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Biomedical subjects

U Schuri

Publications and source records attributed to U Schuri.

17 recordsLinked to original sources
PubMed1999

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.

Amnesia↗
PubMed1997

Time estimation as a neuronal network property: a lesion study.

The neural substrate of estimating short temporal intervals is still unknown. We investigated the ability of patients with infarctions of the middle cerebral artery of either the left or the right hemisphere to estimate verbally and produce time intervals of seconds by counting. Patients showed long-lasting and stable deficits in time estimation in both methods, with either extreme acceleration or deceleration in apparent time compared with healthy controls. A lesion of the posterior part of the supralenticular white matter proved to be responsible for these deficits. Disruption of interneuronal communication therefore leads to a lasting alteration of a learned time-pacing synchronized to conventional time units.

Adult↗
PubMed1993

The possible contribution of the septal region to memory.

A particularly well-documented, intelligent patient (H.I.) with very selective, minute, but most likely bilateral damage of the basal forebrain including the septal region is presented. Though behavioral progress was found for a number of areas, she remained deficient, especially in long-term memory. The severest and largely modality-nonspecific deficits were observed in recall (as opposed to recognition) situations. As a peculiar finding which we would attribute to septal damage, H.I. was mainly affected in tests containing emotional (especially emotionally negative) stimuli, or certain flavours. While this involvement might have helped her in memorizing material judged as positive, it was of negative influence under other circumstances. The septal area may serve as an interface contributing a specific combination of emotional flavour and evaluating (feedback) judgement to a larger (septo-hippocampal-amygdalar) memory and learning processing network.

Affective Symptoms↗
PubMed1993

Mnestic performance profile of a bilateral diencephalic infarct patient with preserved intelligence and severe amnesic disturbances.

The case of a patient with above-average intelligence and educational background, high motivation, and an approximate IQ-MQ difference of 40 points is documented. The patient has been examined repeatedly for nearly a decade. Extensive neuroradiological material of his focal bilateral brain damage in the dorsal diencephalon is available. A widespread range of cognitive tests was used to investigate his actual performance on all relevant aspects of intelligence, attention, subjective memory, immediate retention, learning, skill and problem solving abilities, concept formation, cognitive flexibility, priming, constructional ability, retrograde memory, and long-term retention. The total of more than 50 tests included German-language forms of the revised Wechsler Memory Scale and of the Rivermead Behavioural Memory Test. The patient's short-term memory and attention were, in spite of his advanced years, average or well above average. He gave a number of examples of still intact skills and implicit memory abilities, though there was no uniformity in his performance on implicit memory tests (e.g., with respect to stored vs. new implicit information). He had no awareness of his severe anterograde and retrograde amnesia, documented over a large range of verbal and figural tests. Taken together, the results from our patient confirm the principal dichotomy between declarative and nondeclarative mnestic functions, but give evidence for some restrictions as well. They furthermore demonstrate that focal diencephalic damage may result in profound anterograde and selective retrograde amnesia, especially with respect to data-based material, and that disconnecting portions of the medial and basolateral limbic circuits has devastating consequences on memory.

Aged↗
PubMed1992

The septo-hippocampal pathways and their relevance to human memory: a case report.

The interaction between the septal region and the hippocampal formation appears indispensable for the maintenance of normal memory and learning mechanisms in humans. The disruption of some combination of septo-hippocampal pathways, especially the disruption of the "dorsal route", deteriorates explicit memory functions. The case of a 25-year-old male patient is presented who developed anterograde and to a certain extent retrograde amnesia following rupture and repair of an arteriovenous malformation in the atrium of the left ventricle. A left-sided lesion of the dorsal route involving the posterior cingulate bundle, the longitudinal striae (as part of the supracommissural hippocampus) and the fornix appeared responsible for his mnemonic deficits. The implications of these findings for the understanding of other clinical cases, particularly those with lesions of the septal region, the anterior and posterior singular gyrus/cingulate bundle and the fornix are discussed.

Adult↗
PubMed1988

Verbal memory and learning in unilateral posterior cerebral infarction. A report on 30 cases.

Unilateral posterior cerebral infarction, sparing memory-related structures in the diencephalon, may represent a means of investigating the role of hippocampal afferents and the parahippocampal areas in memory processing. Among 30 patients with unilateral posterior cerebral infarction a group of 12 subjects with left-sided lesions suffered from marked verbal memory and learning dysfunction, whereas the remaining subjects with left or right-sided lesions showed no obvious memory deficit. The impairment was most prominent for verbal learning tasks, while recall of isolated and complex verbal information appeared to be less affected. In some cases the memory disturbance could be detected up to one year after the causative event. Analysis by CT scanning revealed a coincidence of mnestic disturbances with lesions around the left collateral sulcus affecting the posterior parahippocampal gyrus and the collateral isthmus. The latter term refers to the fibre stem of the medial temporal lobe limited by the floor of the lateral ventricle and the depth of the collateral sulcus. Through this bottle-neck, bidirectional fibres run between the posterior parahippocampal gyrus and different sensory-specific and multimodal association areas. A lesion within the collateral isthmus or, more particularly, a combined lesion of the collateral isthmus and the posterior parahippocampal gyrus, deprives the hippocampus itself of its main afferent projection source and, on the other hand, prevents dissemination of the hippocampal output to widespread neocortical areas. It cannot be excluded, at least in some cases, that small lesions in the fimbria-fornix route, in the retrosplenial cortex or in the hippocampal formation itself also contribute to the memory and learning dysfunction. However, these small lesions, so far as they could be detected by CT scanning, were present in patients with and without memory disturbances.

Adult↗
PubMed1985

A contribution to the anatomical basis of thalamic amnesia.

Damage to diencephalic structures is stated to give rise to memory dysfunction. Amnesia is likely to occur following vascular lesions in the ventral portion of the thalamus. The CT findings of 6 of our own cases and 5 patients reported in the literature, all with selective vascular lesions of the thalamus, were studied to determine the critical structures involved in human memory processes more closely. Thalamic amnesia probably depends on intrathalamic white matter lesions more than on nuclear lesions. The mamillothalamic tract and the ventral portion of the lamina medullaris interna are the most likely candidates in the mediation of memory processes and a combined lesion of these structures may be responsible for thalamic amnesia in man. Two patients without significant memory dysfunction had lesions in the ventrobasal portion of the mediodorsal nucleus sparing the mamillothalamic tract and the ventral part of the lamina medullaris interna. Our findings correspond well with the understanding of amnesia as a 'disconnection syndrome' stressed recently by Warrington and Weiskrantz (1982) and with Mishkin's (1982) model of the memory system in monkeys.

Aged↗
PubMed1982

Electrodermal response patterns in neurological patients with disturbed vigilance.

In 18 neurological patients with severely disturbed vigilance and 18 healthy subjects, electrodermal responses to acoustic stimuli were elicited. There were substantial differences between both groups in the temporal patterning of electrodermal responses. Patients reacted significantly less on initial trials than healthy subjects and exhibited their maximal responses on later trials. This response pattern is interpreted as reflecting changes in activation.

Acoustic Stimulation↗
PubMed1980

The Vigilance Scale: an analysis of elicited behavioral responses.

The Vigilance Scale (VS) is a 12-step additive (Guttman scale) that allows assessment of the behavioral deficit in the unconscious state and the state of clouding of consciousness. Despite restrictions on its applicability, which are discussed in detail, the VS seems to be a useful measuring device that indicates the level of brain function a patient with a disturbance of consciousness can actually attain. There are two categories of scale errors to be found, the first being caused by various "instrumental" disorders, i.e., severe motor deficits, the second resulting from the probabilistic approach of the VS to a Guttman scale.

Adolescent↗
PubMed1979

Spontaneous activity of autonomic functions in coma due to drug overdose.

Spontaneous heart rate, respiration rate and electrodermal activity were studied in 32 patients with different grades of severe poisoning by ingestion of various drugs. The degree of their behavioural impairment was determined with the Munich Coma Scale (MCS) which measures stimulus evoked somatomotor responses. There was a significant reduction of spontaneous variations of heart rate and respiration rate with increasing severity of coma. Spontaneous electrodermal fluctuations were present only at the least severe grades of impairment. Thus, cardiorespiratory and electrodermal activity can provide significant information on the level of behavioural impairment in severe poisoning.

Adolescent↗
PubMed1979

Autonomic responses to meaningful and non-meaningful auditory stimuli in coma.

In a group of poisoned patients, the lowest MCS (Munich Coma Scale) vigilance grade at which patients responded when called by their names was determined. In 12 patients at this vigilance grade, the extent to which the meaning of the names contributed to their reactions was investigated. Their first name and a control stimulus (name backwards) were repeatedly presented via headphones. Stimulus intensity was 90 dB(A). During stimulus presentation, changes in heart rate, finger pulse amplitude, and electrodermal activity were recorded. A comparison between responses under both stimulus conditions revealed that the first reactions of poisoned patients to their names are primarily elicited by the physical properties of the stimulus.

Acoustic Stimulation↗