of the lumbosacral Diabetic amyotrophy (ischemic infarction of the lumbosacral plexus)plexus)

Uremia: symmetric sensorimotor axonal neuropathyUremia: symmetric sensorimotor axonal neuropathy Hypothyroidism: sensorimotor neuropathy, entrapment Hypothyroidism: sensorimotor neuropathy, entrapment

neuropathy (carpal tunnel syndrome)neuropathy (carpal tunnel syndrome)

Nutritional etiologies of Nutritional etiologies of polyneuropathiespolyneuropathies

B12 deficiencyB12 deficiency: sensorimotor axonopathy, myelopathy : sensorimotor axonopathy, myelopathy involving the posterior columnsinvolving the posterior columns

B6 deficiency or toxicityB6 deficiency or toxicity: myelopathy and axonal : myelopathy and axonal sensorimotor neuropathysensorimotor neuropathy

Thiamine deficiencyThiamine deficiency: (wernickes-korsakoff syndrome), : (wernickes-korsakoff syndrome), axonal sensorimotor neuropathy, can be rapid onset and axonal sensorimotor neuropathy, can be rapid onset and progression. (thiamine needed for metabolism progression. (thiamine needed for metabolism carbohydrates/amino acids)carbohydrates/amino acids)

Copper deficiencyCopper deficiency: axonal sensorimotor axonopathy, : axonal sensorimotor axonopathy, myelopathymyelopathy

Zinc toxicityZinc toxicity: due to induced copper deficiency, axonal : due to induced copper deficiency, axonal sensorimotor neuopathy, myelopathy with posterior column sensorimotor neuopathy, myelopathy with posterior column (sensory ataxia)(sensory ataxia)

Vitamin E deficiencyVitamin E deficiency: axonal sensorimotor neuropathy, : axonal sensorimotor neuropathy, myelopathymyelopathy

Infectious etiologies of Infectious etiologies of polyneuropathiespolyneuropathies

HIVHIV• Distal symmetric sensori>motor neuropathyDistal symmetric sensori>motor neuropathy• Inflammatory polyneuritis of buillian barre type at the time of Inflammatory polyneuritis of buillian barre type at the time of

seroconversionseroconversion Lyme diseaseLyme disease

• Multifocal spinal root or cranial nerve (often facial nerve palsy)Multifocal spinal root or cranial nerve (often facial nerve palsy)• Demyelinating and axonal neuropathy often with multiple Demyelinating and axonal neuropathy often with multiple

nerve root involvementnerve root involvement Hepatitis C and cryoglobulinemia: Hepatitis C and cryoglobulinemia:

• vasculitis associatedvasculitis associated• Painful, asymmetric sensorimotor polyneuropathy or multiple Painful, asymmetric sensorimotor polyneuropathy or multiple

mononeuropathiesmononeuropathies Diptheria:Diptheria:

• Toxin mediated sensorimotor neuropathyToxin mediated sensorimotor neuropathy• Prominent autonomic disurbanceProminent autonomic disurbance

Toxic etiologies of Toxic etiologies of polyneuropathiespolyneuropathies

AlcoholAlcohol: slowly progressive, distal, painful, : slowly progressive, distal, painful, symmetric sensorimotor axonal neuropathy. symmetric sensorimotor axonal neuropathy. Nutritional factors likely contributeNutritional factors likely contribute

Lead toxicityLead toxicity: motor predominant, often : motor predominant, often presents with radial nerve associated wrist droppresents with radial nerve associated wrist drop

Arsenic toxicityArsenic toxicity: motor predominant : motor predominant sensorimotor demyelinating>axonal neuropathy. sensorimotor demyelinating>axonal neuropathy. Can mimic guillian barreCan mimic guillian barre

Multiple medicationsMultiple medications: nitrofurantoin, : nitrofurantoin, vincristine, amiodarone, phenytoin: usually vincristine, amiodarone, phenytoin: usually produce a sensorimotor axonal neuropathyproduce a sensorimotor axonal neuropathy

Inflammatory/immune mediated Inflammatory/immune mediated etiologies of polyneuropathyetiologies of polyneuropathy

Vasculitis: systemic lupus erythematosis, Vasculitis: systemic lupus erythematosis, sjogrens, polyarterosis nodosum, wegeners sjogrens, polyarterosis nodosum, wegeners granulomatosis, microscopic polyangiitis, granulomatosis, microscopic polyangiitis, rheumatoid arthritisrheumatoid arthritis• Painful mononeuropathies or mononeuropathy multiplexPainful mononeuropathies or mononeuropathy multiplex• Acute or subacute onsetAcute or subacute onset

Paraprotinemic neuropathy: Paraprotinemic neuropathy: • Monoclonal gammaopathy, excessive amounts of Monoclonal gammaopathy, excessive amounts of

abnormal immunoglobulin produced by a single clone of abnormal immunoglobulin produced by a single clone of plasma cellplasma cell

• Several distinct peripheral neuropathy syndromesSeveral distinct peripheral neuropathy syndromes• Symmetric polyneuropathy, (mononeuritis multiplex, Symmetric polyneuropathy, (mononeuritis multiplex,

mononeuropathy), demyelinating>axonalmononeuropathy), demyelinating>axonal

Inflammatory/immune mediated Inflammatory/immune mediated etiologies of polyneuropathyetiologies of polyneuropathy

CIDP (chronic inflammatory demyelinating CIDP (chronic inflammatory demyelinating polyradiculoneuropathy)polyradiculoneuropathy)• Acquired neuropathy due to immune mediated Acquired neuropathy due to immune mediated

demyelinationdemyelination• Chronic progressive or relapsing-remitting neuropathyChronic progressive or relapsing-remitting neuropathy• Symmetric sensorimotor neuropathy with predominant Symmetric sensorimotor neuropathy with predominant

motor symptoms, demyelinating changes on EMGmotor symptoms, demyelinating changes on EMG• Subacute weakness proximally and distally variable Subacute weakness proximally and distally variable

sensory loss, areflexiasensory loss, areflexia• Left untreated: continuously progressive or relapsing Left untreated: continuously progressive or relapsing

remitting courseremitting course• Treatment: corticoids, IVIG, plasma exchangeTreatment: corticoids, IVIG, plasma exchange

Hereditary etiologies of Hereditary etiologies of polyneuropathypolyneuropathy

Hereditary sensory motor neuropathy (HSMN) = Hereditary sensory motor neuropathy (HSMN) = charcot marie tooth (many genetic disorders charcot marie tooth (many genetic disorders identified, with distinct clinical syndromes)identified, with distinct clinical syndromes)• Genetic defect of axonal and myelin proteinsGenetic defect of axonal and myelin proteins• Onset of symptoms is insidious and progression is Onset of symptoms is insidious and progression is

indolent, often onset in childhood/adolenscence or early indolent, often onset in childhood/adolenscence or early adulthood, progresses gradually throughout adult lifeadulthood, progresses gradually throughout adult life

• Significant motor involvement, striking atrophy of the Significant motor involvement, striking atrophy of the muscles of the foot, calf and handsmuscles of the foot, calf and hands

• Hereditary Sensory Motor Neuropathy HSMN-1Hereditary Sensory Motor Neuropathy HSMN-1 Demyelinating polyneuropathyDemyelinating polyneuropathy Autosomal dominant patternAutosomal dominant pattern Striking atrophy calves (stork legs)Striking atrophy calves (stork legs) Large fiber sensory loss with marked reduction in vibratory Large fiber sensory loss with marked reduction in vibratory

perception and proprioceptionperception and proprioception

Distal symmetric polyneuropathyDistal symmetric polyneuropathy

Pattern seen with most metabolic, toxic and nutritional etiologiesPattern seen with most metabolic, toxic and nutritional etiologies Axonal predominantAxonal predominant Length dependent (symptoms begin in the feet and progress Length dependent (symptoms begin in the feet and progress

rostrally), the stocking-glove pattern.rostrally), the stocking-glove pattern.• The offending agent affects protein synthesis in the cell body of the The offending agent affects protein synthesis in the cell body of the

peripheral nerve and then impairs axonal transportperipheral nerve and then impairs axonal transport• Dysfunction first occurs in the distal portions of the longest axons, thus Dysfunction first occurs in the distal portions of the longest axons, thus

in the most distal portions of the extremities in the most distal portions of the extremities • Small diameter axons are most susceptible to metabolic injury because Small diameter axons are most susceptible to metabolic injury because

of their small size and lack of reserveof their small size and lack of reserve Initial symptoms typically include autonomic dysfunction and Initial symptoms typically include autonomic dysfunction and

small fiber sensory modalities, including loss of pain and small fiber sensory modalities, including loss of pain and temperaturetemperature

Clinical presentation: numbness, paresthesias, burning discomfortClinical presentation: numbness, paresthesias, burning discomfort• Loss sensation distal LE, later loss of achilles reflex and weakness Loss sensation distal LE, later loss of achilles reflex and weakness

intrinsic foot musclesintrinsic foot muscles

Distal symmetric polyneuropathyDistal symmetric polyneuropathy

ExamplesExamples• DiabetesDiabetes• AlcoholAlcohol• Nutritional deficienciesNutritional deficiencies• MedicationsMedications

Symmetric or asymmetric Symmetric or asymmetric demyelinating polyneuropathydemyelinating polyneuropathy

Demyelinating more than axonal Demyelinating more than axonal involvementinvolvement

Numbness and weakness in a length Numbness and weakness in a length dependent fashiondependent fashion

Clinically: sensory loss in feet, and Clinically: sensory loss in feet, and weakness (footdrop)weakness (footdrop)

Examples:Examples:• Hereditary sensory motor neuropathiesHereditary sensory motor neuropathies• CIDPCIDP

Multifocal axonal neuropathy Multifocal axonal neuropathy (mononeuropathy multiplex)(mononeuropathy multiplex)

Individual nerves are affected in a patchy Individual nerves are affected in a patchy fashion (ie: left median nruopathy, then fashion (ie: left median nruopathy, then right peroneal neuropathy) right peroneal neuropathy)

Underlying pathology ischemic infarction Underlying pathology ischemic infarction of the vasa nervorumof the vasa nervorum

Painful and cause profound weaknessPainful and cause profound weakness Prognosis for recovery is good assuming Prognosis for recovery is good assuming

the underlying disease can be suppressedthe underlying disease can be suppressed Examples: Examples:

• VasculitisVasculitis• DiabetesDiabetes

Acute polyneuropathiesAcute polyneuropathies

Guillian Barre syndrome (acute Guillian Barre syndrome (acute inflammatory demyelinating inflammatory demyelinating polyradiculoneuropathy):polyradiculoneuropathy):• Rapidly progressiveRapidly progressive• Motor predominenceMotor predominence• Diffuse polyradiculoneuropathyDiffuse polyradiculoneuropathy• Clinical presentation:Clinical presentation:

Nearly symmetric, rapidly ascending motor weakness Nearly symmetric, rapidly ascending motor weakness often with associated paresthesiasoften with associated paresthesias

Often striking autonomic involvement (resting Often striking autonomic involvement (resting tachycardia, fluctuations in blood pressure)tachycardia, fluctuations in blood pressure)

Guillian-Barre syndrome contGuillian-Barre syndrome cont

Often follows a systemic infectionOften follows a systemic infection• Campylobacor jejuni infectionCampylobacor jejuni infection

Weakness reaches its nadir within Weakness reaches its nadir within the first 2 weeks, may require the first 2 weeks, may require intubation and respiratory suppportintubation and respiratory suppport

Rate of recovery is accelerated by Rate of recovery is accelerated by plasma exchange or IVIGplasma exchange or IVIG

Other acute neuropathiesOther acute neuropathies

Neurotoxins:Neurotoxins:• Medications – acute onset symmetric Medications – acute onset symmetric

neuropathyneuropathy• Toxic exposures – heavy metalsToxic exposures – heavy metals

Vasculitic neuropathies – especially if Vasculitic neuropathies – especially if multiorgan involvement, multiorgan involvement, multifocality, or severe painmultifocality, or severe pain

Acute motor weaknessAcute motor weakness

Disorders of neuromuscular Disorders of neuromuscular transmission and muscle should be transmission and muscle should be considered if rapidly progressing considered if rapidly progressing weakness without sensory findingsweakness without sensory findings

General principles of treatment of General principles of treatment of neuropathiesneuropathies

Patient education and counseling, genetic counselingPatient education and counseling, genetic counseling Withdrawal of medications suspected, or toxic exposureWithdrawal of medications suspected, or toxic exposure Correction of nutritional and vitamin deficienciesCorrection of nutritional and vitamin deficiencies Treatment of alcoholismTreatment of alcoholism Blood glucose control in diabeticsBlood glucose control in diabetics Specific drug therapies: chelating agents in lead Specific drug therapies: chelating agents in lead

neuropathy, prednisone in CIDP, plasmapheresis or IVIG for neuropathy, prednisone in CIDP, plasmapheresis or IVIG for GBSGBS

Pain control: gabapentin, carbamazepine, other Pain control: gabapentin, carbamazepine, other anticonvulsants, tricyclics, transcutaneous electrical nerve anticonvulsants, tricyclics, transcutaneous electrical nerve stimulationstimulation

Meticulous foot careMeticulous foot care Orthotic devices and splintsOrthotic devices and splints Surgical correction of entrapment neuropathiesSurgical correction of entrapment neuropathies Physical and occupational therapyPhysical and occupational therapy