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Biomedical subjects

D Leys

Publications and source records attributed to D Leys.

At least 19 recordsLinked to original sources

Frontal lobe dysfunction in unilateral lenticulostriate infarcts. Prominent role of cortical lesions.

Most studies on frontal lobe dysfunction (FLD) in patients with striatal lesions did not consider possible associated cortical lesions not seen on computed tomographic scans. To determine the possible role of such cortical lesions, we assessed FLD in 10 patients with unilateral lenticulostriate infarct on computed tomographic scans. Magnetic resonance imaging revealed an associated cortical infarct not seen on computed tomographic scans in four patients. Using a battery of neuropsychological tests sensitive to FLD, we found that (1) the crossed tapping test was the only FLD test significantly disturbed in patients with pure unilateral lenticulostriate infarcts, (2) FLD was only present in patients with associated cortical infarct, and (3) caudate lesions only account for the number of echopraxic errors in the crossed tapping test. We conclude that unilateral isolated lenticulostriate infarcts might not lead to FLD, even though they may disturb the development of strategies involved in motor procedural learning.

Adolescent

Parkinson's disease and basal ganglia calcifications: prevalence and clinico-radiological correlations.

We reviewed computerized tomograms (CT) for basal ganglia and dentate nucleus calcifications in 79 patients with Parkinson's disease (PD), 54 patients with Alzheimer's disease (AD) and 109 controls aged 50 or more. When it was determined, no patient had disturbances in calcium metabolism. We found: (1) 30 subjects out of 242 (12.3%) with calcification located within the lenticular nucleus in 28. (2) Calcifications were unilateral in 11 and asymmetric in 11. (3) The prevalence of calcifications was 21.5% in PD, 9.2% in AD and 7.3% in controls and were significantly more severe in PD than in C and AD (P less than 0.02). (4) PD patients with calcifications were clinically indistinguishable from those without calcification. (5) Calcifications within the basal ganglia were not associated with a levodopa-resistance. We suggest the basal ganglia calcifications are more frequent in PD, but we cannot explain why, since post-synaptic lesions have never been showed in PD.

Aged

Atrophy of medial temporal lobes on MRI in "probable" Alzheimer's disease and normal ageing: diagnostic value and neuropsychological correlates.

Magnetic resonance imaging (MRI) has shown a great reduction in medial temporal lobe and hippocampal volume of patients with Alzheimer's disease as compared to controls. Quantitative volumetric measurements are not yet available for routine clinical use. We investigated whether visual assessment of medial temporal lobe atrophy (MTA) on plain MRI films could distinguish patients with Alzheimer's disease (n = 21) from age matched controls (n = 21). The degree of MTA was ascertained with a ranking procedure and validated by linear measurements of the medial temporal lobe including the hippocampal formation and surrounding spaces occupied by cerebrospinal fluid. Patients with Alzheimer's disease showed a significantly higher degree of subjectively assessed MTA than controls (p = 0.0005). Linear measurements correlated highly with subjective assessment of MTA and also showed significant differences between groups. Ventricular indices did not differ significantly between groups. In Alzheimer's disease patients the degree of MTA correlated significantly with scores on the mini-mental state examination and memory tests, but poorly with mental speed tests. This study shows that MTA may be assessed quickly and easily with plain MRI films. MTA shown on MRI strongly supports the clinical diagnosis of Alzheimer's disease, is related to memory function, and seems to occur earlier in the disease process than does generalised brain atrophy.

Aged

Prevalence and significance of hyperdense middle cerebral artery in acute stroke.

BACKGROUND AND PURPOSE: Early noncontrast computed tomographic scans may visualize a hyperdense middle cerebral artery before the infarct becomes visible. This sign disappears within a few days, corresponds to the clot itself, and might be associated with a poor prognosis. The aim of the study was to determine its prevalence, diagnostic value, relationship to demographic data, ability to separate embolic from nonembolic causes, short-term prognostic value, evolution over time, and relationship to arterial occlusion on angiography. METHODS: We performed this study using computed tomographic scans performed within 12 hours after onset in 272 consecutive unselected patients with a first acute cerebrovascular event. RESULTS: Seventy-three subjects had the hyperdense middle cerebral artery sign, leading to a prevalence of 26.8% in the whole group and 41.2% in patients with a middle cerebral artery infarct. Specificity was 100%, but sensitivity was only 30%. This sign was not dependent on cerebrovascular risk factors, but was more likely to occur in cortical and in large, deep, middle cerebral artery infarcts (p less than 0.01). It provided only a 3.5% gain in predicting death, and one fifth of patients with the sign recovered within 2 weeks; this sign was not an independent variable of poor outcome on multiple linear regression. It spontaneously disappeared within a few days and was always related to an occlusion of the middle cerebral artery in patients who underwent early angiography. CONCLUSIONS: The hyperdense middle cerebral artery sign is useful in the diagnosis of middle cerebral artery occlusion but does not always predict a poor prognosis.

Acute Disease

[Mixed pre- and postsynaptic neuromuscular block].

We report a new case of neuromuscular block overlap between Myasthenia Gravis and Eaton-Lambert syndrome. A 64-year-old man with a 4-months history of gait disturbance was admitted for ophthalmoplegia worsening during exercise and decreasing at rest. Clinical examination after exercise, revealed limbs weakness and areflexia, palsy of the left eye abduction and a left ptosis. The level of anti-acetylcholin-receptor antibodies was high. Electrophysiological explorations revealed a decrement at 3 Hz and a increment at 30 Hz, with a reduction in amplitude of the initial motor potential. This patient improved under a combination of guanidine and anticholinesterase drugs. From this case and 9 previously reported cases, we propose 4 criteria for the diagnosis of such neuromuscular blocks: 1) exercising symptoms and signs, including areflexia, 2) presence of anti-acetylcholin-receptor antibodies, 3) reduction of the amplitude of the initial motor potential, with a decrement at 3 Hz, and an increment at 30 Hz, and 4) clinical and electrophysiological improvement under guanidine and anticholinesterasic drugs therapy.

Cholinesterase Inhibitors

[Multiple cerebral hemorrhage and amyloid angiopathy of the white matter in a case of Alzheimer's disease].

Amyloid angiopathy is a common pathological finding in Alzheimer's disease. It usually involves leptomeningeal and cortical vessels but spares the white matter. It may cause lobar cerebral hemorrhages at a late stage of the disease. We report a case of Alzheimer's disease at an early stage with diffuse lesions of amyloid angiopathy including some within the white matter, apparently responsible for 2 deep and 1 superficial cerebral hemorrhages.

Alzheimer Disease

Juvenile distal cerebral ischemia: angiographic features. A study of 55 cases.

This study of juvenile distal cerebral ischaemia is based on 55 patients aged from 18 to 30 years. The authors describe the circumstances of discovery, as well as the clinical features and the course of the disease which may be severe and lead to non-resolutive neurological accidents and sometimes dementia. Paraclinical evaluation includes capillaroscopy, finger and toe pads biopsy (which clearly shows a pathological process with fibrocellular promontories narrowing the lumen of arterioles), and above all angiography which displays two typical signs: arterial narrowness and bands of peripheral ischaemia. In advanced forms of the disease angiography reveals classical signs of ischaemic lesions, but charateritically these are very distal. Associated abnormalities of the carotid siphon can also be found. Finally, positive CT scans show an isolated widening of the sulci which is fairly suggestive of the disease.

Adolescent

Early hypopituitarism following cavernous sinus thrombosis: total recovery within 1 year.

Hypopituitarism related to cavernous sinus thrombosis is a very rare event which usually occurs at least 1 year after the acute stage. We report a case which distinguished itself from the previously reported cases through (i) its occurrence during the acute stage and (ii) its total recovery within 1 year. Early anterior hypopituitarism is probably more frequent than expected on the basis of reported cases and it may contribute to the high rate of mortality in cavernous sinus thrombosis. This underscores the need to consider hypopituitarism in every patient with cavernous sinus thrombosis.

Adult

Could Wallerian degeneration contribute to "leuko-araiosis" in subjects free of any vascular disorder?

To determine the possible role of Wallerian degeneration secondary to the grey matter neuronal loss in the pathogenesis of "leuko-araiosis", computerised tomography (CT) of the brain was studied in 98 normotensive and non diabetic subjects free of cardiac diseases: 32 with Alzheimer's disease, 36 with Parkinson's disease, eight with progressive supranuclear palsy, and 22 controls. In Alzheimer's disease, leuko-araiosis scores were greater than in control subjects. Leuko-araiosis was more prominent in anterior periventricular areas in Parkinson's disease and progressive supranuclear palsy, and in posterior periventricular areas in Alzheimer's disease. In two patients with Alzheimer's disease and leuko-araiosis, necropsy revealed diffuse white matter pallor, mild fibrillary astrocytosis, and in one patient limited hyaline thickening of small white matter vessels, without any infarction or hypertensive change. Changes were more severe in white matter close to cortical areas with a great density of neurofibrillary tangles. Leuko-araiosis was more severe or more widespread in Alzheimer's disease than in Parkinson's disease, progressive supranuclear palsy and normal ageing. Differences in the location of leuko-araiosis between the four groups might be due to differences in the location of the grey matter disorder and Wallerian degeneration rather than amyloid in Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy and normal ageing. Wallerian degeneration might be another cause of leuko-araiosis in neuro-degenerative disorders beside previously reported extra-cerebral predisposing factors and amyloid angiopathy.

Aged

Monosporium apiospermum meningoencephalitis: a clinico-pathological case.

Twenty nine cases of central nervous system infection due to Monosporium apiospermum have been reported. Six of them occurred after an aspiration pneumonia following a near drowning. The case of a 53 year old man is reported: M apiospermum was isolated from cerebrospinal fluid, sputum, urine and from the mud of the ditch where the patient had fallen. Though the treatment used recommended doses of intravenous, intrathecal and intraventricular amphotericin B, it was ineffective and the patient died 97 days after the near drowning. Necropsy showed that the ventricular infectious process was more prominent distant from the antifungal ventricular source.

Brain

[Parkinsonian syndrome caused by carbon monoxide poisoning. Preliminary results of the treatment with bromocriptine].

Parkinsonism is the most frequent neurological complication of carbon monoxide intoxication. Its prognosis is severe and Dopa is ineffective. We treated 9 patients (mean age 60.89 +/- 6.10 years) with bromocriptine (5 à 30 mg daily). Webster's scores were improved under treatment. Our study suggests that early administration of bromocriptine might be an effective therapy of carbon monoxide induced parkinsonism.

Adult

[Right unilateral auditory agnosia following left lenticular hemorrhage].

A 33-year old patient who had had left lenticular hemorrhage presented with an inability to understand with the right ear oral language and, in a less dramatic way, nonverbal sounds. This unilateral auditory agnosia was first associated with a right motor underutilization and right motor, sensitive, visual and auditive extinctions. Speech discrimination scores were 100% with the left ear and 15% with the right ear, even less in dichotic conditions. Tonal audiogram, as well as early and late components of the auditory evoked potentials were normal. Cerebral regional perfusion and metabolism were impaired over the left parietotemporal area. There was severe hypoactivation of the left hemisphere with right monaural verbal stimulations. Rehabilitation consisting of non-specific attention tasks and repetitions of words reaching only the right ear was undertaken 15 months after the stroke. The oral language comprehension improved, as did the left hemisphere activation, and the extinction phenomena disappeared, except for the auditory one. The unilaterality of the auditory agnosia could be due, in part, to a peculiar physiological processing in this patient, such as poor performance of his right ipsilateral auditory pathway which could be improved with practice. A striatal lesion could induce a spatial hemi-inattention as reflected by the multimodal extinction in this case. Besides, a lack of selective activation for verbal stimulation of the left hemisphere is suggested.

Adult