Biomedical subjects
Publications and source records attributed to R Khalil.
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.
A 60-year-old man who had Parkinson's disease for 25 years became unable to maintain the upright position of the trunk while standing or walking. Because of a loss of postural fixation, his trunk sank forward until his back was horizontal. Fifteen years before, a bifocal implantation of radioactive yttrium-90 had been performed by a stereotaxic procedure at the level of the globus pallidus (GP) and the ventrolateral thalamus, respectively on the right side. A second operation, 2 years later, had been made by electrocoagulation in the left ventrolateral thalamus. Postmortem examination showed the following features (a) neuronal cell loss in the pigmented nuclei of the brainstem with intracellular Lewy bodies and gliosis. These data corresponded with the usual pathology of idiopathic Parkinson's disease; (b) surgical lesions resulting from the previous stereotaxic operations in the right GP and the ventrolateral thalamus on both sides and (c) neuronal cell loss without gliosis in the right GP that was evident in regions spared by the surgical lesion. Moreover, these degenerative changes were particularly seen in the left GP, which was surgically unlesioned. The ansa lenticularis was demyelinated on both sides. These data might be consistent with a retrograde degenerative process affecting the pallidothalamic projections. Beside the role of the neuronal cell loss affecting the pars compacta of the substantia nigra (SN) in akinesia, the role of the lesions affecting the G.P. in the genesis of postural disorders is suggested.
Thirty-five infants and children with beta-thalassemia major and 12 with beta-thalassemia trait were studied. Their ages ranged between 6 months and 12 years. Thirty-three were males and 14 females. Spontaneous rosette (E1-RFC), total rosette (E2-RFC), enumeration of T lymphocyte subsets using monoclonal antibodies (OKT3, OKT4, and OKT8), migration inhibition factor (MIF) assay and in vivo delayed hypersensitivity skin reactions were tested. Lower mean T cell population was present in thalassemia major but not the trait. The helper/suppressor ratio was decreased in patients with evidence of hypersplenism. Patients who had suffered from pneumonia or hepatitis manifested lower mean T cell count, depletion of helper cells and decreased helper/suppressor ratio. They also showed depressed delayed cutaneous hypersensitivity and MIF activity. Study of the cell-mediated immunity in patients with thalassemia might be useful to detect those who could be-more susceptible to infections.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We describe 2 clinicopathological cases of non-hereditary multiple telangiectasias of the nervous system. In the first case, the general course of the disease was characterized by spells over a period of 7 years and the major lesions successively involved cranial nerves, spinal cord and brain. Neuropathological examination showed both ischemic and hemorrhagic changes. Systematized degenerative changes were found and were similar to those observed in spinocerebellar heredodegenerations (Friedreich's ataxia). In the second case, the 3 years of evolution were characterized by spells of the encephalitic type only. A review of the literature indicates the rarity of this kind of disease, the usual localization of capillary malformations and the clinical polymorphism (epilepsy, strokes, multifocal syndromes masquerading as multiple sclerosis). The pathogenesis of pathological changes is discussed.
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.
Normal subjects and Parkinsonian patients performed a bimanual load lifting task. In this task, one "postural" forearm, held in a horizontal position while supporting a 1 kg weight, was unloaded either by the experimenter's hand (imposed unloading) or by the subject's other hand in response to a tone burst (voluntary unloading). The variables recorded were reaction time (RT: time interval between the tone and beginning of unloading) and movement time (MT: duration of the change in force measured by a force platform on the "postural" forearm). Elbow angle changes were also measured with a potentiometer. The EMG activity from brachioradialis of the "postural" arm and that from the biceps of the "active" arm were recorded. The Parkinsonian patients showed an increase in both RT and MT and an impairment of the co-ordination between movement and posture which was reflected in an increase in amplitude of the elbow rotation after voluntary unloading. Moreover, the decrease in EMG activity in the brachioradialis of the postural arm during unloading was less in Parkinsonian patients than in the normal group. This disorder of postural command was often accompanied by a lack of anticipatory EMG changes. Comparison between treated and non-treated patients showed that dopamine agonists brought about recovery of both RT and MT but did not improve postural co-ordination. The co-ordination was less impaired when the voluntary unloading was performed by the preferred hand. Several hypotheses are discussed concerning the mechanism underlying this impaired co-ordination.
Explore the source record for details and available documents.
Cortical language areas were identified by CT scan or NMR imaging, using planes of horizontal sections parallel to the orbitomeatal plane and therefore indirectly to the bicommissural plane. Sections 45 and 50 mm above the bicommissural plane pass electively through temporal structures i.e. the posterior part of T1 and T2, while sections at 60 and 70 mm pass through the angular gyrus and supramarginal gyrus.
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.
Explore the source record for details and available documents.
A 15 year-old North-African female showed typical symptoms and evolution of Progressive Myoclonus Epilepsy of the Unverricht type. Pathological examination failed to show either inclusion bodies or any other storage material. The only relevant findings included degenerative changes in the inferior olives and, to a lesser extent, in the cerebellar cortex. The site of lesions was remarkable: in the inferior olives, lesions were bilaterally and symmetrically restricted to the external angles (lateral lamellae); in the cerebellum, loss of Purkinje cells and ascending fibres of the molecular layer was prominent in the lateralmost part of the hemispheres (semilunar lobules). Such a topography implies a system disorder involving the olivo-cerebellar pathway, particularly in that part which projects to the neocerebellum. Twelve other clinico-pathological cases of progressive myoclonus epilepsy of the degenerative group are reviewed. It is suggested that, here again, lesions--although more diffuse--may be related to a primarily olivo-cerebellar involvement.
A patient who had a two-month history of nonspecific inflammatory disease experienced symptoms of raised intracranial pressure and meningitis. Computed tomographic scan showed multiple, small ring-enhancing hypodensities consistent with cerebral abscesses. The infective agent proved to be Hemophilus paraphrophilus, a fastidious, particularly slow-growing organism that was identified on blood cultures. An autopsy disclosed disseminated microabscesses and demonstrated typical pathologic changes of endocarditis complicating mitral valve prolapse.