Send to

Choose Destination
J Neurol. 1981;225(2):95-108.

Vitamin B 1, B 2 and B 6 deficiency in neurological disorders.


The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system. The incidence of thiamine deficiency was 31%, of riboflavin deficiency 22% and of pyridoxine deficiency 6%. Alcoholics in particular suffered from deficiencies of vitamin B 1, and B 2. There was a correlation of vitamin B 1 and B 2 deficiency and signs of a cerebellar and/or brainstem lesion. The most frequent symptoms in this connection were gait disturbances and oculomotor signs like spontaneous and gaze nystagmus, disturbed eye tracking, diminished optokinetic nystagmus, decreased ability to suppress vestibular nystagmus by fixation. These signs hardly ever occurred in alcoholic patients who showed no deficiency of vitamin B 1, B 2 or B 6. Whenever they do appear, a vitamin B supplementation has to be performed in order to prevent the manifestation of Wernicke's encephalopathy, cerebral or cerebellar atrophy. Alcoholics showed the same incidence of polyneuropathy, whether they suffered from a deficiency of B vitamins or not. Deficiencies of vitamin B 1, B 2 or B 6 were also found in patients with intestinal malabsorption and polyneuropathy, diabetic polyneuropathy, optic atrophy, myelopathy and cerebellar ataxia of unknown etiology, neurological manifestations of neoplasms arising outside the nervous system, B 12 myeloencephalopathy and Thévenard's syndrome.

[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center