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Memory complaints, memory disorders and focus localization in patients with partial epilepsy.

Our study aimed at analysing effects of epileptic foci on memory function in patients with partial epilepsy. Twenty-eight patients with spontaneous memory complaints and psychometrically established memory disorders were assessed by 21-channel electroencephalography recorded both during cognitive testing and during 99mTc-HMPAO single photon emission computed tomography (SPECT). Computed tomography (CT) was performed on the same day. None of the epilepsy-related factors (seizure type, seizure frequency, type of epilepsy, age at onset of the seizures, type of antiepileptic treatment) could be related directly to severity or type of memory impairment (classified into the categories 'global', 'verbal' and 'non-verbal'). Remarkably, this study found no significant relationship between EEG focus localization and severity of measured memory impairment. Most areas with hypoperfusion on the SPECT were found in the group with global (severe) amnesia, typically with a right frontal localization. Abnormalities on CT were predominantly found in the same group, however, with a right-sided parietal localization. An unanticipated finding was that the majority of temporal CT and SPECT lesions were found in the group with relatively better memory performance.

Adult

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.

Aged

[The mechanisms of memory disorders at the stages in its acquisition and fixation].

The blockade of cholinergic system with scopolamine (10 mg/kg) did not impair the process of memory acquisition in rats but disrupted the process of memory fixation or consolidation, the disturbance stemming from the ketamine-blocked ion-channels of nicotinic receptors. Both scopolamine and ketamine impaired the process of memory recall, being more efficient in the case of ketamine. Piracetam (40 mg/kg) diminished the impair of fixation induced with scopolamine but did not affect the ketamine-induced impairment of memory acquisition.

Amnesia

[Memory disorders and symptoms of frontal dysfunction in 29 patients operated on for an aneurysm of the anterior communicating artery].

Twenty-nine patients operated for an aneurysm of the anterior communicating artery have been submitted to short-term and long-term memory tests and to tests said to be sensitive to frontal lobe dysfunction; anosognosia was also studied. Their performance, as compared to that of 29 matched control subjects, revealed: (a) that this neurological condition induces often memory deficits (with anosognosia) and, even more often, signs of frontal dysfunction; (b) that these deficiencies are not homogeneous, however; and (c) that the classical amnesic syndrome can be observed in some cases. It appears useful to make an in-depth analysis of memory deficits of this kind of patients to reach a better understanding of normal memory processes.

Adult

[Exploration of memory disorders in anxiety states].

According to cognitive model of anxiety, memory process in anxious patients is usually tested by comparing the incidental recall of positive and negative, threatening and non threatening, self and other-referenced words. Contrary to expectation, the results indicate relatively poorer memory for threatening material in anxious patients and no bias in favour of the recall of self referent negative words. At the opposite this memory bias can be evidenced in patients with panic disorder. The bias for anxiety words is better evidenced in the subgroups with the higher arousal level or when there is a mood induction by reading first an anxiogenic text. Consistent with prediction a perceptive pre-attentional bias can be shown for the great majority of the subjects studied in recent researches.

Adult

Possible biochemical basis of memory disorder in Alzheimer disease.

Damage to the hippocampal formation, whether focal or diffuse, leads to severe impairment of short-term memory. The most common presenting symptom of Alzheimer disease is loss of short-term memory, and histologically the hippocampus is characteristically affected. Choline acetyltransferase, which is involved in the synthesis of acetylcholine, is depleted in the hippocampus in the disorder. Anticholinergic drugs administered to normal subjects can simulate some aspects of the memory defect seen in Alzheimer disease. It is postulated that damage to a cholinergic neuronal pathway running to or from the hippocampus underlies the memory disorder. This suggestion implies that it may be possible to improve memory in patients with Alzheimer disease by pharmacological means.

Acetylcholine

Language and memory disorders following closed head trauma.

Patients who suffer closed head trauma may demonstrate communication disorders which have been variously described as aplasia, severe memory impairments, traumatic aphasia, or confusion. The memory and language skills of 14 patients who had suffered closed head trauma were documented after they regained ocnsciousness and at one-month intervals for four monts utilizing the Porch Index of Communicative Ability and the Wechsler Memory Scale. Results indicated that patients initially suffered both reduced memory and language skills. After four months, expressive and receptive language skills were grossly functional for conversational purposes, and all memory taskd with the exception of orientation skills were within normal limits. Significant improvement in both language and memory functioning most often occurred during the first month after regaining consciousness, although gradual improvement in both language and memory skills was noted beyond the one-month period. No significant correlations existed between the length of unconsciousness and the initial and final language and memory scores.

Adult

[Multiple sclerosis in children. Impact of memory disorders].

Three cases of multiple sclerosis, characterized by disorders of superior functions such as memory loss, either isolated (1 case) or as part of a frontal syndrome (2 cases) are reported. The importance of these disorders, often presenting as the main symptoms, their good prognosis and their rarity in adulthood are underlined. From a pathophysiologic point of view, the authors discuss the role of the frontal, near the limbic area, localization of the plaques.

Adolescent

[Mental akinesia and memory disorders following carbon monoxide poisoning].

A 32-year old woman presented with serious memory impairment and a mental syndrome named loss of psychic auto-activation or psychic akinesia following carbon monoxide poisoning. The MRI findings were bilateral pallidal lesions probably associated with thalamic lesions. The evolution was favourable.

Adult

[Verbal memory disorders in local lesions of the right and left hemispheres].

Disturbances of verbal memory were examined in patients with local cerebral affections. The patients were asked to reproduce triads of words selected with regard to their semantic (situation or synonymic associations) or sensor (phonetic association) similarity. The ability to reproduce the triads was found to be different depending on the kind of the triads and the pathological focus localization. Patients with the pathological focus in the posterior divisions of the left hemisphere could hardly reproduce the triads of the semantically-similar words, while those with the pathological focus in the posterior divisions of the right hemisphere had difficulties in reproducing the triads of the phonetically-similar words. There were no differences as regards the triad type in patients with the pathological focus localization in the frontal divisions of the left hemisphere. A problem of multi-channel coding of the information for its processing and storage is discussed.

Brain Diseases