Cases reported "Amnesia"

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1/35. 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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2/35. 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.
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3/35. 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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4/35. Transient crossed aphasia and persistent amnesia after right thalamic haemorrhage.

    A 45-year-old right-handed woman suffered transient aphasia and persistent amnesia after a right thalamic haemorrhage. This patient appeared to have crossed aphasia, although it disappeared within 8 weeks. It is noteworthy that the patient had a unilateral right thalamic lesion but exhibited both verbal and non-verbal memory impairment. Computed tomography and magnetic resonance imaging revealed cerebral haemorrhage in the right thalamus involving the ventral anterior nucleus, medioventral nucleus, mamillothalamic tract, internal medullary lamina, and mediodorsal nucleus. An amytal test was performed and suggested that the right hemisphere was dominant for language functions and the left hemisphere was dominant for visuospatial functions. Single photon emission CT revealed a low perfusion area only in the right thalamus. These findings suggest that the right hemisphere might be dominant for both verbal and non-verbal memory function in this patient, although visuospatial function was lateralized in the left hemisphere.
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5/35. Memory disorder in Korsakoff's psychosis: a neuropathological and neuropsychological investigation of two cases.

    Neuropathological findings in the brains of two alcoholic patients with Korsakoff's psychosis are reported. Their memory defects had been studied in detail quantitatively over a period of nine years in one case and three years in the other, relevant details of which are presented. Both patients had had a relatively pure long-term memory impairment in the absence of other cognitive deficits and in the absence of a short-term memory impairment. Their retrograde amnesia for public events and famous faces had been measured and found to have extended backwards over at least twenty-five years. There was severe impairment in anterograde recognition memory for both verbal and non-verbal material. On a newly prepared memory quotient battery both patients had scored well below the bottom of the normal scale (less than 60, where 100 is the mean with a standard deviation of /- 15). Both patients had also shown the characteristic differential improvement in retention when tested by cued recall and also the characteristic 'prior learning effect', i.e. normal retention of one list of words when tested by cued recall but impaired retention of a second list sharing the same cues as the first list. There had been a slight but significant deterioration in intelligence in one of the patients in the two years prior to his death, although his IQ still fell within the normal range. The other patient remained undeteriorated until his death, and his IQ also was close to an estimated measure of his premorbid IQ. In the brains of both patients there was marked gliosis, shrinkage and discolouration bilaterally in the medial nuclei of the mammillary bodies. In addition there was a thin band of gliosis bilaterally between the wall of the third ventricle and the medial dorsal nucleus, the rostral limit lying anterior to the medial dorsal nucleus. In the patient with no intellectual deterioration these were the only pathological changes that were seen. In neither patient was there evident local loss of nerve cells, gliosis or any other qualitative evidence of abnormality in the hippocampi, the white matter of the temporal lobes or the greater part of the medial dorsal nuclei, although it is difficult to be certain whether there was any overlap between the band of gliosis and the most medial region of the medial dorsal nueleus and other adjacent thalamic nuclei. In the other patient there was also a small zone of softening in the cerebellum and an increase in astrocytes in other regions of the cerebral hemispheres, including the basal ganglia, amygdala, and brain-stem, but without noticeable loss of cells. The question of the minimal lesion for the alcoholic Korsakoff amnesic state, and some aspects of the related anatomy, is discussed in the context of other reports in the literature which are, however, difficult to assess in the absence of details of the specificity, severity and character of the memory disorders.
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6/35. 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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7/35. A case of frontal network amnesia.

    A 63 year old man developed an amnesic syndrome coupled with an array of "frontal lobe" signs after bilateral small subcortical infarcts. His amnesia was characterised by severe difficulty in voluntary recall of recently memorised verbal and non-verbal materials, while his recognition for the same materials was less affected. The symptoms remained unimproved at a follow up evaluation eight months after onset. magnetic resonance imaging showed two small circumscribed lesions, one in the dorsomedial nucleus of the left thalamus and the other in a region of the right globus pallidus and anterior limb of the right internal capsule. The mammillothalamic tracts and anterior nuclei of the thalami were clearly spared bilaterally. The left dorsomedial nucleus lesion disrupted the thalamofrontal circuit, while the anterior limb lesion of the right internal capsule disconnected the same circuit by damaging part of the anterior thalamic radiation. Thus the amnesia in this patient may have been caused by disruption of the bilateral thalamofrontal circuits. This type of amnesic pathology should be separated from more conventional types of amnesia that are produced by disruption of the so called Papez circuit or the Delay-Brion memory system.
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8/35. amnesia following a discrete basal forebrain lesion.

    Destructive lesions of the basal forebrain are associated with memory impairment in both humans and experimental animals. The basal forebrain is thought to contribute to memory function by providing cholinergic innervation to critical memory structures such as the hippocampus and amygdala. In previously reported clinical cases of basal forebrain amnesia, multiple neuroanatomical regions have been damaged, preventing identification of the minimal critical lesion necessary to produce an amnestic syndrome. We describe a patient who developed persistent, global anterograde and retrograde amnesia following resection of a low-grade glioma. Post-surgical magnetic resonance imaging studies revealed a small discrete lesion, centred in the right diagonal band of broca, that included the preoptic area, the anterior hypothalamus, the lamina terminalis and the paraterminal gyrus. The septal nuclei and the cell bodies of the nucleus basalis of Meynert appeared to have been spared, as were other structures in the medial temporal lobe and diencephalon. Our case provides critical support for the independent contribution of the basal forebrain, in particular the diagonal band nuclei, in memory function. We propose that our patient's amnesia resulted from disconnection of pathways between the diagonal band nuclei and the hippocampal region, depriving the hippocampus of cholinergic innervation.
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9/35. Pathologically proven frontotemporal dementia presenting with severe amnesia.

    Early and severe memory impairment is generally held to be an exclusion criterion for the clinical diagnosis of frontotemporal dementia (FTD). However, clinical experience suggests that some patients with otherwise typical FTD can be amnesic from presentation, or even present solely with amnesia. A review of severe amnesia at presentation in patients with pathologically proven FTD is therefore warranted. The present study examined the records of all patients in the joint Cambridge-Sydney neuropathological series of patients with dementia and a pathological diagnosis of FTD to identify those for whom memory complaints were dominant at presentation. Eight of 71 patients met these criteria. For two patients, memory loss was the only complaint; for one patient, memory loss was accompanied by personality change; for two patients, memory loss was accompanied by prominent dysexecutive symptoms; and for three patients, memory loss was accompanied by apathy but no other behavioural changes. In seven patients local specialist teams initially diagnosed Alzheimer's disease; four patients entered anticholinesterase drug trials. All eight later developed behavioural features: in four, the diagnosis was revised to FTD, while in four the diagnosis of FTD was made only on neuropathological examination after death. In conclusion, severe amnesia at presentation in FTD is commoner than previously thought and the clinical consensus criteria for the diagnosis of FTD may need to be revised. The underlying basis of the memory impairments in patients with FTD may be heterogeneous, with different explanations in different subgroups.
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10/35. Autobiographical amnesia and accelerated forgetting in transient epileptic amnesia.

    BACKGROUND: Recurrent brief isolated episodes of amnesia associated with epileptiform discharges on EEG recordings have been interpreted as a distinct entity termed transient epileptic amnesia (tea). patients with tea often complain of autobiographical amnesia for recent and remote events, but show normal anterograde memory. OBJECTIVE: To investigate (a) accelerated long term forgetting and (b) autobiographical memory in a group of patients with tea. methods: Seven patients with tea and seven age matched controls were evaluated on a range of anterograde memory tasks in two sessions separated by 6 weeks and by the Galton-Crovitz test of cued autobiographical memory. RESULTS: patients with tea showed abnormal long term forgetting of verbal material, with virtually no recall after 6 weeks. In addition, there was impaired recall of autobiographical memories from the time periods 1985-89 and 1990-94 but not from 1995-1999. CONCLUSIONS: tea is associated with accelerated loss of new information and impaired remote autobiographical memory. There are a number of possible explanations including ongoing subclinical ictal activity, medial temporal lobe damage as a result of seizure, or subtle ischaemic pathology. Future analyses should seek to clarify the relationship between aetiology, seizure frequency, and degree of memory impairment.
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