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Generate QR Code JIS X 0510 in Microsoft Office DEMENTIA AND THE AMNESIC (KORSAKOFF) SYNDROME

DEMENTIA AND THE AMNESIC (KORSAKOFF) SYNDROME
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Table 21-5 Classi cation of the amnesic states I Amnesic syndrome of sudden onset usually with gradual but incomplete recovery A Bilateral or left (dominant) hippocampal infarction due to atherosclerotic-thrombotic or embolic occlusion of the posterior cerebral arteries or their inferior temporal branches B Bilateral or left (dominant) infarction of anteromedial thalamic nuclei C Infarction of the basal forebrain due to occlusion of anterior cerebral anterior communicating arteries D Subarachnoid hemorrhage (usually rupture of anterior communicating artery aneurysm) E Trauma to the diencephalic, inferomedial temporal, or orbitofrontal regions F Cardiac arrest, carbon monoxide poisoning, and other hypoxic states (hippocampal damage) G Following prolonged status epilepticus H Following delirium tremens II Amnesia of sudden onset and short duration A Temporal lobe seizures B Postconcussive states C Transient global amnesia D Hysteria III Amnesic syndrome of subacute onset with varying degrees of recovery, usually leaving permanent residua A Wernicke-Korsakoff syndrome B Herpes simplex encephalitis C Tuberculous and other forms of meningitis characterized by a granulomatous exudate at the base of the brain IV Slowly progressive amnesic states A Tumors involving the oor and walls of the third ventricle and limbic cortical structures B Alzheimer disease (early stage) and other degenerative disorders with disproportionate affection of the temporal lobes C Paraneoplastic and other forms of immune limbic encephalitis
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anisms that govern immediate registration, which remains intact in even the most severely damaged patients with the Korsakoff amnesic syndrome Equally obscure are the anatomic arrangements that enable the patient with virtually no capacity to retain any newly presented factual information to still learn some simple perceptualmotor and cognitive skills, even though there may be no memory of having been taught these skills in the rst place Other psychologic features of human memory that must be accounted for by any model purporting to explain this function are the importance of cueing in eliciting learned material and the imprecision of past memories, allowing for unwitting embellishment and false recollection, to the point of fabrication The latter aspect has been a topic of considerable importance in children who have (or have not) been subjected to sexual abuse and in adults and children whose memories of past abuse have been suggested by the examiners (see Schacter) Also of interest are the separate roles of the thalamus, the hippocampi, and the frontal lobes in memory and whether the nature of the amnesia resulting from damage at one site differs from the others That isolated thalamic lesions, without implicating medial temporal areas, can cause a Korsakoff syndrome is evident from the experience with alcoholism Graff-Radford and colleagues have found that with purely thalamic lesions, as appreciated by imaging studies, anterograde learning is more affected than retrograde recall; but comparing these functions quantitatively seems to us quite dif cult Kopelman, in reviewing his own studies and those of others, concludes that the differences are subtle and pertain mostly to temporal ordering and the modality of information, which is degraded more with diencephalic-temporal lesions than with frontal lobe damage The cellular mechanisms involved in learning and the formation of memories are only beginning to be understood Whether physiologic phenomena such as long-term potentiation or anatomic changes in the dendritic structure of neurons are at the center of memory storage is not known; certainly both are likely to be involved The neurochemical systems that are activated during formation and recall of memory are also obscure Kandel has provided a detailed review of information on this subject (see the References)
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imperfectly and with no regard for their normal temporal relationships, giving them a ctional quality and explaining many instances of confabulation Another noteworthy fact is that long-standing social habits, automatic motor skills, and memory for words (language) and visual impressions (visual or pictorial attributes of persons, objects, and places) are unimpaired Long periods of repetition and usage have made these implicit or procedural memories virtually automatic; they no longer require the participation of the diencephalic-hippocampal structures that were necessary to learn them originally All of this suggests that these special memories, or coded forms of them, through a process of relearning and habituation, come to be stored or led in other regions of the brain; ie, they acquire a separate and autonomous anatomy Several fundamental questions concerning the amnesic syndrome remain unanswered Not known is how a disease process, acting over a brief period of time, not only impairs all future learning but also wipes out portions of a vast reservoir of past memories that had been rmly established for many years before the onset of the illness Also unknown are the anatomic and physiologic mech-
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