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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43 year old man with a traumatic amnesic syndrome experienced only a brief, if any, loss of consciousness following an injury to the head. Four years after this injury, his results on standard psychometric assessment were normal. Long-latency evoked response potentials results were normal, and the neurological examination and computed tomography scans were unhelpful in explaining his amnesic symptoms. He had no history of alcohol abuse, yet his neuropsychological profile was that of a Korsakoff-like amnesia with frontal lobe features. Magnetic-resonance images demonstrated evidence of extensive frontal lobe damage, while cerebral blood flow studies provided additional evidence of bilateral frontal lobe dysfunction. The case highlights the need for those giving opinions in medico-legal head trauma cases to go beyond a reliance on routine indicators, such as duration of coma, results of standard psychometric assessment and computed tomography scans, to more specialised neuropsychological evaluations and magnetic-resonance imaging scans.
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PMID:Neuropsychological assessment and brain imaging technologies in evaluation of the sequelae of blunt head injury. 233 82

Nearly 10% of a sample of men charged with a variety of offences claimed amnesia for their offence. The amnesia occurred only among those who had committed violence and was most frequent following homicide. All the amnesics had a psychiatric disorder, four having a primary depressive illness and the remainder being almost equally divided between schizophrenia and alcohol abuse. None of the amnesias had any legal implications. The circumstances of the offences suggested a variety of mechanisms to account for the amnesia, including repression, dissociation and alcoholic black-outs. Psychological defence mechanisms were probably of some importance, even when alcohol was an important factor.
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PMID:Amnesia for criminal offences. 649 66

The transient amnesia produced by lorazepam has been suggested to have much in common with the permanent amnesia associated with organic brain damage. The present study examined the amnesia associated with chronic alcoholism and acute lorazepam administration and hypothesised that because alcoholics have prior impairment, their response to lorazepam induced amnesia would differ from that of non-alcoholics. Memory functioning was tested in 20 chronic alcoholics and 20 non-alcoholic controls both before and after administration of either 2 mg lorazepam or a placebo. It was found that, although there were some discrepancies on some of the memory tests, both long term alcohol abuse and acute lorazepam administration impaired visual and verbal episodic memory but did not impair semantic or short-term memory (STM).
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PMID:A comparison of the amnesic effects of lorazepam in alcoholics and non-alcoholics. 787 Aug 81

The consequences of the severe head injuries should be estimated 1-2 years following the injury. The evaluation must be based upon certain postulates which are to be obligatory for the team of experts (neuropsychiatrist, otologist, ophthalmologist, neuro-radiologist, clinical psychologist). They must work simultaneously as a team for it is the only way to establish the precise qualification of the damage in question. The clinical work up to now has shown many weak points. The first postulate is the information on the state of health prior to the injury: previous injuries and their sequelae, psychopathological manifestations, alcohol abuse, disturbances of the consciousness, vertigo, disturbances of the sight and hearing etc. The second postulate is the review of the case history regarding the acute period of the injury: the qualification of the injury, the duration of the state of unconsciousness and post-traumatic amnesia, focal neurological signs, psychological disturbances, EEG, CT etc. The third postulate is a detailed clinical examination including paraclinical parameters neurological examination (focal neurological signs, hemicerebral syndrome and very seldom-parkinsonism) with consultation of otologist (vestibularis, audiogram) and ophthalmologist (visus, fundus, campus, intraocular pressure), EEG (longitudinal follow-up), possible evoked cerebral potentials. The epilepsy syndrome must be based upon clinical and EEG criteria, while the selection must be very strict. In there are structural brain changes the collaboration with the neuroradiologist is important. Psychological disorders: neurasthenic neurosis, personality disorders, and rarely dementia. It should be clinically confirmed accompanied by psychological tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A doctrinaire approach to evaluation of sequelae of craniocerebral injuries]. 796 91

The performance of amnesic Korsakoff patients in delay eyeblink classical conditioning was compared with that of recovered chronic alcoholic subjects and healthy normal control subjects. Normal control subjects exhibited acquisition of conditioned responses (CRs) to a previously neutral, conditioned tone stimulus (CS) following repeated pairings with an unconditioned air-puff stimulus, and demonstrated extinction of CRs when the CS was subsequently presented alone. Both amnesic Korsakoff patients and recovered chronic alcoholic subjects demonstrated an impairment in their ability to acquire CRs. These results indicate that the preservation of delay eyeblink conditioning in amnesia must depend on the underlying neuropathology of the amnesic syndrome. It is known that patients with amnesia caused by medial temporal lobe pathology have preserved conditioning. We have now demonstrated that patients with amnesia caused by Korsakoff's syndrome, as well as recovered chronic alcoholic subjects, have impaired conditioning. This impairment is most likely caused by cerebellar deterioration resulting from years of alcohol abuse.
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PMID:Impaired delay eyeblink conditioning in amnesic Korsakoff's patients and recovered alcoholics. 856 Dec 80

This case study presents a 37 year old man, P.P., who shows evidence of both profound executive impairment and diencephalic amnesia associated with two discrete lesion sites following a Sub Arachnoid Haemorrhage. The executive impairment is unusual in type and severity, amounting to a gross impairment in the initiation and organisation of action. The thalamic lesion provides a rare example of diencephalic damage resulting in an extensive retrograde amnesia of the type that is often associated with Korsakoff's syndrome, but which in this case is not associated with prolonged alcohol abuse. Some of the problems caused by the co-occurrence of two such profound and disabling impairments are discussed.
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PMID:Co-occurrence of executive impairment and amnesic syndrome following sub arachnoid haemorrhage: a case study. 944 72

A 38-y-old male with occult inhalant abuse underwent an 18-mo evaluation for presumed seizure disorder. Although past medical history was significant for alcohol abuse, his wife confirmed a 6-y histoy of abstinence. His seizures were characterized as episodes of unconsciousness preceded by a feeling of "things slowing down". No muscular activity was witnessed during these episodes, and upon regaining consciousness the patient had slurred speech, disorientation, dissociative amnesia, and bizarre behavior that resolved spontaneously. Despite 4 emergency department visits, 4 hospital admissions, 5 neurologic and 7 psychiatric outpatient evaluations, extensive work-up was non-diagnostic. These episodes recurred until his wife found him huffing trichloroethylene. Questioning of the patient revealed that huffing always preceded these episodes and that he started huffing after discontinuing alcohol. The patient underwent addiction treatment. Toxic inhalants should be suspected as a substitute drug of abuse in patients attempting abstention. Disorientation clinically similar to dissociative amnesia can occur following loss of consciousness during an episode of trichloroethylene use.
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PMID:An unusual presentation of inhalant abuse with dissociative amnesia. 1182 66

Alcohol-related amnesia ("blackout") is a common even in people who are not alcohol dependent. The average duration of simple alcohol-induced amnesia in our alcohol dependent male patients was almost 8 hours (7.96, SD=23.96). Alcohol-induced amnesia is considered to be a risk factor for long-term impairment of cognitive functions, if alcohol abuse continues. On the other hand cognitive functions in alcohol dependent persons who abstain from alcohol often improve remarkably because of reorganisation and restoration of neuronal networks. This process can be enhanced by vitamin B1, appropriate treatment of withdrawal syndrome, memory training, coping with stress and depression (relaxation techniques can be used), balanced life-style, and nootropic drugs. Alcohol-related amnesia often motivates alcohol dependent patients to overcome their problem, especially if it is appropriately used in psychotherapy.
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PMID:[Alcohol-related amnesia ("blackout") in broader perspective]. 1573 Feb 21

The neuropathology associated with chronic alcohol abuse varies across studies, though research suggests generalized reductions in cortical and subcortical grey and white matter. Neuropsychological findings also differ within the literature. The inconsistent findings with respect to the neuropathology and neurobehavior of patients with histories of alcohol abuse may be due, at least in part, to differing nosology and the highly variable inclusion/exclusion criteria employed by researchers. Oslin et al. [Int J Geriatr Psychiatry 1998;13:203-212] have proposed and recently validated specific criteria for probable alcohol-related dementia (ARD). We were interested in comparing the neuropsychological profile of ARD patients with the neurocognitive profiles of typical cortical and subcortical dementia patients. Participants included 14 ARD patients, 15 patients diagnosed with Alzheimer's disease (AD), 13 patients diagnosed with subcortical vascular dementia (VaD), and 20 normal controls. Patient subgroups were similar with respect to age (mean = 79), education (mean = 12 years) and dementia severity (MMSE; mean = 22.1). The three dementia patient subgroups demonstrated significantly worse performance than the normal controls subgroup on all neuropsychological tests. The ARD subgroup exhibited very similar executive control deficits to VaD patients. However, the different neurocognitive profiles of the patient subgroups suggest that ARD patients may also, in fact, demonstrate some degree of amnesia given that they perform slightly worse than subcortical patients on delayed verbal free recall and recognition. Nonetheless, the ARD patients did not display as severe impairment as the AD patients on the memory tasks. No significant differences between the three patient groups were identified on language tests. In sum, we present preliminary evidence of a distinct neuropsychological profile for ARD patients that includes impairment on both executive control and memory tests. This pattern of performance suggests that long-term alcohol abuse, in comparison to AD and VaD, may be associated with both cortical and subcortical neuropathology.
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PMID:The neuropsychological profile of alcohol-related dementia suggests cortical and subcortical pathology. 1616 75

Korsakoff syndrome is a chronic form of amnesia resulting from thiamine deficiency. The syndrome can develop from unrecognized or undertreated Wernicke encephalopathy. The intra-individual course of Wernicke-Korsakoff syndrome has not been studied extensively, nor has the temporal progression of gait disturbances and other symptoms of Wernicke encephalopathy. Here we present the detailed history of a patient whose acute symptoms of Wernicke encephalopathy were far from stable. We follow his mobility changes and the shifts in his mental status from global confusion and impaired consciousness to more selective cognitive deficits. His Wernicke encephalopathy was missed and left untreated, being labeled as "probable" Korsakoff syndrome. Patients with a history of self-neglect and alcohol abuse, at risk of or suffering with Wernicke encephalopathy, should receive immediate and adequate vitamin replacement. Self-neglecting alcoholics who are bedridden may have severe illness and probably active Wernicke encephalopathy. In these patients, mobility changes, delirium, or impaired consciousness can be an expression of Wernicke encephalopathy, and should be treated to prevent further damage from the neurologic complications of thiamine deficiency.
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PMID:Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy. 2553 41


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