Which physical findings are characteristic of toxic neuropathy?

Updated: Dec 06, 2017
  • Author: Jonathan S Rutchik, MD, MPH, FACOEM; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
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Answer

Kimura, in Electrodiagnosis in Diseases of Nerve and Muscle, notes that polyneuropathy presents clinically as a "triad of sensory changes in a glove and stocking distribution, distal weakness, and hyporeflexia." The sensory changes include sensory loss in a stocking-glove distribution. Often, progression is distal to proximal. This is consistent with the commencement of axonal degeneration. Early loss of symmetrical ankle jerk is noted. In severe cases, motor dysfunction such as abnormal gait and foot drop also may occur. In some patients with exclusively small fiber neuropathy, the motor and reflexes examination may be normal.

Spencer and Schaumberg emphasized a gradual insidious onset, as well as slow recovery. Recovery proceeds at a rate of 2 mm/day and may take months or several years, or may never be complete. Function is restored in reverse order to the sequence of loss. Coasting may be noted, that is, intensification may occur for weeks before improvement. This often reflects continued axonal degeneration and reconstitution.

Signs of CNS disease also may be present at examination. This occurs in some patients recovering from certain toxic neuropathies. Dorsal column or corticospinal tract degeneration may be present. These clinical signs of degeneration are not prominent early in the illness; however, the patient may manifest hyperreflexia, Babinski responses, and stiff-leg ataxic gait with corticospinal tract disease or diffusely decreased proprioceptive and vibratory sensations and gait ataxia with dorsal column degeneration.

Involvement of the autonomic nerves may lead to a different clinical presentation–miosis, anhydrosis, orthostatic hypotension, sphincter symptoms, impotence, and vasomotor abnormalities. These may occur with or without evidence of a peripheral neuropathy. Tachycardia, rapid alterations in blood pressure, flushing and sweating, and abnormalities in gastrointestinal motility may be present.

Spencer and Schaumberg reported the association of sensory ganglion cell loss in pyridoxine-associated sensory neuropathy with 9 clinical features; they are as follows:

  • Rapid or subacute onset may occur following massive intravenous administration.

  • Initial sensory loss may occur anywhere; the gasserian ganglion often is affected simultaneously with the dorsal root ganglion, and thus facial numbness may be noted.

  • Diffuse sensory loss with ataxia and preservation of motor power may be present. Proprioceptive deficit is noted to be greater than the loss of pain or temperature sensation.

  • Tendon reflexes may be absent.

  • NCV results usually are normal; sensory nerve potentials may be abnormal or absent. Recovery is variable, reflecting the death of nerve cell bodies and consequent permanent loss of axons. Collateral sprouting from surviving axons may account for the extent of recovery in these conditions.

  • No signs of CNS disease are present.

  • Cholinergic symptoms follow (see Organophosphates and disorders of neuromuscular transmission).


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