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blockers, and both older and newer anticonvulsant drugs such as gabapentin, which may reduce the requirement for sedative drugs There is little to choose among the primary drugs in respect to their therapeutic ef cacy More importantly, there are few data to indicate that any one of them can prevent hallucinosis or delirium tremens or shorten the duration or alter the mortality rate of the latter disorder (Kaim et al) In general, phenothiazine drugs should be avoided because they reduce the threshold to seizures Probably, the use of any of the diazepine medications is as effective as a single dose of lorazepam in prophylactically suppressing seizures (see earlier discussion) If parenteral medication is necessary, we prefer 10 mg of diazepam or chlordiazepoxide given intravenously and repeated once or twice at 20- to 30-min intervals until the patient is calm but awake; we have also favored midazolam in closely controlled circumstances Beta-blocking agents, such as propranolol and atenolol, are helpful in reducing heart rate, blood pressure, and the tremor to some extent Lofexidine, an alpha2 agonist that blocks autonomic out ow centrally, and clonidine are similarly effective in reducing the severity of most of the withdrawal symptoms, but they are not recommended as the sole treatments Corticosteroids have no place in the treatment of the withdrawal syndrome
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Nutritional Diseases of the Nervous System (See Chap 41)
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Alcoholism provides the ideal setting for the development of nutritional diseases of the nervous system Although only a small proportion of alcoholics develop nutritional diseases, the overall number of these diseases is substantial because of the frequency of alcoholism The importance of the alcohol-induced de ciency diseases relates to the fact that they are preventable and, if neglected, may lead to permanent disability These illnesses are discussed fully in the preceding chapter, Diseases of the Nervous System Due to Nutritional De ciency
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Disorders of Uncertain Pathogenesis Associated with Alcoholism
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Also discussed in Chap 41 are so-called alcoholic cerebellar degeneration and Marchiafava-Bignami disease The former is almost certainly of nutritional origin; in the latter a nutritionalmetabolic etiology seems likely but has not been established Central pontine myelinolysis, though frequently observed in alcoholics, is more appropriately considered with the acquired metabolic disorders (Chap 40) Certain disorders of skeletal and cardiac muscle associated with alcoholism (acute alcoholic myopathy and cardiomyopathy) are described in Chap 51, with the myopathies due to drugs and toxins There remain to be discussed several diverse disorders that have been attributed to alcoholism but whose causal relationship to alcohol abuse, nutritional de ciency, or some other factor is not clear Alcoholic Dementia and Cerebral Atrophy The term alcoholic dementia is used widely and often indiscriminately to designate a presumably distinctive form of dementia that is attributable to the chronic, direct effects of alcohol on the brain Unfortunately, a syndrome subsumed under the title of alcoholic dementia and its many synonyms that appear in the older literature (alcoholic deteriorated state, chronic alcoholic psychosis, chronic or organic brain syndrome due to alcohol) has never been delineated satisfac-
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torily, either clinically or pathologically In the Comprehensive Textbook of Psychiatry, it has been de ned as a gradual disintegration of personality structure, with emotional lability, loss of control, and dementia (Sadock and Sadock) Purported examples of this state show a remarkably diverse group of symptoms, including jealousy and suspiciousness; coarsening of moral ber and other personality and behavioral disorders; deterioration of work performance, personal care, and living habits; and disorientation, impaired judgment, and defects of intellectual function, particularly of memory In recent years, there have been attempts to rede ne alcoholic dementia Cutting and also Lishman have expressed the view that the term Korsakoff psychosis should be limited to patients with a fairly pure disorder of memory of acute onset and that patients with more global symptoms of intellectual deterioration, of gradual evolution, be considered to have alcoholic dementia These are rather weak diagnostic criteria As pointed out in Chap 41, Korsakoff psychosis may have an insidious onset and gradual progression, and patients with this disorder, in addition to an amnesic defect, characteristically show disturbances of cognitive functions that depend little or not at all on memory More importantly, in none of the patients designated by these authors as having alcoholic dementia was there a neuropathologic examination, without which the clinical assessment must remain arbitrary and imprecise The pathologic changes that purportedly underlie primary alcoholic dementia are even less precisely de ned than the clinical syndrome Courville, whose writings have been quoted most frequently in this respect, described a series of cerebral cortical changes that he attributed to the toxic effects of alcohol Some of them turn out on close inspection to be quite nonspeci c, re ecting nothing more than the effects of aging or the insigni cant artifacts of tissue xation and staining More recently, Harper and colleagues have reported that the mean brain weight is decreased in alcoholics and the pericerebral space is increased in volume ndings that do no more than con rm the brain shrinkage that is demonstrable by CT scans in many alcoholics and is to some extent reversible with sustained abstinence (see later) Also, using an automated cell-counting method, these authors reported a reduction in the number of neurons in the superior frontal cortex Other investigators, using more accurate (stereologic) counting methods, have not duplicated these ndings (Hansen et al; Jensen and Pakkenberg), nor have experimental studies in animals settled the problem In our experience, the majority of cases that come to autopsy with the label of alcoholic dementia prove simply to have the lesions of the Wernicke-Korsakoff syndrome Traumatic lesions of varying degrees of severity are commonly added Other cases show the lesions of Marchiafava-Bignami disease, hepatic encephalopathy, or an unrelated communicating hydrocephalus, Alzheimer disease, ischemic necrosis, or some other disease quite unrelated to alcoholism Practically always in our material, the clinical state can be accounted for by one or a combination of these disease processes, and there has been no need to invoke a hypothetical toxic effect of alcohol on the brain This has also been the experience of Torvik and associates; with a few exceptions, such as coincidental Alzheimer disease, all their cases that had been diagnosed as having alcoholic dementia turned out, on neuropathologic examination, to have the chronic lesions of Wernicke-Korsakoff disease In brief, the most serious aw in the concept of a primary alcoholic dementia is that it lacks a distinctive, well-de ned pathology Until such time as the morphologic basis is established,
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