Biomedical subjects

N Hebel

Publications and source records attributed to N Hebel.

5 recordsLinked to original sources

PubMed1997

Patterns of oculomotor scanning in patients with unilateral posterior parietal or frontal lobe damage.

Eye movements were recorded during the inspection of dot patterns in control subjects and in patients with acquired unilateral brain damage involving posterior parietal or frontal cortical regions. Normal subjects adapted their oculomotor scanning pattern effectively to the stimulus configuration. Patients' oculomotor scanning patterns were characterized by a rather rigid sequence of fixations and saccades, with no evidence for a systematic and flexible spatio-temporal organization. In a stimulus condition where dots were grouped, patients with frontal damage accurately shifted their gaze between the dot groups, but had difficulties with dot sampling. These observations suggest that the posterior parietal damage mainly affected the visuo-spatial guidance of the scanpath, whereas the frontal damage impaired its planning. It is concluded that both, posterior parietal and frontal brain structures, and their reciprocal connections, are part of a distributed neural network subserving visually-guided oculomotor scanning, and that the spatio-temporal organization of the scanpath depends critically on both structures and their close co-operation.

Adult↗

PubMed1989

[Disorders of learning and memory in focal cerebral tissue lesions].

Memory and learning in man depend on complex cognitive systems, and thus on efficient associative information stores in different neocortical areas of our brain. In addition, phylogenetically older, "limbic" brain structures are needed, in order to manage these huge accociative stores in our telencephalon. This "operating system" manages memory and learning capabilities considering the "milieu interne", and especially biological and individual priorities. Our contribution attempts to sketch the anatomical outlines of this limbic operating system. Two interdependent neuronal networks may be of pivotal importance: 1. a medial limbic loop with Papez circuit as the main structure, and 2. a basolateral limbic loop including the amygdala, the subcallosal area (and the septum verum?) as well as the mediodorsal thalamic nucleus. Based on the anatomical evidence of (largely) selective, i.e. focal brain lesions the likelihood for all these relay stations as memory-related structures is discussed. Our working hypothesis assumes that combined, bilateral lesions of both limbic neuronal networks make severe, global and lasting deficits in memory and learning performance fairly likely. The lesion of only one of these limbic loops seems to cause modality-specific deficits. Unilateral lesions of the retrocommissural hippocampal formation may also account for lasting amnesia.

Brain Damage, Chronic↗

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↗

PubMed1987

[On the posterior infarct].

The article deals with infarctions in the territory of the posterior cerebral arteries. For a better understanding of pathoanatomical and pathogenetical factors influencing posterior cerebral infarctions embryological, orthological and pathological data on the posterior cerebral artery and on its leptomeningeal anastomoses to other cerebral arteries were reported in the first two chapters. Chapter 3 includes a review of findings on the predilection sites for occlusions of the posterior cerebral artery, on the relative incidence and also on pathogenetical factors of posterior cerebral infarctions. The few papers especially dealing with the posterior cerebral infarctions in the CCT were indicated likewise. Chapter 4 contains our own findings on 180 patients with posterior cerebral infarctions, who were all examined with CCT (the slices were done parallel to the fronto-occipital line); data on age, sex and hemispheric distribution of the sample and on combinations with other cerebral infarctions were reported. 159 posterior cerebral infarctions (of 144 patients including 15 with bilateral infarctions) could be described "anatomically". As to the maximum infarction areas referred to 8 defined slice levels, differences to the findings reported so far in the literature were observed; they comprise the (ventro-) lateral borders of the infarction areas including the longitudinal fibre projections (e.g. the optic radiation), the cranial extension of the posterior cerebral infarctions and the splenial as well as thalamic lesions. The posterior cerebral infarctions were classified as uni-territorial, bi-territorial and subtotal subtypes. Among the uni-territorial posterior cerebral infarctions calcarine infarctions outweighed those in the territory of the posterior temporal (temporo-occipital) artery and of the parieto-occipital artery by a ratio of 2:1:1. The overlap areas of the uni-territorial posterior cerebral infarctions are shown in figures. The second, less frequent bi-territorial subtype is a combination of infarctions in the territories of the calcarine and the parieto-occipital arteries. The calcarine, the medio-basal and the subtotal subtype occurred in about 23% of the "anatomically" evaluated posterior cerebral infarctions. At length, thalamic and splenial infarctions associated with any of the subtypes were observed in about a quarter of all posterior cerebral infarctions. As to the subtotal posterior cerebral infarctions additional thalamic and splenial infarctions can be expected in about 40%.

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↗