Biomedical subjects
Publications and source records attributed to J Cambier.
Electro-oculographic recordings in a patient with an oculomotor disorder due to hemorrhage of the vermis showed macrosaccadic oscillations. Data from reported cases suggest the specific significance of this type of disorder for acute cerebellar lesions.
Both thresholds of nociceptive flexion reflex and pain sensation were studied in 6 normal subjects and in 6 patients with typical thalamic pain. In these patients, on the painful side, these thresholds were found increased (98 p. 100; 89 p. 100 respectively) compared to the normal side. Values obtained in this latter did not significantly differ from those observed in normal subjects. After 8 days of indalpine treatment, the nociceptive reflex threshold was furthered increased in the painful side while the pain threshold was not modified by this drug. In the normal side, changes observed after indalpine were similar to that obtained in normal subjects. All the indalpine-induced modifications were reversed by naloxone in both patients and normals. These results are discussed in the context of the possible mechanisms of thalamic hyperpathia.
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.
27 cases of patients who presented language disorders of aphasic nature consecutive to a strictly subcortical lesion of vascular origin are reported. From a topographic point of view, the population is divided into 3 groups: thalamic lesions (15 cases), striatal lesions (9 cases), isolated lesions of the white matter (3 cases). The results of the neurolinguistic analysis of the aphasia show a great symptomatological variety. Nevertheless, in spite of this apparent diversity, certain semiologic elements appear to be common to all of the observed linguistic profiles, no matter where the lesion is: hypophonia, non fluent speech, verbal paraphasias, normal repetition, comprehension generally good. A discussion is proposed as to the specific part which certain structures, notably the thalamus, might play in the origin of these various disturbances.
Stenotic lesions of the cervical arteries due to atherosclerosis or irradiation may provoke the development of a Moya-Moya type collateral network. Rupture of a vessel participating in this collateral circulation may be the cause of a hemorrhagic accident. The hemorrhage may be subarachnoid, intracerebral or more usually intraventricular. Intraventricular hemorrhage occurred in a patient who had developed a Moya-Moya type collateral circulation secondary to atherosclerotic stenosis of a carotid artery. The hemorrhagic incident occurred during carotid endarterectomy, suggesting a predisposing role for hemodynamic modifications resulting from the operation.
In a patient with a history of sudden onset of an isolated sensory syndrome of the right side of the body the sensory deficit was exclusively related to lemniscal sensitivity. NMR imaging showed a small hemorrhage in the left paramedian portion of the pontine tegmentum, corresponding precisely to the location of the median lemniscus.
The anterior choroidal artery syndrome is extremely rare. When complete, it includes hemiplegia, hemianaesthesia and homonymous lateral hemianopsia. The diagnosis is provided by computerized tomography which shows a low-density area located in the posterior part of the posterior limb of the internal capsule, sparing the thalamus medially but involving the tip of the pallidum externally and corresponding to the territory of the anterior choroidal artery. Incomplete forms of the syndrome have been described. The syndrome may also be associated with neuropsychological disorders, including left neglect syndrome in right-sided lesions and disorders of speech in left-sided lesions. The anatomico-clinical correlations are discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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.
In newborn rats, passive immunity is acquired from the mother by selective transport across the gut wall of immunoglobulin (IgG) present in colostrum and milk. Ultrastructural and physiologic studies of this mechanism have shown that the binding and uptake of IgG exhibits saturation kinetics and stereochemical specificity consistent with it being a receptor-mediated process. We report here the isolation and purification of a protein from membranes of neonatal rat enterocytes that binds immunoglobulins. The basis of our purification procedure is the extraction of this IgG-binding protein from isolated membranes in the absence of detergents and its biospecific elution from an IgG affinity column. This purified protein consists of two similar polypeptides of 52,000 and 48,000 Mr. The interaction of this purified protein with immunoglobulin is isotype dependent, with specificity for IgG and its Fc fragment, and pH dependent, with optimal binding at the intraluminal pH of 6.0. This intestinal IgG-binding protein is found in enterocytes of the proximal intestine during the early postnatal period, but is absent after weaning when transport of IgG ceases. Our results suggest that this purified intestinal IgG-binding protein functions in the transepithelial transport of IgG in rat neonates.
A 74 year-old woman was admitted with a right hemiplegia resulting from a left infarct that had totally destroyed the territory supplied by the middle and anterior cerebral arteries. The patient presented with anosognosia and hemiasomatognosia and negligence of the right half-field. She was aprosodic, not aphasic, and there was a severe apraxia and total agraphia. These neuropsychological disorders are discussed in relation to the contradictory data relative to the manual lateralization of the patient. Findings in this case of a "crossed apraxia" show that management of language and of the propositional gestures are not necessarily ensured by the same hemisphere. It also appears that manual preference may be a poor clue for interpretation in terms of functional lateralization.
CT showed a rapid and almost total regression of the lesions of a primary cerebral lymphoma during corticoid therapy. Such results assists the evaluation of changes provoked by radiotherapy and chemotherapy, since corticoids are often combined with these treatments.
Anticoagulant treatment after cerebral infarcts is still debated due to the imperfectly evaluated risk of hemorrhagic transformation. In the case reported here the hemorrhage developed during anticoagulant treatment instituted 18 days after the onset of the infarct. The role of previously administered aspirin is discussed.
A 24 year-old man experienced a left retrobulbar neuritis which improved completely after 2 months of non-steroid antiinflammatory therapy. One month after the end of the treatment he developed a Korsakoff-like amnestic syndrome. Three months later he complained of horizontal diplopia. A CT Scan showed a diffuse enhancement of the periventricular areas, corpus callosum and fornix. Diplopia and CT scan abnormalities disappeared after the administration of tetracosactide. Subsequently a progressive worsening of the neurological condition developed, including a 1 1/2 syndrome of Fisher. In C.S.F. proteins ranged from 35 to 66 mg/dl, gammaglobulins from 4 to 5 per cent, cells from 2.2 to 6.8 per mm3 without abnormal cells. Rounded areas of enhancement were observed on CT scan in pons and right occipital lobe. Usual biological tests, abdominal echography and lymphography were normal. Death occurred 15 months after the onset of symptoms. Neuropathological examination showed: 1) a cerebral lymphoma of probable B origin with distinct masses in right occipital lobe and pontine tegmentum and a more diffuse perivascular infiltration on the left side in the amygdaloid nucleus, fourth temporal gyrus, sublenticular area, hypothalamus and in the right internal capsule; 2) multiple small clear-cut foci of demyelination with myelin-axonal dissociation bilaterally in the optic pathways, periventricular regions, corona radiata, cerebral and cerebellar white matter, sublenticular areas, temporal lobes, splenium of the corpus callosum and fornices with secondary atrophy of the mamillary bodies. Both recent and old plaques were observed. Inflammatory perivascular cuffing, when present, consisted of small nontumoral lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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.
Explore the source record for details and available documents.