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:T435,

Introduction

"Wernicke's encephalopathy" is the term applied to a disease process characterized pathologically by symmetrical lesions in the mammillary bodies, the walls of the third ventricle, the periaqueductal areas, and the floor of the fourth ventricle. Clinically, the disease is said to be characterized by disturbances of consciousness, paralysis of the external ocular muscles, ataxia, and sometimes polyneuritis.^1,2The disease results from a thiamine deficiency due to inadequate intake, faulty absorption due to gas trointestinal disturbances, or to unusually increased requirements such as in fever.^3-8Lesions resembling Wernicke's encephalopathy have been observed as a familial disease in infants in the absence of the above-mentioned circumstances, probably because of a defect in the metabolic pathways in which thiamine is usually involved.⁹ Due to the modern diet, often supplemented with vitamins, the avitaminoses have become relatively rare. Individuals addicted to alcohol, however, form a group in which the lack1f:T7ec,

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References