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berculosis Symptoms of neuropathy appeared between 3 and 35 weeks after treatment was begun and affected about 10 percent of patients receiving therapeutic doses in the upper range (10 mg/kg daily) The initial symptoms are symmetrical numbness and tingling of the toes and feet, spreading, if the drug is continued, to the knees and occasionally to the hands Aching and burning pain in these parts then becomes prominent In addition to sensory loss, examination usually discloses a loss of tendon re exes and weakness in the distal muscles of the legs Severe degrees of weakness and loss of deep sensation are observed only rarely Isoniazid produces its effects on the peripheral nerves by interfering with pyridoxine metabolism, perhaps by inhibiting the phosphorylation of pyridoxine (the collective name for the B6 group of vitamins) and decreasing the tissue levels of its active form, pyridoxal phosphate The administration of 150 to 450 mg of pyridoxine daily, in conjunction with the isoniazid, completely prevents the neuropathy The same mechanism is probably operative in the neuropathies that occasionally complicate the administration of the isoniazid-related substances such as ethionamide, used sometimes in the treatment of tuberculosis, and the now littleused antihypertensive agent hydralazine Paradoxically, the taking of extremely high doses of pyridoxine over a prolonged period may, as alluded to earlier, actually cause a disabling, predominantly sensory ganglionopathy (Schaumburg et al) A relatively mild sensory neuropathy (acral paresthesia) associated with optic neuropathy occasionally complicates chloramphenicol therapy The chronic administration of metronidazole (used in the treatment of Crohn disease and anaerobic infections) may have the same effect A predominantly motor neuropathy has been reported with the chronic administration of dapsone, a sulfone used to treat leprosy and certain dermatologic conditions Stilbamidine, used in the treatment of kala azar, may also induce a purely sensory neuropathy with a propensity to affect the trigeminal nerves The introduction in 1952 of nitrofurantoin for the treatment of bladder infections was soon followed by reports of neurotoxicity attributable to the drug The earliest symptoms are pain and tingling paresthesias of the toes and feet, followed shortly by similar sensations in the ngers If the drug is not discontinued, the disorder progresses to a severe, symmetrical sensorimotor polyneuropathy Patients with chronic renal failure and azotemia are particularly prone to neurotoxicity from nitrofurantoin because of diminished drug excretion resulting in high tissue levels To make matters more complex, the uremic state itself may be responsible for a similar polyneuropathy, so that the distinction between uremic and nitrofurantoin neuropathy in the presence of chronic renal failure may be impossible The neuropathologic studies of Lhermitte and colleagues disclosed an axonal degeneration in peripheral nerves and sensory roots Cardiac Drugs Amiodarone, a drug that is commonly used for treating recalcitrant ventricular tachyarrhythmias, induces a motorsensory neuropathy in about 5 percent of patients after several months of treatment Perhexiline maleate, another drug for the treatment of angina pectoris, may also cause a generalized, predominantly sensory polyneuropathy in a small proportion of patients Affected persons show a striking neuronal lipidosis Patients taking niacin to lower blood cholesterol levels may experience intense distal and truncal paresthesias, but no neuropathy has been identi ed Disul ram (Antabuse) The development of a sensorimotor neuropathy similar to that produced by INH is sometimes associated.

In broad terms, all motor disorders may be considered to consist of certain functional de cits (or negative symptoms) and, the opposite, excessive motor activity (positive symptoms), the latter being ascribed to the release or disinhibition of the activity of undamaged parts of the motor nervous system When diseases of the basal ganglia are analyzed along these classic lines, bradykinesia, hypokinesia, and loss of normal postural re exes stand out as the primary negative symptoms, and tremor, rigidity, and involuntary movements that constitute a category of dyskinesias that include chorea, athetosis, ballismus, and dystonia as the positive ones Disorders of phonation, articulation, and locomotion are more dif cult to classify In some instances they are clearly a consequence of rigidity and postural disorders, while in others, where rigidity is slight or negligible, they seem to represent primary de ciencies Stress and nervous tension characteristically worsen both the motor de ciency and the abnormal movements in all extrapyramidal syndromes, just as relaxation improves them The speci c symptoms of basal ganglia disease are elaborated below