1c:I[419806,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/30036bedc5269936.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/cd5e572bc3e4eb92.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/d4ac9dcf27f6ff52.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 1d:T453,Introduction Clinical Observations The Natural History of the Disease Clinical and Pathological Case Reports A Quantitative Estimation of the Changes in the Cerebellar Cortex Comment A. Clinical Features B. Nature and Significance of the Pathological Findings C. Clinical and Pathological Correlation D. Etiological Considerations E. Review of the Medical Literature F. Spontaneously Occurring Cortical Cerebellar Degenerations in Animals G. Restricted Cortical Cerebellar Degeneration in the Alcoholic Patient—a Clinical-Pathological Entity Summary and Conclusions

Introduction

The relationship of cerebellar cortical degeneration to chronic alcoholism has been a controversial matter for many years. There are now several published accounts of a cerebellar syndrome in alcoholic patients, but these are purely clinical, and one has no way of ascertaining the nature of the pathological changes and of deciding whether they differed in any way from the other known types of cerebellar atrophy. Isolated, pathologically verified instances of primary cerebellar degeneration have been described in1e:T459,Anemias associated with frank megaloblastic changes in the bone marrow are usually caused by a deficiency of either cyanocobalamin (vitamin B₁₂) or folic acid. The clinical differentiation of these deficiencies is almost entirely circumstantial and often difficult. The presence of cyanocobalamin deficiency is almost certain when a megaloblastic anemia is associated with combined system disease of the spinal cord and is probable when the secretion of gastric intrinsic factor is defective. The latter association may be suspected or established, in order of increasing certainty, by the demonstration of (1) gastric achlorhydria, (2) gastric achylia, (3) failure to absorb oral radioactive cyanocobalamin unless this is accompanied by an intrinsic factor preparation.¹Occasionally the diagnosis of vitamin B₁₂deficiency is facilitated by obtaining a history of total gastrectomy or, more rarely, of long-standing vegetarianism.²Circumstantial clinical evidence of folic-acid deficiency is less specific than that of cyanocobalamin deficiency and diagnosis is usually

	Year	Citations

References