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Biomedical subjects

F Viader

Publications and source records attributed to F Viader.

At least 37 records · Page 2Linked to original sources
PubMed1988

[Alzheimer's disease with early association of a hemi-parkinsonian syndrome].

A 66 year-old woman presented with severe memory disorders followed several months later with tremor of Parkinsonian type of the right upper limb totally relieved by treatment with levodopa-benserazide. Four years later she was admitted with memory disturbances, temporospatial disorientation, constructional and ideatory apraxia, dressing apraxia and language difficulties. Eight years later she had become bed-ridden, with deviation of head and eyes towards the left, hypertonus tremor and stereotyped movements. Neuropathologic examination showed neuronal loss in substantia nigra and left locus ceruleus, dorsal nucleus of the pneumogastric nerve and Meynert's basal nuclei on both sides. Neurofibrillary tangles affected the peri-aqueductal grey matter and Lewy's bodies were observed in the substantia nigra. Neurofibrillary tangles and granulovacuolar degeneration together with senile plaques were numerous in the hippocampus, but senile plaques and neurofibrillary tangles were rare in the remainder of the cortex. Combined Alzheimer's disease and Parkinson's disease could be due to simple coincidence, one of the diseases possibly predisposing to the appearance of the other.

Aged↗
PubMed1988

[Crying provoked by sound stimuli in a case of probable dementia of Alzheimer's type].

A case of pathological crying elicited only by non-verbal auditory stimulations in a woman with probable dementia of the Alzheimer type is reported. As neuropsychological data available in this case have suggested a greater involvement of left than right temporal cortex, the authors propose that the crying phenomenon could have been explained by a similar inter-hemispheric asymmetry in pathological involvement of the limbic structures.

Acoustic Stimulation↗
PubMed1987

[Study of the cerebral blood flow by intravenous injection of xenon-133 in thalamic and juxtathalamic lesions].

Sixteen patients with subcortical vascular lesions of one hemisphere, (7 left, including 4 aphasics and 9 right, 4 of which had a left neglect syndrome) and 4 controls without noticeable cerebral pathology underwent cerebral blood flow (CBF) measurements with intra-venous Xe 133, both at rest and during activation. The latter consisted of listening to a text together with eye opening and was considered non specific. At rest, a non significant CBF lowering on the side of the lesion was found in most patients, mainly in right brain damaged ones. Hypoperfusion areas (HA) were noted, predominantly in parieto-temporal cortex in right lesions, and in lower and middle frontal areas as well in left lesions. HA persisted during activation on both sides, except on the right side in left damaged patients. Activation resulted in a bilateral and roughly symmetrical mean CBF increase, which was not significant in left lesions nor in controls, but was significant (p less than .05) in right brain damaged patients without neglect syndrome. Conversely, patients with right lesions resulting in left neglect exhibited conspicuous mean CBF asymmetry during activation with depression on the right side. Right-left difference in mean CBF was significantly higher in this group than in right sided lesions without neglect (p less than .05). These facts are consistent with an activation imbalance between hemispheres as the mechanism of unilateral neglect syndromes, and support the view that right subcortical pathways and especially the thalamus, play a part in the activation of both cerebral hemispheres.

Adult↗
PubMed1987

[A case of aphasia with speech disorders by infarction of the left caudate nucleus and putamen].

An infarction involving the left putamen, caudate nucleus and the anterior limb of the internal capsule, resulted in aphasia with semantic paraphasias, verbal incoherence and verbal memory impairment. Cerebral blood flow (CBF) studies with 133Xe inhalation at 20 days post onset showed, on one hand, a bilateral lowering of cortical blood flow and on the other hand a left frontal-parietal hypoperfusion area. Spontaneous recovery occurred within 2 months. While the mean CBF became normal at 14 months post onset, a relative hypoperfusion area persisted on the anterior left hemispheric cortex. On the basis of these findings and current CBF and metabolic studies carried out in patients with subcortical lesions, the authors discuss the role of cortical and subcortical structures in subcortical aphasic syndromes. The importance of reciprocal connections between cortex, striatum and thalamus is stressed.

Aphasia↗
PubMed1987

[Hemodynamic study of obstructive lesions of the internal carotid artery: value of coupled measurement of regional cerebral blood flow and volume].

A study of 130 patients having presented either a transient ischemic attack or a completed stroke, or admitted for an asymptomatic carotid stenosis, allowed the following investigations: CT-scan, doppler, angiography, measurement of the regional cerebral blood flow (rCBF) by the study of 133Xe clearance (Novocerebrograph (R)), and measurement of the regional cerebral blood volume (rCBV) made by gamma emission tomography after autotransfusion of 99m Tc-labeled erythrocytes with an Elscint Apex 415 ECT (R) camera. Our aim was to look in which case a rCBF and/or a rCBV interhemispheric asymmetry was observed, by comparing the previous hemodynamic parameters with clinical, CT-scan and angiographic data. Although a rCBF and/or a rCBV asymmetry appeared more often among patients presenting with infarction than among those of the asymptomatic category, this does not seem specific for any clinical grade. The same statement applies to the comparison between hemodynamic parameters and CT data. The arterial lesions were classified in 4 groups: no stenosis (12 cases), uni or bilateral moderate carotid stenosis (40 cases), unilateral severe carotid stenosis or occlusion (65 cases), bilateral carotid severe stenosis or occlusion (13 cases). We observed a rCBF asymmetry among some patients in the 4 groups, although this was more frequent among the two latter groups. Nevertheless no case of a rCBV asymmetry was observed in the 2 first groups. Such an asymmetry was present in 31 percent of the patients belonging to the two latter groups. In patients of the third group the asymmetry was always due to a relative increase of rCBV beyond the carotid lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial Occlusive Diseases↗
PubMed1987

[Peripheral neuropathy in severe mixed cryoglobulinemia syndrome].

A syndrome of polyneuropathy and cryoglobinemia is reported in a 76-year-old woman. Nerve biopsy showed severe demyelination and vascular involvement was demonstrated in a muscle biopsy. Peripheral neuropathy is discussed in the context of the Gougerot-Sjögren syndrome, associated with cryoglobins in the blood. Prompt treatment of this disease should be initiated and consists mainly of plasmapheresis.

Aged↗
PubMed1986

Subcortical neglect.

The unilateral neglect syndrome is defined as a lack of directed attention to one half of the space or the body. It has been reported mainly after cortical lesions of the right parietal or frontal lobe in man. However, there is strong experimental and clinical evidence for the existence of neglect syndromes of subcortical origin. The unilateral neglect syndrome is not the result of elementary sensory deficits. The failure in directed attention is dependent on an imbalance of hemispheric activation.

Aged↗
PubMed1986

[Thalamic neglect].

Thalamic lesions can provoke negligence behavior with various, sometimes dissociated manifestations: motor negligence or reduction in use of one half of the body whatever the direction of the gesture or the half-space in which it occurs; extinction phenomena demonstrated without difficulty for visual, somatesthetic and auditory modalities; spatial negligence involving attentional and intentional components, often difficult to distinguish. Negligence of this type is mainly the result of right sided lesions, with several non-exclusive explanations: natural predominance of the left hemisphere, activating role of language with respect to the left hemisphere, capacity of the right hemisphere to be "attentive" to bath half-spaces in contrast to the left hemisphere, attentive to the right half-space only.

Aged↗
PubMed1985

Subcortical dementia. Frontal cortex hypometabolism detected by positron tomography in patients with progressive supranuclear palsy.

The dementia associated with progressive supranuclear palsy (PSP) is considered to be subcortical because the cerebral cortex, unlike the subcortical structures, is usually free from major neuropathological lesions; the characteristic symptoms point to a dysfunction of the prefrontal lobe. The regional cerebral metabolic rate of glucose (rCMR Glu) was studied by positron emission tomography and 18F-fluoro-2-deoxyglucose18FDG in 6 patients presumed to have PSP and was compared with values found in 8 control subjects of similar age. The results obtained showed a highly significant rCMR Glu decrease in the prefrontal cortex of our patients. The loss of several subcortical afferents to prefrontal cortex may be responsible for the frontal cortical hypometabolism present in PSP.

Aged↗
PubMed1985

[Lead encephalopathy with thrombosis of the superior longitudinal sinus].

A 32 year old obese, diabetic and hypertensive woman presented with signs of increasing intracranial pressure: diplopia, partial lateralised Jacksonian seizures followed by alternating post-ictal hemiplegia. She was also anaemic. Investigation revealed lead poisoning and thrombosis of the superior sagittal sinus. She recovered rapidly with heparin and calcium EDTA therapy, except for persistent optic atrophy due to the papilloedema. The authors discuss the relation of lead encephalopathy and dural sinus thrombosis, and the contribution of each condition to this patient's clinical symptoms.

Adult↗
PubMed1985

[Frontal syndrome of progressive supranuclear palsy].

Neuropsychological findings in 10 clinical cases of progressive supranuclear palsy are presented. Patients were aged 52 to 80 and the duration of their illness was 1 to 5 years. Severe psychological disturbances e.g. depression or outbursts of irritability were prominent features in 5 patients. Formal neuropsychological testing disclosed mental slowing, impaired attention, reduced verbal fluency and elaborated linguistic abilities, poor abstract thinking and reasoning, mild to moderate memory loss, dynamic apraxia, grasping, motor impersistence, imitation and utilization behaviour. The clinical similarities between these neuropsychological changes and frontal lobe syndromes, together with the lack of cortical involvement, suggest that the "dementia" of progressive supranuclear palsy could be explained by deactivation of the frontal cortex by subcortical lesions. The special importance of pallidal and mesencephalic reticular involvement in the syndrome is hypothetized.

Aged↗