1/172. A fugue-like state associated with diazepam use.diazepam is a long-acting benzodiazepine. Although diazepam is commonly associated with a variety of side effects, it is generally not believed to cause fugue-like states or retrograde amnesia. This report presents the case of an active duty patient who developed a brief fugue-like state with retrograde amnesia. This was associated with the short-term oral use of diazepam. There was no other apparent cause for his symptoms, which resolved within 24 hours after the diazepam was discontinued. This case suggests that short-term use of diazepam can lead to a brief fugue-like state with retrograde amnesia that has not been reported previously.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
2/172. Amnestic state in a holocaust survivor patient: psychogenic versus neurological basis.Differentiation between psychogenic and organic amnesia is sometimes quite difficult. This paper focuses on the psychogenic and organic components of a complex case of amnesia rooted in remote and prolonged traumatic stress and manifested under circumstances evoking dissociated memories. The Transient Global amnesia (TGA) of a concentration camp survivor who developed sudden amnesia during a psychiatric intake interview was clearly triggered by the pressure of repressed holocaust memories. The importance of distinguishing between TGA and dissociative amnesia is emphasized, and the role of psychological upset as a precipitant in TGA is stressed.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
3/172. Amnestic syndrome presenting as malingering in a man with developmental disability.The authors report an unusual presentation of amnestic syndrome mislabeled as malingering in a man with mild developmental disability. The case highlights the challenges to medical personnel in treating persons who visit emergency rooms often, particularly individuals with mental retardation. Diagnostic overshadowing was a primary factor in the failure to diagnose amnestic syndrome. Overshadowing occurs when a patient's problematic behaviors are attributed to mental retardation, and no attempt is made to search for the root causes of the problem. The case also highlights the need for emergency room personnel to maintain links with agencies involved in the day-to-day care of persons with developmental disabilities.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
4/172. Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?OBJECTIVE: To analyse amnesia caused by basal forebrain lesions. methods: A single case study of a patient with amnesia after bleeding into the anterior portion of the left basal ganglia. Neuropsychological examination included tests of attention, executive function, working memory, recall, and recognition of verbal and non-verbal material, and recall from remote semantic and autobiographical memory. The patient's MRI and those of other published cases of basal forebrain amnesia were reviewed to specify which structures within the basal forebrain are crucial for amnesia. RESULTS: attention and executive function were largely intact. There was anterograde amnesia for verbal material which affected free recall and recognition. With both modes of testing the patient produced many false positive responses and intrusions when lists of unrelated words had been memorised. However, he confabulated neither on story recall nor in day to day memory, nor in recall from remote memory. The lesion affected mainly the nucleus accumbens, but encroached on the inferior limb of the capsula interna and the most ventral portion of the nucleus caudatus and globus pallidus, and there was evidence of some atrophy of the head of the caudate nucleus. The lesion spared the nucleus basalis Meynert, the diagnonal band, and the septum, which are the sites of cholinergic cell concentrations. CONCLUSIONS: It seems unlikely that false positive responses were caused by insufficient strategic control of memory retrieval. This speaks against a major role of the capsular lesion which might disconnect the prefrontal cortex from the thalamus. It is proposed that the lesion of the nucleus accumbens caused amnesia.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
5/172. Naming people ignoring semantics in a patient with left frontal damage.Studies about proper name anomia generally assume that persons' names are harder to recall than other semantic information one knows about them and that name retrieval is not possible without biographical knowledge. We describe a patient, SB, who, after a left frontal haemorrhage, was unable to recall any biographical information about people she could name. Moreover, she had a normal score in an Object Picture Naming Test, but gave confabulatory answers in a Semantic Questionnaire involving the same items. The role of frontal function in producing this pattern of impairment is discussed, together with the possible existence of a direct route from visual perception to proper name retrieval.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
6/172. memory lost and regained following bilateral hippocampal damage.We present a longitudinal neuropsychological study (31 examinations over a period of 18 months) of patient DE DF demonstrated bilateral atrophy of the hippocampal formation and globus pallidus resulting from carbon monoxide poisoning. Eighteen months after the event, the volume of the hippocampal formation was reduced by 42% on the left side and 28% on the right. The patient initially presented with a severe global amnesia. Then, he showed a gradual, yet selective recovery of episodic memory function. Verbal free recall and spatial memory performance remained reduced, whereas immediate word recall and recognition memory, as well as picture learning and memory, improved to levels at the lower range of normal performance. Interestingly, nonspatial associative learning was never much impaired and recovered completely by the end of testing. These data are taken as evidence that the human hippocampal formation does not equally support different forms of episodic memory.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
7/172. Neuroimaging and behavioral correlates of recovery from mnestic block syndrome and other cognitive deteriorations.OBJECTIVE: We conducted a follow-up study on a patient with enduring psychic shock-induced cognitive impairment to study by neuropsychological and functional imaging methods the degree of his recovery process on the brain and cognitive levels. BACKGROUND: Based on the assumption that trauma and stress conditions can alter the functions of the nervous systems, we report on a patient whom we studied 2 and 12 months after he suffered "mnestic block syndrome" and additional cognitive deterioration symptoms. methods: We report on a patient studied 2 and 12 months after he suffered "mnestic block syndrome" and additional cognitive deterioration symptoms. magnetic resonance imaging and fluorodeoxyglucose positron emission tomography were used for neural and detailed neuropsychological testing for cognitive deficits. RESULTS: The patient initially manifested severe intellectual decline, including severe anterograde and retrograde amnesia. His symptoms were correlated with major, although selective, reductions in his brain metabolism (2-3 SD below those of controls). Presently, he shows a normal brain metabolism and has regained parts of his memory and many of his other intellectual capabilities. Nevertheless, he still has long-term memory impairments. CONCLUSIONS: This case demonstrates a close relation between brain metabolism and cognitive performance, with major deficits of both at 2 months and major recovery of both at 12 months after a shocking event. It can serve as an example for possible stress-related deteriorations in certain brain regions, which can be partly corrected by psychotherapeutic interventions, passing time, and favorable environmental conditions.- - - - - - - - - - ranking = 4keywords = ms (Clic here for more details about this article) |
8/172. Medial temporal lobe amnesia: a case study for nursing.Maintaining and enhancing cognitive function is a crucial but challenging intervention for patients with memory problems. research on the medial temporal lobe (MTL) memory system has yielded much information that can guide nurses in planning, evaluating, and performing effective interventions. A patient, Mrs. N, with a diagnosis of anaplastic astrocytoma of the left medial temporal lobe provides an example. Information from research guides assessment of Mrs. N and affords development of specific patient-centered interventions to maintain function, cope, and compensate. Data have been gathered from the patient, relatives, and caregivers to compare with and augment existing research, because few nursing case studies of amnesia involving patients with left medial temporal lobe tumors are available for analysis.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
9/172. Priming arithmetic reasoning in an amnesic patient.The present study elucidates the role of implicit memory in problem solving by evaluating priming effects in a severely amnesic patient. An arithmetic series completion task was adopted to investigate the effects of lags, of items difficulty, as well as the influence of different distractor tasks on priming numerical reasoning. The results indicated that the priming effect was maximized in difficult trials and disappeared after long lags. On the other hand, the facilitation effect was not modulated by the nature of the distractor tasks. Critically, the experimental design controlled for peripheral facilitation of visual input and verbal output processes and a recognition task indicated that the effect may not be attributed to explicit memory. Thus, the facilitation must be located to a more central stage, possibly at the stage in which the abstract formula of the underlying algorithm are generated (Langdon & Warrington, 1997).- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
10/172. Loss of psychic self-activation after paramedian bithalamic infarction.BACKGROUND AND PURPOSE: Loss of psychic self-activation has been described after bilateral lesions to the globus pallidus, striatum, and white matter of the frontal lobes, but it is a very rare sign of bithalamic lesions. The exact functional-anatomic mechanism underlying loss of psychic self-activation following bithalamic lesions remains to be elucidated. CASE DESCRIPTION: We present clinical, neuropsychological, structural, and functional neuroimaging data of an 18-month follow-up period of a man with prominent loss of psychic self-activation after coronary arteriography. Except for memory decline, accompanying symptoms remained restricted to the acute phase. The neurobehavioral syndrome consisted mainly of apathy, indifference, poor motivation, and flattened affect, and this remained unchanged during the entire follow-up period. MRI showed a bithalamic infarction involving the nucleus medialis thalami bilaterally. Single-photon emission CT revealed a severe relative hypoperfusion of both thalami, a relative hypoperfusion of both nuclei caudati, and a relative hypoperfusion mesiofrontally. CONCLUSIONS: Single-photon emission CT data support the hypothesis that the neurobehavioral manifestations after bithalamic paramedian infarction are caused by disruption of the striatal-ventral pallidal-thalamic-frontomesial limbic loop. Probably, bilateral disruption at different levels of the striatal-ventral pallidal-thalamic-frontomesial loop may lead to a similar clinical picture consisting of loss of psychic self-activation.- - - - - - - - - - ranking = 1keywords = ms (Clic here for more details about this article) |
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