Cases reported "Vitamin B Deficiency"

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1/4. Acute axonal polyneuropathy in chronic alcoholism and malnutrition.

    In contrast to the classic, slowly progressive polyneuropathy in alcoholic patients, acute forms, clinically mimicking guillain-barre syndrome, are rare. We present a patient who developed motor weakness and sensory loss in all four limbs within four days. Laboratory data were consistent with long-term alcohol abuse and documented thiamine deficiency. Repeated cerebrospinal fluid examinations were normal. Electrophysiological studies showed an acute sensorimotor polyneuropathy with predominantly axonal involvement. We conclude that acute alcoholic neuropathy has to be distinguished from guillain-barre syndrome and other forms of acute polyneuropathy by using clinical, laboratory, and electrophysiological data. Both ethanol toxicity and vitamin deficiency could play a role in the pathogenesis.
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2/4. Vitamin deficiency in the elderly.

    The oral manifestations of vitamin deficiencies are often the first indications of malnutrition. This is especially true among the elderly, whose more frequent physical and/or psychological disorders may prevent them from eating a balanced diet. The following is a guide to the dentist, who is often the first health professional to recognize nutritional deficiencies in this age group.
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3/4. vitamin b deficiency neuropathy. case reports.

    Poor nutrition is common throughout the third world. The US also has examples among recent Asian and Latin American immigrants, alcoholics, the homeless, and former prisoners of war. All of these groups are susceptible to long-term pathologic damage, depending on the degree of malnutrition which they experience. The peripheral nervous system is quite vulnerable to impairment and damage from vitamin B loss.
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4/4. 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 Thevenard's syndrome.
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