Chronic peripheral neuritis

Thiamin deficiency can result in three distinct syndromes a chronic peripheral neuritis, beriberi, which may or may not be associated with heart ilure and edema acute pernicious (fulminating) beriberi (shoshin beriberi), in which heart failure and metabolic abnormalities predominate, without peripheral neuritis and Wernicke s encephalopathy with KorsakofPs psychosis, which is associated especially with alcohol and dmg abuse. The central role of thiamin diphosphate in... 

A. Ethambutol is associated with retrobulbar neuritis, resulting in loss of central vision and impaired red-green discrimination. Ethionamide (B) is an analogue of isonicotinic acid and is associated with GI intolerance and peripheral neuropathy, but not the optic neuritis or color vision discrimination problems. Aminosalicylic acid (C) can cause GI irritation and bleeding problems, so caution is required in peptic ulcer patients. It has no neurological side effects. Rifampin (D) is associated with red-orange discoloration of saliva, tears, and urine but not the color vision problems. Isoniazid (E) is associated with peripheral neuritis in chronic alcoholics and malnourished individuals and requires pyridoxine supplements. It is not associated with optic neuritis. 

It is used exclusively for urinary tract infections. The side effects include nausea, vomiting, diarrhoea, anorexia, leukopenia, haemolytic anaemia, jaundice, dizziness and headache. On chronic use can lead to peripheral neuritis and interstitial pulmonary fibrosis. 

Chronic deficiency of thiamin, especially associated with a high carbohydrate diet, results in beriberi, which is a symmetrical ascending peripheral neuritis. Initially the patient complains of weakness, stiffness, and cramps in the legs, and is unable to walk for more than a short distance. There may be numbness of the dorsum of the feet and ankles, and vibration sense may be diminished. 

The signs of chronic heart failure may be seen without peripheral neuritis. The arteriolar dilatation, and possibly also the edema, probably results from high circulating concentrations of lactate and pyruvate, a result of impaired activity of pyruvate dehydrogenase. 

Hydralazine (Apresoline) Directly relaxes arterioles (not veins) independent of sympathetic interactions. Causes decrease in blood pressure leading to reflex tachycardia and increased cardiac output. Directly increases renal blood flow. Moderate hypertension. May be used in pregnant women who are hypertensive. Reflex tachycardia, palpitations, fluid retention, systemic lupus erythematosis-liKe syndrome. Chronic therapy may lead to peripheral neuritis (due to interference with vitamin B6 metabolism in neural tissue). 

B. Chronic toxicity. Peripheral neuritis with chronic use is thought to be related to competition with pyridoxine. The mechanism of chronic hepatic injury and INH-induced systemic lupus erythematosus (SLE) is not discussed here. 

B. Chronic therapeutic INH use may cause peripheral neuritis, hepatitis, hypersensitivity reactions inciuding drug-induced lupus erythematosus, and pyri-doxine deficiency. 

The heart may also be affected in beriberi, with dilatation of arterioles, rapid blood flow, increased pulse rate and pressure and increased jugular venous pressure leading to right-sided heart failure and oedema - so-called wet beriberi. The signs of chronic heart failure may be seen without peripheral neuritis. The arteriolar dilatation, and possibly also the oedema, probably result from high circulating concentrations of lactate and pyruvate as a result of impaired activity of pyruvate dehydrogenase. 

In its more severe forms thiamine deficiency can present as (1) wet beri-beri with generalized oedema 2md tendency to heart failure, (2) dry beri-beri, a chronic polyneuropathy with degenerative changes in the peripheral nerves, (3) infantile beri-beri, a chronic marasmic state also frequently associated with sudden heart failure, and (4) Wernicke s encephalopathy, which may be seen in chronic alcoholics and may be regarded as a cerebral beri-beri . Less severe states of thiamine deficiency usually manifest themselves as a chronic polyneuropathy. Problems of differential diagnosis from other forms of peripheral neuritis therefore arise, and it is in this connection that studies of pyruvate metabolism may be of help. 

After initial contradictory reports it is now established that arsenic can cross the blood-brain barrier and produces alternations in whole rat brain biogenic amines levels in animals chronically exposed to arsenite (Tripathi et al, 1997). The neurological effects are many and varied. Usually, peripheral neuropathy, sensory neuropathy (Hafeman et al, 2005), and encephalopathy are the initial complaints associated with acute arsenic poisoning. Acute exposure to arsenic in humans has been shown to result in problems of memory, difficulties in concentration, mental confusion, and anxiety (Hall, 2002 Rodriguez et al, 2003). Other neurological symptoms arising due to arsenic are primarily those of a peripheral sensory neuritis, predominantly numbness, severe paresthesia of the distal portion of the extremities, diminished sense of touch, pain, heat and cold, and symmetrically reduced muscle power (Menkes, 1997). 

Prolonged TCE exposure has been associated with impairment of peripheral nervous system function, persistent neuritis and temporary loss of tactile sense and paralysis of the fingers after direct solvent contact. Chromosomal effects have been reported in those involved in the use of TCE for degreasing and symptoms of systemic lupus erythematosis have been reported after chronic TCE exposure. In addition, organic dementia has been noted after occupational exposure to TCE and there have been some reports of an association between exposure and scleroderma, an autoimmune disease. 

C. Chronic lower-level exposure can cause parkinsonism and other poorly reversible CNS impairments, optic neuritis, peripheral neuropathy, and atherosclerosis. Based on animal data, carbon disulfide exposure is likely to be associated with adverse reproductive outcomes. 

Australian children exposed to chalking Pb paint Acute and chronic encephalopathy, peripheral motor and sensory neuropathy, ocular neuritis First modem documentation of young children as at high risk for Pb paint poisoning Gibson et al. (1892), Gibson (1904)... 

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