Cases reported "Amnesia"

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1/510. A case of amnestic syndrome caused by a subcortical haematoma in the right occipital lobe.

    A case of an amnestic syndrome caused by a subcortical haematoma in the right occipital lobe is reported. A 62-year-old right-handed man presented with a sudden onset of headache to the hospital. On admission, he had a left homonymous hemianopsia, disorientation and recent memory disturbance, but had normal remote memory and digit span. Computed tomography (CT) and magnetic resonance imaging (MRI) revealed a subcortical haematoma in the right occipital lobe. These findings suggest that the patient's amnesia was caused by a lesion of the retrosplenial region in the non-dominant hemisphere. ( info)

2/510. Recovery from anterograde and retrograde amnesia after percutaneous drainage of a cystic craniopharyngioma.

    A case is reported of a cystic craniopharyngioma involving the floor and walls of the third ventricle. Pronounced anterograde and retrograde amnesia were documented preoperatively by formal testing. Rapid improvement in both new learning capacity and remote memory occurred after percutaneous twist drill drainage of the cystic portion of the tumour. The relevance of these observations to the amnesic syndrome and its neuropathological basis is discussed. ( info)

3/510. Observations on two natural amnesias.

    The role of interpersonal sequences in determining amnesias has not been as explored as the role of intrapsychic conflict. This paper examines two natural amnesias, emphasizing their function as part of the process of sequencing phenomena. ( info)

4/510. Contributions of prefrontal cortex to recognition memory: electrophysiological and behavioral evidence.

    To clarify the involvement of prefrontal cortex in episodic memory, behavioral and event-related potential (ERP) measures of recognition were examined in patients with dorsolateral prefrontal lesions. In controls, recognition accuracy and the ERP old-new effect declined with increasing retention intervals. Although frontal patients showed a higher false-alarm rate to new words, their hit rate to old words and ERP old-new effect were intact, suggesting that recognition processes were not fundamentally altered by prefrontal damage. The opposite behavioral pattern was observed in patients with hippocampal lesions: a normal false-alarm rate and a precipitous decline in hit rate at long lags. The intact ERP effect and the change in response bias during recognition suggest that frontal patients exhibited a deficit in strategic processing or postretrieval monitoring, in contrast to the more purely mnemonic deficit shown by hippocampal patients. ( info)

5/510. Retrograde temporal order amnesia resulting from damage to the fornix.

    Some amnesic patients show an impairment of temporal order memory that cannot be accounted for by content memory deficits. The performance of an amnesic patient on memory tasks assessing the patient's content and temporal memories for remotely acquired material is described, after a lesion including the bilateral anterior fornix and adjacent anterior thalamus. The patient displayed a deficit in the temporal order tasks for remotely acquired information. Neither frontal cognitive deficits nor recognition deficits can account for this patient's poor temporal memory. This retrograde temporal order memory impairment without content memory deficits were not seen in previously reported thalamic amnesic patients. Accordingly, the present patient's poor retrograde temporal memory could hardly be explained by only a thalamic lesion. It is concluded that the patient's impairment of temporal order memory for the retrograde material is probably due to the direct disconnection between the frontal lobe and the hippocampus by disruption of the fornix. ( info)

6/510. 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. ( info)

7/510. 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. ( info)

8/510. 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. ( info)

9/510. 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. ( info)

10/510. Confabulation and delusional misidentification: a four year follow-up study.

    We describe a patient, AZ, who showed, in addition to an amnesic syndrome which eventually improved, longstanding confabulation and delusional misidentification following bilateral frontal and right temporal post-traumatic lesions. Confabulation appeared in personal recollections and on long-term verbal memory testing. Misidentification concerned mainly his wife and house. During the four year follow-up AZ's confabulation progressively shrinked so as to become restricted to verbal memory tasks. By contrast, misidentification persisted. General semantic memory was unimpaired throughout, while performance on frontal tests was initially poor and partly improved in time. We argue that confabulation and misidentification, though often intermingled and occurring after similar lesion pattern, should be considered as different neuropsychological entities. ( info)
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