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Key Features

  • Can be categorized on the basis of the structure primarily affected

  • Predominant pathologic feature may be axonal degeneration (axonal or neuronal neuropathies) or paranodal or segmental demyelination

  • Distinction may be possible on the basis of neurophysiologic findings

Clinical Findings

  • Common mononeuropathies

    • Lead to a sensory, motor, or mixed deficit that is restricted to the territory of the affected nerve

    • A similar clinical disturbance is produced by peripheral nerve tumors, but these are rare except in patients with neurofibromatosis type 1

    • Multiple mononeuropathies suggest a patchy multifocal disease process such as

      • Vasculopathy (eg, diabetes, arteritis)

      • Infiltrative process (eg, leprosy, sarcoidosis)

      • Radiation damage

      • Immunologic disorder (eg, brachial plexopathy)

  • Diffuse polyneuropathies

    • Lead to a symmetric sensory, motor, or mixed deficits, often most marked distally

    • Examples include

      • Hereditary, metabolic (eg, diabetic, hyperthyroidism and hypothyroidism, amyloidosis), infectious (eg, syphilis), and toxic (eg, alcohol, lead) disorders

      • Idiopathic inflammatory polyneuropathy (Guillain-Barré syndrome)

      • Nonmetastatic complication of malignant disease (paraneoplastic antineuronal antibodies)

    • Tendon reflexes are depressed or absent

    • Paresthesias, pain (dysesthesia, neuralgia), and muscle tenderness may also occur

Diagnosis

  • Blood glucose, serum gamma glutamyl transferase (GGT), thyroid stimulating hormone (TSH), serologic test for syphilis, heavy metals screen, antibodies associated with neoplasia (eg, anti-Hu antibodies, also known as anti-neuronal nuclear antibody type 1 [ANNA-1])

  • Nerve conduction velocity and electromyography

    • Motor and sensory conduction velocity are measured in accessible segments of peripheral nerves

    • In axonal neuropathies

      • Nerve conduction velocity is normal or only mildly reduced

      • Needle electromyography provides evidence of denervation in affected muscles

    • In demyelinating neuropathies

      • Nerve conduction velocity may be slowed considerably in affected fibers

      • In more severe cases, conduction is blocked completely, without accompanying electromyographic signs of denervation

  • Sural nerve biopsy may be required to establish a pathologic diagnosis in some conditions (eg, amyloidosis, hereditary neuropathies)

Treatment

  • Treatment is directed at underlying disease process (eg, control of blood glucose in diabetes; surgery, chemotherapy and/or radiation for malignancy)

Medications

  • Agents useful in control of dysesthesia and neuralgia include

    • Gabapentin, 300–3600 mg orally daily in divided doses

    • Tricyclic antidepressants (eg, desipramine, 25–50 mg orally nightly)

    • Pregabalin, 50–100 mg orally three times daily

    • Duloxetine, 60–120 mg orally daily

    • Opioid agent (submaximal dose particularly in combination with submaximal dose of gabapentin)

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