Cases reported "Amnesia"

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1/72. 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.
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2/72. 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.
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3/72. 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.
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keywords = visual
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4/72. 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).
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5/72. Functional anatomical study of psychogenic amnesia.

    Psychogenic amnesia is characterized by an inability to recall information already stored in the patient's memory. It is usually related to a stressful or traumatic event that cannot be explained by manifest brain damage. To examine the underlying functional disturbance of brain areas in this condition, we performed a positron emission tomography (PET) activation study on a psychogenic amnesic patient and on 12 normal control subjects. A task requiring explicit retrograde memory of faces was compared with a control task. To assess functional modifications associated with the processes of recovery, a second PET study was performed on the patient 12 months after onset. During the task, activation of the right anterior medial temporal region including the amygdala was increased in the psychogenic amnesic patient. Activation of the bilateral hippocampal regions increased only in the control subjects. During recovery, the right anterior medial temporal region became less active while the right hippocampal region became more active. Activation levels also differed in the anterior cingulate cortex, prefrontal cortex and some other cortical regions between control subjects and the patient. These findings suggest that the changes in these limbic and limbic-cortical functions are related to symptoms of the psychogenic amnesia.
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6/72. Voxel-based mapping of brain hypometabolism in permanent amnesia with PET.

    In this study, we used voxel-based mapping methods to compare the resting cerebral metabolic rate of glucose (CMRglc) measured with PET in five patients with permanent amnesia (three with chronic Wernicke-Korsakoff and two with postanoxia syndrome) to that of nine healthy age-matched subjects. We assessed (i) a group pattern of relative hypometabolism; and (ii) the consistency of this group pattern, if any, in individual subjects, according to etiology. The results from the group analysis documented that permanent amnesia is associated with hypometabolism in the thalamus, posterior cingulate cortex, and mesial prefrontal cortex (near the anterior cingulate gyrus), bilaterally, as well as in the left supramarginal and middle temporal gyri. The individual analysis showed that this group pattern was found in essentially each patient, regardless of the cause of amnesia. Thus, permanent amnesia is subtended by dysfunction in structures belonging to Papez/limbic circuits as well as in left-hemisphere areas typically concerned with verbal functions, probably through a mechanism of thalamo-cortical disconnection and possibly involved in retrograde amnesia. The use of a voxel-based method allowed us to map a common network of synaptic dysfunction in a neuropsychological syndrome regardless of etiology. Our results indicate that this should be a powerful method in functional neuropsychology.
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7/72. Hypothalamic amnesia with spontaneous confabulations: a clinicopathologic study.

    Previous studies demonstrated that patients producing spontaneous confabulations fail to suppress currently irrelevant memory traces and have anterior limbic lesions, particularly involving the orbitofrontal cortex or the basal forebrain. Here, a woman is described who had sarcoidosis damaging the medial hypothalamus and endocrine dysfunction, and a severe memory failure characterized by spontaneous confabulation, disorientation, and severely impaired free recall with preserved recognition. Isolated hypothalamic damage may produce the same type of memory disorder as orbitofrontal damage.
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8/72. Selective sparing of face learning in a global amnesic patient.

    OBJECTIVE: To test the hypothesis that visual memory for faces can be dissociated from visual memory for topographical material. METHOD: A patient who developed a global amnesic syndrome after acute carbon monoxide poisoning is described. A neuroradiological examination documented severe bilateral atrophy of the hippocampi. RESULTS: Despite a severe anterograde memory disorder involving verbal information, abstract figures, concrete objects, topographical scenes, and spatial information, the patient was still able to learn previously unknown human faces at a normal (and, in some cases, at a higher) rate. CONCLUSIONS: Together with previous neuropsychological evidence documenting selective sparing of topographical learning in otherwise amnesic patients, this case is indicative of the fact that the neural circuits involved in face recognition are distinct from those involved in the recognition of other visuoperceptual material (for example, topographical scenes).
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keywords = visual
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9/72. Verbal encoding deficits in a patient with a left retrosplenial lesion.

    Over the past decade, memory impairments associated with retrosplenial damage have received increased attention among neuroscientists, although the exact role of the retrosplenial region in memory has not been clearly defined. Evidence from lesion studies and functional neuroimaging has implicated the retrosplenial region in verbal episodic memory, temporal ordering of information, and topographical memory. In addition, recent positron emission tomography studies have shown increased activation of the retrosplenial cortex during tasks involving both the encoding and retrieval of episodic information. The objective of this study was to define more clearly the nature of memory impairments observed in retrosplenial amnesia. A 47-year-old amnesic male with a left retrosplenial arteriovenous malformation was examined on neurocognitive tasks of automatic and directed encoding, temporal ordering of information, and remote memory. Despite normal performance on frontal cognitive tasks, intact memory for remote information, and a superior IQ, this individual exhibited a profound deficit in the encoding of information, evidenced by poor release from proactive interference, poor category clustering on word list recall, poor semantic encoding on a levels of processing task, and mild impairments in temporal ordering. These results imply that the retrosplenial region plays a role in the verbal encoding of information, which contributes to the profound verbal memory impairment reported in previous case studies of patients with retrosplenial damage.
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10/72. Dorsal thalamic lesion in a noted case of human memory dysfunction.

    The extensively studied patient N.A. has had a severe verbal memory deficit since 1960, when he sustained a stab wound to the brain with a miniature fencing foil. His amnesia occurs in the absence of any other known cognitive defect. Recent CT scans have localized a lesion in the left dorsal thalamus of this patient in a position corresponding to the dorsomedial nucleus; there is no radiographic evidence of other damage in the diencephalon or cerebral cortex. The dorsomedial thalamus may be critical in the neuropathology of diencephalic amnesia and, in humans, may be required for normal memory functions.
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