Nutritional Disorders of the Nervous System
The central and/or peripheral nervous system may suffer from deprivation of several nutrients. Important among them are the deficiencies of thiamine (Vitamin B1), pyridoxine (Vitamin B6), cyanocobalamine (Vitamin B12), nicotinic acid (Vitamin B3) and pantothenic acid.
Nutritional Polyneuropathy: This may result from the deficiencies of thiamine, pyridoxine, cyanocobalamine, niacin and pantothenic acid, singly or in combination.
Thiamine deficiency: This leads to Cardiac or neurological ill-effects, the latter is known as dry beriberi. Though originally described among persons subsisting on polished rice as the main energy intake, at present beriberi is seen more among alcoholics. The neurological lesion takes the form of symmetrical sensorimotor polyneuropathy, clinically characterized by tingling, numbness and hyperalgesia of the distal parts of the extremities. The motor phenomena are bilateral lower motor neuron lesions characterized by loss of ankle jerk, foot drop and wrist drop. There is deep hyperaesthesia, giving rise to calf-tenderness. Some cases may develop Wernicke’s encephalopathy as well.
Neuropathy resulting from deficiency of Vitamin B12 may coexist with myelopathy in many cases. Neuropathy may be demonstrable in 50-60% of subjects suffering from pellagra and subclinical form of niacin deficiency. Vitamin B6 deficiency produces polyneuropathy. It is more floridly seen as a complication of therapy with isonicotinic acid hydrazide (INH). Administration of 6mg of vitamin B6 prevents the development of this type of neuropathy.
Burning feet syndrome (also known as Gopalan’s condition in which the subject experiences burning pain in the feet, especially severe during night, so as to interrupt sleep. Examination may reveal pallor, cyanosis, excessive sweating and areas of capillary dilatation over both feet. A third of these patients may show loss of sensation. More often, hyperalgesia may be present. Many patients respond dramatically to injections of pantothenic acid suggesting that deficiency of this vitamin may play a major role in the pathogenesis of this syndrome.