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Depressed or absent tendon reflexes May be family history of neuropathy May be history of systemic illness or toxic exposure The cause of polyneuropathy or mononeuritis multiplex is suggested by the history, mode of onset, and predominant clinical manifestations Laboratory workup includes a complete blood count and sedimentation rate, serum protein electrophoresis, and immunophoresis, determination of plasma urea and electrolytes, liver and thyroid function tests, tests for rheumatoid factor and antinuclear antibody, HBsAg determination, a serologic test for syphilis, fasting blood glucose level, urinary heavy metal levels, cerebrospinal fluid examination, and chest radiography These tests should be ordered selectively, as guided by symptoms and signs Measurement of nerve conduction velocity is important in confirming the peripheral nerve origin of symptoms and providing a means of following clinical changes, as well as indicating the likely disease process (ie, axonal or demyelinating neuropathy) Cutaneous nerve biopsy may help establish a precise diagnosis (eg, polyarteritis, amyloidosis) In about half of cases, no specific cause can be established; of these, slightly less than half are subsequently found to be heredofamilial Treatment is of the underlying cause, when feasible, and is discussed below under the individual disorders Physical therapy helps prevent contractures, and splints can maintain a weak extremity in a position of useful function Anesthetic extremities must be protected from injury To guard against burns, patients should check the temperature of water and hot surfaces with a portion of skin having normal sensation, measure water temperature with a thermometer, and use cold water for washing or lower the temperature setting of their hot-water heaters Shoes should be examined frequently during the day for grit or foreign objects in order to prevent pressure lesions Patients with polyneuropathies or mononeuritis multiplex are subject to additional nerve injury at pressure points and should therefore avoid such behavior as leaning on elbows or sitting with crossed legs for lengthy periods Neuropathic pain is sometimes troublesome and may respond to simple analgesics, such as aspirin or nonsteroidal anti-inflammatory agents, and to gabapentin Opioids may be necessary for severe hyperpathia or pain induced by minimal stimuli, but their use should be avoided as much as possible The use of a frame or cradle to reduce contact with bedclothes may be helpful Many patients experience episodic stabbing pains, which may respond to gabapentin, pregabalin, phenytoin, carbamazepine, or tricyclic antidepressants Symptoms of autonomic dysfunction are occasionally troublesome Postural hypotension is often helped by wearing waist-high elastic stockings and sleeping in a semierect position at night Fludrocortisone reduces postural hypotension, but doses as high as 1 mg/d are sometimes necessary in diabetics and may lead to recumbent hypertension Midodrine, an -agonist, is sometimes helpful in a dose of 25 10 mg three times daily Impotence and diarrhea are difficult to treat; a flaccid neuropathic bladder may respond to parasympathomimetic drugs such as bethanechol chloride, 10 50 mg three or four times daily.

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A Charcot-Marie-Tooth Disease (HMSN Type I, II)

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Several distinct varieties of Charcot-Marie-Tooth disease can be recognized There is usually an autosomal dominant mode of inheritance, but occasional cases occur on a sporadic, recessive, or X-linked basis The responsible gene is commonly located on the short arm of chromosome 17 and less often shows linkage to chromosome 1 or the X chromosome It has also been linked to several other chromosomes, emphasizing the genetic heterogeneity of the disorder Clinical presentation may be with foot deformities or gait disturbances in childhood or early adult life Slow progression leads to the typical features of polyneuropathy, with distal weakness and wasting that begin in the legs, a variable amount of distal sensory loss, and depressed or absent tendon reflexes Tremor is a conspicuous feature in some instances Electrodiagnostic studies show a marked reduction in motor and sensory conduction velocity (hereditary motor and sensory neuropathy [HMSN] type I) In other instances (HMSN type II), motor conduction velocity is normal or only slightly reduced, sensory nerve action potentials may be absent, and signs of chronic partial denervation are found in affected muscles electromyographically The predominant pathologic change is axonal loss rather than segmental demyelination A similar disorder may occur in patients with progressive distal spinal muscular atrophy, but there is no sensory loss; electrophysiologic investigation reveals that motor conduction velocity is normal or only slightly reduced, and nerve action potentials are normal

B Dejerine-Sottas Disease (HMSN Type III)

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