Surveillance for exposure to HTLV-I in Egyptian infants and children with various malignancies.
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Biomedical subjects
Publications and source records attributed to R Khalil.
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Two fatal cases of deep cerebral venous system thrombosis are reported in adults. The first case looked like a diencephalic tumor or encephalitis but the diagnosis was made antemortem by means of cerebral angiography. Autopsy found bilateral infarction of basal ganglia. The second patient presented with a hemorrhagic infarction of right thalamus and basal ganglia. Deep cerebral venous occlusion was diagnosed at autopsy. In spite of a few cases of survival, the thrombosis of the galenic system remains often fatal. The pathological changes and indications for anticoagulation are discussed.
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Cell-mediated immunity (CMI) to myelin components has been implicated in Multiple Sclerosis (MS) pathogenesis: two targets were suggested, Myelin Basic Protein with controversial results and, more recently, gangliosides. In order to investigate their possible involvement, we have performed Leukocyte Migration inhibition (LMI) tests in the presence of human brain gangliosides. Thirty nine MS patients (twenty four being "definite", according to McDonald and Halliday's classification), twenty nine patients with Other Neurological Diseases (OND), thirty six patients with Inflammatory diseases (ID) and forty healthy controls were tested. MS patients were divided into two groups, depending on the clinical stage of the disease. The mean migration inhibition percentage of the MS-attack group was found to be significantly different from the four others (p less than 0.01) (24.4 +/- 16.2 versus 10.9 +/- 8.5 in MS without attack, 4.4 +/- 12.9 in OND, 3.9 +/- 13.9 in ID and 11.1 +/- 12.1 in healthy subjects). LMI to gangliosides is therefore significantly increased during the attack stage in MS. These results support the notion of a Delayed Type Hypersensitivity to these glycolipids during the active stage of the disease.
We report the pictorial evolution of a well-known French painter, before and after a left hemiplegia. Before the stroke he was famous not only for his drawings but also for his paintings. The evolution comprised 3 periods. Just after the stroke, the painter presented with severe exacerbation of a chronic depression. The second period was characterized by a rich pictorial production, with an excellent spatial organization of drawings; the style remained well recognizable and the favourite topics were unchanged: streets' scenes, country women, bunches of flowers. Shapes, drawings and volumes were well preserved. The neglect concerned not only the left hemispace but also the "microspaces" on the left side of which the painter's gaze attention had been fixed. Analysis of the production for this period supports the hypothesis according to which the neglect would be explained by a selective defect in automatic orientation of the attention on the left side. In the last period the aggravation appeared to bear more on the instrumental processes than on the esthetic capacities.
A 59-year-old hypertensive patient presented with transient global amnesia without neurological signs or symptoms. During the following 3 years, he experienced several attacks of vertebrobasilar insufficiency and a cerebellar infarction. CT scan and MRI found a partially thrombosed dolichoectatic basilar artery but no significant lesion within the limbic system. These data suggest transient global amnesia was due to a transient ischemia in the basilar artery distribution.
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The authors report on a series of 100 patients, who underwent an ischemic cerebrovascular accident (CVA) (8 transient attacks, 15 minor CVAs and 77 completed strokes) which revealed internal carotid artery occlusion (unilateral in 93 cases and bilateral in 7), proven by ultrasonography and/or angiography. The computerized tomography scan was normal in 8 cases. The middle cerebral artery territory was involved in 84 patients (isolated or associated (25 patients) with another site), whereas an isolated watershed infarction was the only lesion in the other 8 patients. Twenty-two patients died during the acute phase. Among the 68 survivors followed for a long time, 28 were severely incapacitated. The occlusions were not atherosclerotic in 18 cases (8 spontaneous dissections, 5 cardiogenic emboli, 3 radiation-induced arteries, 2 multiple causes). Eighty-two patients had atherosclerotic thromboses (67 men and 15 women, mean age 63.1 +/- 12.7 years). Among them, 24 had previously experienced minor ischemic strokes. In this group, the two year survival rate was 63 p. 100. Patients with non-fatal atherosclerotic thromboses were followed for an average of 22.2 months, during which time 28.2 p. 100 experienced another stroke.
We report 2 cases (n. 1 and 2) of cerebral infarction caused by a left atrial myxoma, and 1 case (n. 3). of dementia associated with a large left atrial myxoma. Cerebral emboli and neurological symptoms which can occur prior to cardiac obstructive and/or systemic signs require echocardiography. The cardiac post-operative condition was dramatically improved in cases revealed by an hemiplegia.
Neurological examination and Doppler sonography of a 50-year-old patient were suggestive of a spontaneous dissection of the left internal carotid artery (left-sided headaches, amaurosis fugax, Horner's syndrome and hemispheric stroke). Four-vessel angiogram performed several days after the onset of the symptoms showed dissection of both extracranial carotid arteries, more pronounced on right side where the dissection was clinically asymptomatic. Angiogram follow-up demonstrated a recanalization of both carotid arteries. A review of 15 other documented reports indicates that bilateral internal carotid dissection is usually associated with fibromuscular dysplasia. A large majority of cases does not clinically differ from unilateral carotid artery dissection.
The aim of the present experimental series was to investigate the central organization of the coordination between posture and movement in a bimanual load lifting task. The seated subject was instructed to maintain horizontal one forearm (postural arm) which was loaded with a 1 kg weight. The unloading was performed either by the experimenter (imposed unloading) or by a voluntary movement of the other arm (bimanual unloading). With the bimanual unloading, the movement control was accompanied by an anticipatory adjustment of the postural forearm flexors activity, which resulted in the maintenance of the forearm position despite the unloading. No change in the anticipatory postural adjustment was observed in one patient with complete callosal section. It was reduced in 5 patients with lesion of the SMA region, but only when the postural forearm was contralateral to the lesion. It is suggested that the SMA region contralateral to the postural forearm may select the circuits responsible for the phasic postural adjustments which are necessary to ensure postural maintenance, whereas the motor cortex contralateral to the voluntary movement controls both the movement and, via collaterals, the preselected circuits responsible for the associated postural adjustment.
The Authors report a case of ataxic hemiparesis caused by a lacunar infarct involving the posterior limb of the right internal capsule, in a 64-year-old hypertensive man who completely recovered in about two weeks. The lesion was detected by MRI four days after the onset of illness, when the CT scan was normal. In patients presenting with ataxic hemiparesis, MRI is the most accurate tool in locating very small causative infarcts of the brainstem or the subcortical white matter.
The authors have reported on 20 cases of cerebral venous thrombosis and reviewed the literature. In most of these 20 cases, CT scan findings were non-specific. Digital subtraction angiography was used for diagnosis in 6 cases. In 7 cases, no etiology was found. 12 patients received anticoagulant treatment despite CT scan showed hemorrhagic infarct in 4 of them. No neurological complication was reported after anticoagulation. Venous thrombosis was fatal in 3 non-anticoagulated patients. 4 others showed mild or severe sequellae after discharge.
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The primary stimulus for activation of vascular smooth muscle is an increase in the cytosolic free Ca2+ concentration. The level of activating Ca2+ is determined by a variety of Ca2+ homeostatic mechanisms. Ca2+ entry from the extracellular space occurs through the resting Ca2+ leak and the excitable Ca2+ channels: viz. voltage-gated, receptor-operated and stretch-activated channels. Ca2+ release from sarcoplasmic reticulum is induced by inositol triphosphate (IP3) and, possibly, by Ca2+ itself. Activating Ca2+ binds to calmodulin, forming a complex which induces myosin light chain phosphorylation and initiates smooth muscle contraction. The continuous Ca2+ entry together with the higher Ca2+ sensitivity of the contractile apparatus can then maintain smooth muscle tension. Ca2+ buffering by the sarcoplasmic reticulum and Ca2+ extrusion by Ca2+ pumps serve to lower the cytosolic free Ca2+ concentration. These Ca2+-lowering mechanisms are possibly regulated by cyclic nucleotides.
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In 2 patients receiving a long-term lithium carbonate therapy, persistent cerebellar, pyramidal, and extrapyramidal signs were observed, following a febrile pulmonary event. The mechanism of these disturbances is discussed, emphasizing the lithium-neuroleptics interaction as well as the possible role of hyperthermia.
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