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Numbness, Tingling, Pain and Weakness:
EVALUATING THE PATIENT WITH A PERIPHERAL NEUROPATHY
Peter D. Donofrio, M.D.Department of Neurology
Vanderbilt University School of Medicine
EVALUATING THE PATIENT WITH A PERIPHERAL NEUROPATHY
Introduction
• Focused General and Neurologic Examination• Edx Study as Extension of the Neurologic Examination• Sensory Nerve Conduction Studies• Motor Nerve Conduction Studies• Late Responses• Needle Electromyography (EMG)• Autonomic Nervous System Testing
Table 1Features of the Clinical Examination Important in the
Evaluation of Suspected Neuropathy
General InformationOnset and temporal profile of motor, sensory, and autonomic complaints.Type and distribution of paresthesia, hyperesthesia and hyperpathia.Distribution of weakness.Industrial and medical history for toxin or drug exposures.Family history, including bony deformities such as pes cavus or hammer toes.Social habits including recreational drug use.Antecedent illness or symptoms of underlying disease.
Table 1 (continued)Features of the Clinical Examination Important in the
Evaluation of Suspected Neuropathy
Clinical ExaminationGeneral
Findings most prominent in distal lower extremities.Relative symmetry.Associated findings such as ataxia, tremor, skin lesions, bonydeformities (pes cavus or hammer toes).Palpate peripheral nerves (tenderness, paresthesia, hypertrophy).
Motor (emphasis upon distal muscles)Intrinsic hand muscles, finger and wrists extensors.Toe extensors and foot dorsiflexors.
Table 1 (continued)Features of the Clinical Examination Important in the
Evaluation of Suspected Neuropathy
SensoryDemonstrate distal to proximal sensory loss gradient.Identify involved modalities.
Large fiber: vibration, light-touch, touch-pressure (common); joint position sensation (JPS) when severe.Small fiber: temperature, pin-pain, deep pain.
Discriminative sensations less helpful in peripheral disorders.Absence of sensory level on the trunk.Vibratory loss to iliac crest and JPS loss may suggest spinal cord lesion.
Table 1 (continued)Features of the Clinical Examination Important in the
Evaluation of Suspected Neuropathy
ReflexesAchilles reflexes usually absent.Diffusely hypoactive reflexes not necessarily abnormal.Absence of pathologic reflexes (e.g., Babinski response).
Autonomic Nervous SystemPostural hypotension.Sluggish pupillary reaction to light.Abnormality of sweating.Bowel, bladder, or sexual dysfunction.Vasomotor changes in the feet more than hands.
Table 2Expectations for the Edx Evaluation of Neuropathy
Document evidence of a peripheral abnormalityDetect presence.Document location (diffuse, focal, multifocal).
Identify peripheral modalities involvedSensory fibers.Motor fibers.Autonomic fibers.
Table 2 (continued)Expectations for the Edx Evaluation of Neuropathy
Identify the predominant pathophysiologyAxonal loss.Uniform demyelination.Multifocal demyelination with partial or complete conduction block.Conduction slowing suggestive of membranopathy.Combination of above.
Establish temporal profile when possible (acute, chronic, old, ongoing)Exclude accompanying or alternative disordersDetermine prognosis
Table 3Checklist: Evaluating the Edx Report
Clinical findings consistent with your evaluation?Limb temperatures monitored and recorded?Cool limbs warmed (31°C to 32°C minimum)?Measurement techniques described?Individual measures reported?
Sensory studies (amp, DL, CV).Motor studies (amp, DL, CV, F-wave latency).Needle examination (insertional activity, fibrillation potentials, MUAP recruitment, amp, and % poly).
Table 3 (continued)Checklist: Evaluating the Edx Report
Presence or absence of partial or complete conduction block described?Normal values provided?Sufficient evaluation to
Document the problem?Exclude alternative explanations (avoid errors of omission)?
Appropriate negative findings described?Interpretation consistent with clinical findings?
Figure 1
Figure 2
Figure 3
Clinical Examinations in Neurology, 1976
Needle Examination
Table 4Proposed Edx Studies in Evaluating Neuropathy
Strategy differs depending upon severityTest most involved site if mild or moderate.Test least involved site if severe.
Peroneal motor. If no response:Tibial motor.
If no peroneal or tibial responses, study:Peroneal motor, recording anterior tibialis.Ulnar motor.Median motor.
Table 4 (continued)Proposed Edx Studies in Evaluating Neuropathy
Sural sensoryMedian sensoryTest Additional nerves if finding equivocalDefinite abnormalities should result in test of:
Opposite extremity.Evaluation of suspected abnormality.
Table 5Motor or Motor > Sensory, Axonal Loss
Polyneuropathy
Charcot-Marie-Tooth Disease (Hereditary Motor Sensory Neuropathy Type II)
DapsoneDisulfiramAcute motor axonal neuropathy (AMAN)Acute motor sensory axonal neuropathy (AMSAN)HyperinsulinismNitrofurantoinOrganophosphate PoisoningPorphyriaParaneoplastic motor neuropathy (lymphoma or carcinoma)Vincristine Toxicity
Charcot-Marie-Tooth Disease
Table 6Motor > Sensory, Uniform Conduction Slowing
Polyneuropathy
AmiodaroneCharcot-Marie-Tooth Disease Type I (Hereditary Motor Sensory
Neuropathy Type I)Cytosine arabinoside (ara-C)Dejerine-Sottas disease (Hereditary Motor Sensory Neuropathy Type III)DoxorubicinHexacarbon ToxicityPerhexiline maleateSodium channel blockers
Table 7Motor > Sensory, Multifocal Conduction Slowing
Polyneuropathy
Arsenic (acute intoxication)Acute Inflammatory Demyelinating Polyneuropathy (AIDP)Subacute Inflammatory Demyelinating Polyneuropathy (SIDP)Chronic inflammatory demyelinating polyneuropathy (CIDP)Chronic dysimmune polyneuropathy
Monoclonal gammopathy of undetermined significance (MGUS)Osteosclerotic myelomaMultiple myeloma (substantial proportions are axonal)
Table 7 (continued)Motor > Sensory, Multifocal Conduction Slowing
Polyneuropathy
Systemic lupus erythematousWaldenstrom’s macroglobulinemiaGamma heavy chain diseaseCryoglobulinemiaCastleman’s diseaseLymphomaCarcinomaHIV
Multifocal motor neuropathy (MMN) with conduction block
Figure 4
Table 8Sensory, Axonal Loss
Polyneuropathy
CisplatinCongenitalMetronidazoleParaneoplastic
PyridoxineSjögren’s syndromeStyreneThalidomide
Table 9Sensory > Motor, Axonal Loss
Polyneuropathy
AcromegalyAmyloidosisCritical illness neuropathyConnective tissue diseases
Rheumatoid arthritisPeriarteritis nodosaChurg-Strauss vasculitis
Degenerative disordersFriedreich’s ataxiaOlivopontocerebellar
PharmaceuticalsAmitriptylineColchicineEthambutolIsonicotine hydrazine (INH)MetronidazoleNitrous oxidePhenytoinThalliumVincristine
Table 9 (continued)Sensory > Motor, Axonal Loss
Polyneuropathy
GoutHypothyroidismMetals
Arsenic (chronic)GoldLithiumMercury
NutritionalB12 deficiencyFolate deficiencyPost-gastrectomyThiamine deficiency
Polycythemia veraSarcoidosisToxic
AcrylamideCarbon disulfideEthyl alcoholHexacarbons (glue sniffing)Organophosphorous esters
Multiple myelomaMyotonic dystrophy
Rheumatoid ArthritisVasculitic Neuropathy
Table 10Sensory and Motor, Conduction Slowing
and Axon-Loss Polyneuropathy
Diabetes mellitusEnd-stage renal disease
Interpretation of NCS ResultsHelpful Tips
Absent responses unhelpful => axon loss vs. demyelination.SNAPs normal in lesions proximal to DRG.SNAPs abnormal in lesions distal to DRG.Weak + atrophy + low CMAPs => LMN process.Low CMAPs => any LMN process including myopathy.
Electrodiagnostic ConsultantImportant Role
Exclude disorders that mimic or complicate neuropathyPolyradiculopathyAnterior horn cell disorderMononeuritis multiplexDistal myopathiesNeuromuscular junction disordersMyelopathies
EVALUATING THE PATIENT WITH A PERIPHERAL NEUROPATHY
Summary
• Confirm or Refute Presence of Neuropathy• Identify Fibers Affected• Identify Predominant Pathophysiology• Suggest Temporal Profile (Acute, Subacute, Chronic,
Ongoing)• Document Location (Diffuse, Focal, Multifocal)• Parallel Clinical Exam• Create Focused List of Differential Diagnosis
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