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Biomedical subjects

J Cambier

Publications and source records attributed to J Cambier.

At least 55 records · Page 3Linked to original sources
PubMed1990

Positron emission tomography study in progressive supranuclear palsy. Brain hypometabolic pattern and clinicometabolic correlations.

In 41 patients with progressive supranuclear palsy (PSP) that was diagnosed on the basis of eight clinical criteria (25 patients with all eight criteria [probable PSP] and 16 with six or seven criteria [possible PSP]), we studied cerebral energy metabolism by using positron emission tomography and the fludeoxyglucose F 18 or the oxygen 15 method. Compared with age-matched controls, each of the cortical and subcortical metabolic values was significantly reduced, with a predominance in the frontal cortex, in both groups of patients with probable and possible PSP, without a difference between these two groups, suggesting similar underlying disease. The frontal metabolic value decreased with disease duration, but the relative frontal hypometabolism (expressed as the fronto-occipital metabolic ratio) was apparently already present in the early stages of the disease. The parkinsonian motor score was correlated with the caudate and thalamic metabolic values. The intellectual deterioration index was significantly correlated with both the frontal and the nonfrontal metabolic values. Finally, the frontal neuropsychological score was significantly correlated with only the fronto-occipital metabolic ratio. Hence, in PSP, a degenerative brain disease with subcortical lesions, the prominent frontal lobe-like syndrome essentially depends on the relative hypometabolism of the frontal cortex.

Aged↗
PubMed1990

[Improvement of Joseph's disease with sulfamethazole-trimethoprim].

A case of Joseph's disease characterized by spasticity in all 4 limbs, dystonia and disorders of ocular motility was considerably improved by cotrimoxazole, which confirms a recently published case. Further studies are required to establish this therapeutic effectiveness.

Adult↗
PubMed1989

[Physiopathologic mechanisms of coma].

The occurrence of coma betrays a deficiency of the ascending reticular activating system (ARAS) of the brain stem, which constitutes the neurophysiological support of wakefulness. Multiple factors, acting separately or jointly, may be responsible for coma. They include diffuse lesions or circumscribed lesions with repercussions on the ARAS metabolic and toxic factors, intracranial hypertension, cerebral oedema, epileptic activity, and so forth. Owing to the influence it exerts on the management of coma, the physiopathological approach is as necessary as the aetiological approach.

Brain Diseases↗
PubMed1989

[Cranial pachymeningitis of unknown origin. Study of 3 cases].

The clinical picture in three cases of chronic cranial pachymeningitis of unknown origin was dominated by headache, disturbed balance, a confusional state and cranial nerve lesions. The erythrocyte sedimentation rate was increased and the CSF showed inflammatory changes. CT scan imaging showed thickening of the tentorium cerebelli, which took up contrast intensely. Meningeal biopsy showed the dura-mater to be the site of a non-specific inflammatory process. No precise cause was found. Clinical manifestations in these three patients were remarkably corticosensitive but lesions did not regress on CT. The development of a state of corticodependence led to an attempt at treatment with radiotherapy and/or azathioprine, but follow up is insufficient to evaluate results.

Adult↗
PubMed1989

[Visual object agnosia: current conceptions].

Visual agnosia for objects is a difficulty in recognizing objects presented visually. This difficulty can not be explained by a mental deterioration, a disorder of attention or a lack of familiarity with the object. Two criteria are essential but disputed: the absence of visual sensory difficulty necessary for adequate perception; possible recognition of the object by another sensory modality. An object is characterized by a triple representation: formal, semantic, lexical. The clinical, cognitive, pathophysiological analysis lead to distinguish 3 types of visual agnosia. 1) Aperceptive visual agnosia: patients see badly with morphological errors; the disorder concerns visual informations processing that is a necessary condition for identifying the formal representation of the object; the lesions are bilateral and involve the occipito-temporal cortex. 2) Associative visual agnosia: patients can copy, are not aphasic, but give erroneous verbal responses; the disorder concerns the links between formal representations and semantic, lexical representations; the lesions are unilateral and involve the left gyrus angularis connections. 3) Asemantic visual agnosia: patients have lost the meanings of objects and words; the disorder concerns semantic representations; the lesions are bilateral and involve the temporo-limbic cortex.

Agnosia↗
PubMed1989

[Unilateral paralysis of saccades caused by pontine tuberculoma].

A unilateral lesion of the paramedian pontine reticular formation results in an ipsilateral laterality paralysis with abolition of all saccadic movements directed to the side of the lesion. It is generally accepted that the oculocephalic reflex alone enables the eyes to be deviated beyond the median line of the affected side. In the present case of a paramedian pontine tuberculoma, a paralysis of laterality in accordance with the above mentioned opinion was observed initially. Treatment led to recovery of an ipsilateral pursuit of normal amplitude, contrasting with the persistent abolition of ipsilateral saccadic movements. The significance of this dissociation is discussed together with that of the later reappearance of slow voluntary movements (slow saccadic movements) towards the affected side.

Adult↗
PubMed1989

[Myelopathy, polymyositis and systemic manifestations associated with the HTLV-I virus].

A case of HTLV-I associated myelopathy in a 51 year-old Haitian woman is reported. MRI showed high signals in the cerebral white matter on T2-weighted images. There also was clinical and electrophysiological evidence of myositis, and a biopsy of the quadriceps muscle showed dense inflammatory infiltrates surrounding several small perimysial blood vessels. The virus was not demonstrated in the muscle. The presence of several systemic abnormalities (polyclonal gammapathy, circulating immune complexes, Sjögren's syndrome) and the vasculitis suggest an immunopathological mechanism for this HTLV-I associated myositis.

Antigen-Antibody Complex↗
PubMed1989

[Cerebral infarct and pure sensory deficit].

Twenty cases of pure sensory deficit of vascular origin are reported in patients aged 36 to 79 years. This type of attack in usually presumed to be due to a thalamic lacuna in the ventro-postero-lateral nucleus. However, other reported cases have shown other causal mechanisms and lesional sites. In the present series, CT scan and MRI in 11 cases demonstrated: infarctions in 9 and hemorrhages in 2 patients. The ventro-postero-lateral nucleus was involved in only 4 cases. An infarct of the posterior limb of the internal capsule (anterior choroidal artery territory) was present in 4 cases. The lesions in the other patients were: a thalamic hemorrhage and a small pontine hemorrhage lesion. The likely cause was embolism of cardiac origin in 4 cases, hypertension in 11 cases and diabetes in 4. One patient had an aneurysm of the posterior cerebral artery.

Adult↗
PubMed1989

[Myelin lesions in the central nervous system caused by disturbances in plasma osmolarity: pontine and extra-pontine myelinolysis].

Central pontine myelinolysis is defined by a symmetric area of myelin damage in the center of the basis pontis. In 10% of these cases, symmetric extra-pontine lesions of similar histological type are found in other parts of the brain. The MRI has provided information about the natural history of this demyelinating process. Disorders of plasma osmolarity appear to be a crucial factor in the pathogenesis of central pontine myelinolysis: rapid correction of hyponatremia or sometimes severe plasma hyperosmolarity. Alcoholic patients and, more generally, those afflicted with a serious debilitating illness are more susceptible to a hyperosmolar insult, absolute or relative. In such cases, the management of hyponatremia must be very cautious, owing to the risk of myelinolysis.

Adult↗
PubMed1988

[Effect of pathologic gaze deviation caused by brain stem lesion on interhemispheric equilibrium. Study using a non-verbal dichotic listening test].

Three cases of patients with lateral gaze palsy due to brainstem lesion were studied. They underwent a non-verbal dichotic listening test which evidenced a significant decrease of performance in the ear located on the same side as the lesion. This result can be interpreted as an inter-hemispheric imbalance linked to the pathological gaze deviation.

Abducens Nerve↗
PubMed1988

Ligand-induced desensitization of B-cell membrane immunoglobulin-mediated Ca2+ mobilization and protein kinase C translocation.

Binding of ligand to B-cell membrane immunoglobulin (mIg) can lead to activation of a number of distinct biologic responses, including altered expression of genes encoding c-fos, c-myc, and Ia, as well as proliferation and immunologic tolerance. Tolerance could reflect a functional uncoupling of receptors from systems that generate intracellular second messengers (i.e., receptor desensitization). To better understand the molecular basis of immune regulation, we examined the ability of mIg to function as a signal transducer after the cell's initial contact with mIg-binding ligand. The results show that ligand binding to as little as 2-10% of mIgM or mIgD renders the cell unresponsive to ligand binding to the reciprocal isotype as judged by Ca2+ mobilization and protein kinase C translocation responses. This heterologous receptor desensitization lasts longer than 24 hr and does not reflect loss of receptor from the cell surface. Studies with the calcium ionophore ionomycin, 1,2-dioctanoyl-sn-glycerol, and the protein kinase inhibitor staurosporine indicate that both protein kinase C-dependent and protein kinase C-independent (staurosporine-insensitive) mechanisms mediate heterologous desensitization after mIg crosslinking.

Animals↗