Cases reported "Amnesia"

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1/108. 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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2/108. Sensorimotor skill learning in amnesia: additional evidence for the neural basis of nondeclarative memory.

    We investigated sensorimotor skill learning, a form of nondeclarative (implicit) memory, in 28 subjects with declarative (explicit) memory defects caused by either mesial temporal (n = 15) or basal forebrain (n = 13) damage and in 66 normal control subjects. All 28 amnesics had normal learning of a rotor pursuit task. We also studied in detail the sensorimotor skill learning of patient Boswell. As a result of bilateral damage to both mesial and lateral aspects of the temporal lobes and to the basal forebrain, Boswell has one of the most severe impairments ever reported for learning of all types of declarative knowledge. Compared to matched controls, Boswell acquired and retained normally the skills associated with performing motor tasks. We conducted a long-term (2-year) followup study of Boswell's retention of the rotor pursuit task, and we found that he retained the skill as well as normal controls. Our study builds on previous work in the following respects: (1) It provides evidence, for the first time, that skill learning is normal in basal forebrain amnesics; (2) it shows that patient Boswell has normal learning and long-term retention of sensorimotor skills, in spite of his extensive damage; and (3) it offers additional evidence that mesial temporal lobe damage spares skill learning. These findings demonstrate unequivocally that sensorimotor skill learning does not require structures in mesial and lateral temporal regions nor in basal forebrain.
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3/108. 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.
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ranking = 0.71791451253664
keywords = brain, nervous system
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4/108. Amnesic syndrome with bilateral mesial temporal lobe involvement in Hashimoto's encephalopathy.

    A 25-year-old woman presented with a subacute confusional state, headaches, unsteadiness, myoclonus, seizures, and an amnesic syndrome as a manifestation of Hashimoto's encephalopathy. Investigations showed biochemical hypothyroidism, raised thyroid microsomal antibodies, and weakly positive antineuronal antibodies. A T2-weighted MRI of the brain showed bilateral symmetric areas of increased signal in the mesial temporal lobes and hippocampi that had a low signal intensity on T1-weighted imaging. Despite clinical and radiologic improvement after steroid and thyroid hormone replacement therapy, a severe amnesic syndrome with associated localized MRI abnormalities persists.
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keywords = brain
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5/108. Amnesic confabulatory syndrome after focal basal forebrain damage.

    A 73-year-old woman developed amnesic confabulatory syndrome after a right focal basal forebrain hemorrhage. The confabulation, despite persistent antegrade amnesia, gradually subsided with improvement of the frontal executive function. The lesion appeared to disrupt connections of the medial and lateral limbic circuits important for memory. Simultaneous dysfunctioning of the two circuits involving the medial temporal and frontal lobes may be necessary for the development of this syndrome.
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keywords = brain
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6/108. Electronic memory aids for outpatient brain injury: follow-up findings.

    The introduction of highly portable computers extends the range of tools potentially useful to persons with functional impairments of prospective memory resulting from brain injury. This study reviews the experience of 12 patients with brain injury undergoing outpatient treatment using palmtop computers to assist with memory dependent activities in their everyday lives. During the initial supervised trial period, each was provided a palmtop computer based memory aid capable of generating audible and visible reminder cues. Subsequently, patients were contacted for follow-up between 2 months and 4 years after initial trial usage, and surveyed as to the utility of the computer. Nine patients found palmtop computers were useful during supervised trials. Seven of nine patients actually continued to use such devices after the usage trials had ended. Experience with this technology has shown it to be useful in a high proportion of patients for assisting with memory dependent functions.
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ranking = 0.85714285714286
keywords = brain
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7/108. 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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ranking = 0.28571428571429
keywords = brain
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8/108. limbic encephalitis and antibodies to Ma2: a paraneoplastic presentation of breast cancer.

    A patient with atypical medullary breast cancer is described who presented with symptoms of limbic encephalitis. The patient's serum and CSF contained antibodies that reacted with the nervous system and the tumour. These antibodies recognised Ma2, a neuronal protein related to paraneoplastic limbic and brainstem encephalitis in men with testicular tumours. This report highlights the importance of testing for paraneoplastic antineuronal antibodies in cases of unexplained limbic encephalitis and suggests screening for breast cancer in women with antibodies predominantly directed to Ma2.
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ranking = 0.14648594110807
keywords = brain, nervous system
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9/108. Acquisition and transfer of new verbal information in amnesia: retrieval and neuroanatomical constraints.

    Four experiments examined new associative learning in amnesia by contrasting the performance of 2 amnesic participants-1 (C.C.) with basal forebrain damage and the other (R.H.) with medial temporal lobe damage--and 3 controls. Both amnesic individuals were severely impaired on explicit memory measures but showed intact perceptual priming. On the new associations measures, only C.C., not R.H., exhibited learning by producing correct targets (HIJACKER) in the absence of perceptual cues for them (e.g., STAFF shot ???). When the perceptual cue (e.g., medicine cured _I_C_P) was provided, both C.C. and R.H. showed learning. Transfer to information containing conceptually related targets (e.g., TERRORIST or BELCH) was reliably observed only in C.C. This finding was replicated with further reduction in perceptual overlap across original (lightning torched JUNGLE) and transfer (lightning burned wilderness) sentences. Together, these findings delineate the role of experimental conditions, severity of amnesia, and different neuroanatomical structures in mediating new verbal learning in amnesia.
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ranking = 0.14285714285714
keywords = brain
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10/108. Quantitative modeling of category learning in amnesic patients.

    Category rule learning was examined in two amnesic patients using the perceptual categorization task (e.g., Ashby & Gott, 1988; Filoteo & Maddox, 1999). Traditional accuracy-based analyses as well as quantitative model-based analyses were performed. Unlike accuracy-based analyses, the model-based approach allowed us to examine both categorization rule learning and variability in the trial-by-trial application of the participant's categorization rule. The results indicated that the amnesic patients were as accurate as the controls in learning a complex, nonlinear rule over a large number of trials. The model-based analysis indicated that, in general, the amnesic patients learned the categorization rule as well as controls and applied their rule as consistently as controls. Categorization performance on a second day of testing revealed that amnesic patients can retain the categorization rule over a 24-h period. These results suggest that the brain regions damaged in amnesia are not involved in category learning or memory for the category structures.
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keywords = brain
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