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    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach to Amnesia
    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach to Amnesia
    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach to Amnesia
    Ebook322 pages5 hours

    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach to Amnesia

    By Nelson Butters and Laird S. Cermak

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    About this ebook

    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach To Amnesia presents an overview of one of the theories of amnesia, namely, the extent to which it represents an information-processing deficit. The book discusses the clinical symptoms, neuropathology, and etiology of the alcoholic Korsakoff's syndrome; the influence of the original memory model on the research in amnesia; and the functional differences among long-term memory, short-term memory, and sensory memory. The text also describes encoding deficits; the depth of encoding and visuoperceptive deficits; as well as alternative theories of amnesia. Sensory capacities and the memory and cognitive disorders of chronic alcoholics are also considered. The book further reviews the differences among various amnesic and dementing populations. Neurologist, neuropsychologists, and students taking related courses will find the book invaluable.
    LanguageEnglish
    PublisherAcademic Press
    Release dateJun 28, 2014
    ISBN9781483216867
    Alcoholic Korsakoff's Syndrome: An Information-Processing Approach to Amnesia

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      Alcoholic Korsakoff's Syndrome - Nelson Butters

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      1

      Clinical Symptoms, Neuropathology, and Etiology

      Publisher Summary

      This chapter discusses the clinical symptoms, neuropathology, and etiology of alcoholic Korsakoff’s syndrome. In 1881, Carl Wernicke described a neurological syndrome in three patients that included ataxia, optic abnormalities, and confusional state. Six years following the publication of Wernicke’s paper, S. S. Korsakoff published the first of a series of reports in which he detailed the amnesic and confabulatory symptoms that often accompanied disorders involving polyneuropathy. Although long-term alcoholism often preceded these mental changes, Korsakoff noted that the symptoms also followed a number of other conditions such as persistent vomiting, typhoid fever, and intestinal obstruction. On the basis of his observations, he concluded that the presence of a substance toxic to the peripheral and central nervous systems must have been the common denominator in his reported cases. Although neither Wernicke nor Korsakoff could be specific with regard to etiology and both seemed unaware that their two syndromes often occurred sequentially in the same patients, their clinical descriptions of the symptomatology were accurate and represented important initial steps in the identification and understanding of the Wernicke–Korsakoff syndrome. The major symptoms of the Wernicke stage include a global confusional state, opthalmoplegia, nystagmus, ataxia, and polyneuropathy of the legs and arms. The Korsakoff patients’ anterograde amnesia is the most striking feature of their disorder. They are unable to learn new verbal and nonverbal information from the time of the onset of their illness.

      In 1881, Carl Wernicke described a neurological syndrome in three patients (two male alcoholics, one woman with sulfuric acid poisoning) that included ataxia, optic abnormalities, and a confusional state. Postmortem examination of these three patients showed small punctate hemorrhages that were symmetrically located in the gray matter around the third and fourth ventricles of their brains. Wernicke characterized these findings, which now bears his name, as an acute inflammatory disease of the ocular–motor nuclei, and noted that the symptoms were progressive and led to death in approximately 2 weeks. Six years following the publication of Wernicke’s paper, S. S. Korsakoff published the first of a series of reports in which he detailed the amnesic and confabulatory symptoms that often accompanied disorders involving polyneuropathy. Although long-term alcoholism often preceded these mental changes, Korsakoff noted that the symptoms also followed a number of other conditions, such as persistent vomiting, typhoid fever, and intestinal obstruction. On the basis of his observations, he concluded that the presence of a substance toxic to the peripheral and central nervous systems must have been the common denominator in his reported cases. Although neither Wernicke nor Korsakoff could be specific with regard to etiology, and both seemed unaware that their two syndromes often occurred sequentially in the same patients, their clinical descriptions of the symptomatology were accurate and represented important initial steps in the identification and understanding of the Wernicke-Korsakoff syndrome.

      The major symptoms of the Wernicke stage include a global confusional state, opthalmoplegia, nystagmus, ataxia, and a polyneuropathy (e.g., pain, loss of sensation, weakness) of the legs and arms. Of these neurological symptoms, the global confusional state is perhaps most germane to our interests. The patient is disoriented regarding time and place, is unable to recognize familiar people, is apathetic, inattentive, and, most significantly, is unable to maintain a coherent conversation. It is important to note that this confusional state makes assessment of memory during the Wernicke phase of an illness both difficult and of questionable validity. Memory capacities can only be assessed if it is certain that the material to be learned is attended to and comprehended, and such certainties cannot be guaranteed during the Wernicke phase of an illness. Thus, all the neuropsychological assessments described in the following chapters were conducted when the patients had passed into the chronic Korsakoff stage of their illness.

      If patients with Wernicke encephalopathies are not treated with large doses of thiamine, they are in danger of having fatal midbrain hemorrhages. If, however, patients receive proper vitamin therapy, their neurological symptoms will evidence marked improvement. In most cases, the ocular problems will almost disappear, the ataxia and peripheral neuropathies will improve, and the confusional state will clear. That is, after 2 or 3 weeks of thiamine treatment, patients will realize that they are in a hospital, recognize their spouse and children, and be able to maintain an intelligible conversation with their physicians. At this point, the patients have passed the acute Wernicke phase and have entered the chronic Korsakoff stage. Very few patients in the Wernicke phase show a complete recovery to their premorbid intellectual state.

      The Korsakoff patients’ anterograde amnesia is the most striking feature of their disorder. They are unable to learn new verbal and nonverbal information from the time of the onset of their illness. Learning the name of their physician, nurses, the name of the hospital, and even the location of their bed, may require weeks or months of constant repetition and rehearsal. Events that occurred hours or even minutes before will be lost to the amnesic individual. Not only do they fail to learn the names of important people and places, but often they will not remember previous encounters with these individuals. If the patients spend 3 hours completing a number of psychometric tasks, they will fail to recall the entire test session 2 hours after it has ended. Three common words read to the patient cannot be recalled 10 sec later. As one of our patients described his existence, I always feel as though I am just waking up. I don’t remember what happened a minute ago. I don’t know the meaning of what’s going on. Experimentally, this severe anterograde problem is exemplified by the severe difficulty the Korsakoff patient has in learning even short lists of five or six paired-associates. When alcoholic Korsakoff patients are shown a list of word pairs (e.g., man-hammer) in which they must learn to associate the second word with the first, the acquisition of these associations may require 70 or 80 trials instead of the three or four presentations needed by intact

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