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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Memory and forgetfulness have been viewed since antiquity from perspectives of physical, emotional, and spiritual states of well-being, and conceptualized philosophically. Numerous discussions of memory loss, or case reports, existed, but a fundamental advance in conceptualization of memory loss as a pathological clinical phenomenon originated when Sauvages classified "amnesia" as a medical disorder, in 1763. Originally, amnesia was recognized as a weakening or dissolution of memory, according to a taxonomy that ascribed known causes to the disorder. Etiologic factors included neurological disorders of stroke, hemorrhage, and head injury, metabolic dysregulation, alcohol and substance abuse, toxicity, anoxia, and other acute or chronic (sometimes progressive) brain disorders. Clinical descriptions of amnesia appeared internationally in medical dictionaries and scientific encyclopedias in the early 19th century. The possibility that amnesia could be either idiopathic, or symptomatic of another illness, was proposed based on the wide range of recognized etiologies and associations. Debate ensued regarding the status of amnesia as an illness or a symptom, but regardless, amnesia was soon recognized as an independent disorder of memory, distinguishable from disorders of global intellect, or of consciousness, or of language. Distinctions of amnesia considered its temporal gradient, duration and natural course, nature of onset, severity or depth of memory loss, course, and prognosis. Concepts of retrograde (forgetting knowledge preceding onset) and anterograde (difficulty learning, recalling new information) further specified the nature of amnestic memory difficulty. Alcoholic amnesia in Korsakoff's syndrome generated much attention. Amnesia as a clinical feature was critical to the development of notions of dissociation of conscious from subconscious recall in hysteria, and differentiation of neurogenically-based from psychogenically-based amnesia became central to understanding post-traumatic states. Amnesia studied as a disorder of memory remains an avenue to enrich clinical understanding of a condition that continues to be powerfully challenging to this day.
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PMID:Early History of Amnesia. 3122 Aug 49

Hallucinations, delusions, and confabulations are common symptoms between neurology and psychiatry. The neurological diseases manifesting with such symptoms (dementia, epilepsy, Korsakoff's disease, brain tumors, Parkinson's disease, migraine, right hemisphere stroke and others) would be the key to understand their biological mechanisms, while the cognitive sciences, neuropharmacology and functional neuroimaging would be the tools of such researches. It is possible to understand the perceptive rules of the mind and the mechanisms of the human consciousness based on these symptoms. However, hallucinations and delusions manifest with extraordinary vehemence with psychiatric disorders such as psychosis and schizophrenia, with which there is no evidence of brain lesions. Furthermore, they are subjective symptoms, and they do not have biological markers. Hence, they are prone to high inter-individual variability and depend on other variables (such as education, history of trauma), and are therefore difficult to reduce to unequivocal constructs. Causative mechanisms are probably multiple. For understanding these symptoms, a common framework between neurology and psychiatry is still missing. The psychopathology of French alienists over the 19th century, of S. Freud, and of Henry Ey over the 20th century gave way, in the second half of the 20th century, to the adoption of the DSM and neurosciences, to pursue a pure neurological perspective. However, although psychodynamic models seem nowadays (in a technological era) less influential, detailed clinical evaluations focusing on emotional-cognitive paradigms are probably the only way to lead to new neurobiological researches.
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PMID:Neurology versus Psychiatry? Hallucinations, Delusions, and Confabulations. 3122 Aug 56

A diagnosis of alcohol use disorder is associated with a higher risk of dementia, but a dose-response relationship between alcohol intake consumption and cognitive impairment remains unclear. Alcohol is associated with a range of effects on the central nervous system at different doses and acts on a number of receptors. Acute disorders include Wernicke's encephalopathy (WE), traumatic brain injury, blackouts, seizures, stroke and hepatic encephalopathy. The most common manifestations of chronic alcohol consumption are Korsakoff's syndrome (KS) and alcohol-related dementia (ARD). There is limited evidence for benefit from memantine in the treatment of ARD, but stronger evidence for the use of high-dose parenteral thiamine in the progression of neuropsychiatric symptoms for WE. Accumulating evidence exists for pharmacological treatment in the prevention of hepatic encephalopathy. Rehabilitation of people with ARD may take several years, and requires an approach that addresses physical and psychosocial factors.
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PMID:Alcohol use disorders and the brain. 3211 74


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