Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

Clinical features of ten Japanese children with cerebrovascular Moyamoya disease are reported and non-Japanese paediatric cases of the disease are reviewed from the world literature. The most common initial manifestations were headache in four cases (40%), motor deficit and convulsion in three cases (30%). As their recurrent and/or residual symptoms, eight children (80%) developed motor deficit consisting of hemiplegia in five cases and paresis or weakness of the extremities in three cases, and four (40%) had headaches. The mode of presentation in our cases was similar to that of non-Japanese cases, in addition to a female preponderance. Electroencephalographic findings of prominent high voltage delta bursts following hyperventilation and slowness of returning to the normal pattern, seen in all hyperventilated cases, is one of the features. Of 15 carotid arteries visualised in ten patients, sites of occlusion or stenosis were seen between the bifurcation of the posterior communicating artery and that of the anterior cerebral artery or the middle cerebral artery in 13 arteries, with a vascular network in the basal ganglia. This study suggests that if hyperventilation procedures produce prominent high voltage delta bursts during electroencephalography in children with headache and/or motor deficit, cerebrovascular disease, especially Moyamoya disease, should be suspected.
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PMID:Cerebrovascular Moyamoya disease. 637 Jun 99

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.
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PMID:Experimentally induced thiamine deficiency in beagle dogs: clinical observations. 719 32

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma]. 761 89

This study reports the effects of Ca2+ channel blockers (Ca antagonists) on intraneuronal Ca2+ ([Ca2+]i) movements and on the disturbance of rotarod performance produced in rats by intracerebroventricular administration of paraquat. Paraquat (50 nmol) produced a decrement in rotarod performance which was present at 30 min. and maximal at 60 min. and was not associated with overt behavioural changes; larger doses of paraquat (100-400 nmol intracerebroventricularly) produced paresis and convulsions which severely disrupted rotarod behaviour. The disruption of rotarod performance after paraquat (50 nmol intracerebroventricularly) was significantly reduced by giving Ca antagonists (flunarizine, verapamil and nicardipine) not only intraperitoneally 15 min. after paraquat but also intracerebroventricularly immediately before paraquat. The order of pharmacological potency was flunarizine > or = verapamil > nicardipine. In contrast, intracerebroventricular administration of Bay K 8644, a Ca agonist, enhanced the disruption of rotarod performance caused by paraquat (50 nmol). In in vitro studies, paraquat markedly potentiated the rapid increase in [Ca2+]i levels evoked by 50 mM KCl in rat brain synaptosomal fraction, although paraquat alone produced a small prolonged rise in [Ca2+]i levels which had a slow onset. The above results suggest that paraquat induced neurotoxicity is associated with increased [Ca2+]i levels in brain neuronal cells, and that paraquat might effect on membrane activity instability.
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PMID:Inhibitory effects of calcium channel antagonists on motor dysfunction induced by intracerebroventricular administration of paraquat. 769 Apr 78

Cranial CT scanning was performed in twenty-two patients with severe neurological complications secondary to eclampsia. All patients had repetitive and/or prolonged convulsions. In addition, three patients were in prolonged coma, and three had cortical blindness. One of the patients had central facial paresis, and two had hemiparesis. In seventeen patients, abnormal CT findings were identified. Diffuse cerebral edema was determined in four patients. The most frequent finding was bilateral low-density areas in the parietal and/or occipital lobes (7 cases). In three patients, CT revealed bilateral low-density areas in the basal ganglia. All women but three recovered completely. Two of the three patients who died had intracranial massive hemorrhage. Follow-up CT examinations demonstrated complete resolution of the low-density areas and slight cortical atrophy in three of four patients. Complete recovery of the patients associated with complete resolution of the low-density lesions suggested that these lesions corresponded to edema. We concluded that CT is useful in patients with complicated eclampsia because it may orientate management.
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PMID:The diagnostic value of cranial computed tomography in complicated eclampsia. 811 69

Osteopetrosis is an inherited skeletal condition characterized by increased bone radiodensity. There are three clinical groups: infantile-malignant autosomal recessive, fatal within the first few years of life (in the absence of effective therapy); intermediate autosomal recessive, appears during the first decade of life but does not follow a malignant course; and autosomal dominant, with full-life expectancy but many orthopaedic problems. The infantile variant shows a myelophthisic anemia, granulocytopenia, and thrombocytopenia, and patients eventually die from infection or bleeding or both. Neurologic sequelae include cranial nerve compression (optic nerve, blindness; auditory nerve, deafness; facial nerve, paresis), hydrocephalus, convulsions, and mental retardation. Radiographs show uniform bone density without corticomedulary demarcation, broadened metaphyses, "bone within a bone" or endobone phenomena (tarsals, carpals, phalanges, vertebra, ilium), and thickened growth plates if there is superimposed rickets. Transverse pathologic fractures occur, often followed by massive periosteal bone formation. Computed tomographic scans, magnetic resonance imaging, and bone scans provide specific information. Iliac crest bone biopsy is valuable to quantitate osteoclast and marrow changes by light and electron microscopy. Medical treatments involve high-dose calcitriol to stimulate osteoclast differentiation and bone marrow transplantation to provide monocytic osteoclast precursors. Orthopaedic problems in the intermediate and autosomal dominant forms include increased fractures, coxa vara, long-bone bowing, hip and knee degenerative arthritis, and mandibular and long-bone osteomyelitis. Cranial nerve compression also occurs. Osteotomy, plating, intramedullary rodding, and joint arthroplasty can be done, but are difficult because of bone hardness.
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PMID:Osteopetrosis. Current clinical considerations. 835 40

The effect of fludarabine (9-beta-D-arabinosyl-2-fluoroadenine-5'- monophosphate), an adenine nucleoside analogue, on the tolerance of the spinal cord to fractionated irradiation was studied in a rat model. Anesthetized female Fisher 344 rats received irradiation to 2 cm of the cervical spine with a telecobalt unit (dose rate 1.14 Gy/min). Radiation was administered in two, four or eight fractions spread over a 48-h period with or without fludarabine. Animals assigned to combined therapy received two daily intraperitoneal injections of fludarabine (150 mg/kg) given 3 h prior to the first daily radiation fraction. It was found that fludarabine reduced the iso-effect dose required to induce leg paresis at 9 months after irradiation for all fractionation schedules. Dose modification factors of 1.23, 1.29 and greater than 1.27 were obtained for two, four and eight fractions, respectively. Fitting the data with the direct analysis method of Thames et al. with an incomplete repair model [18] showed that the potentiating effect of fludarabine may be mediated through reduction in the number of 'tissue-rescuing units' (InK). Alpha and beta values were slightly but not significantly decreased, whereas the alpha/beta ratio was unchanged. These features suggest that fludarabine did not significantly inhibit cellular repair processes but rather reduced the spinal cord tolerance by a fixed additive toxic effect on the same target cells. In rodent models, the combination of fludarabine and fractionated radiation has previously been found to yield a therapeutic gain, i.e., the drug enhanced tumor response to a greater extent than it reduced normal tissue tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of intra-peritoneal fludarabine on rat spinal cord tolerance to fractionated irradiation. 852 25

We compared the clinical characteristics of 46 patients from three unrelated families with familial hemiplegic migraine (FHM) linked to chromosome 19, with those of 20 patients from two families with FHM not linked to chromosome 19. We found no significant differences for age at onset, frequency and duration of attacks, duration of the paresis, and occurrence of basilar migraine symptoms. In the linked families, significantly more patients reported unconsciousness during attacks (39% vs 15%; p < 0.05) and provocation of attacks by mild head trauma (70% vs 40%; p < 0.05). In one linked family patients also displayed chronic progressive cerebellar ataxia, whereas in one unlinked family benign infantile convulsions occurred in addition to FHM. Interestingly, so far an association with cerebellar ataxia was only described in chromosome 19-linked families. FHM linked to chromosome 19 and FHM unlinked to chromosome 19 do not differ with respect to clinical features.
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PMID:Familial hemiplegic migraine: a clinical comparison of families linked and unlinked to chromosome 19.DMG RG. 873 65

When rabbits were given intravenously purified verotoxin 2 (VT2) at 5 microg/kg of body weight, they developed hemorrhagic diarrhea, flaccid paresis, an ataxic gait, an opisthotonic posture, and convulsions. To examine the effects of VT2 toxemia on the rabbit central nervous system, magnetic resonance imaging and ultrastructural studies were performed. At 24, 57, and 80 h after injection of VT2 into 12 rabbits, T2-weighted images of the central nervous system were obtained. The initial lesion was noted at 24 h in the hypothalamic areas of all experimental animals. At 57 h, the T2 value increased in the medulla of the cerebral hemisphere or the hippocampus, with a brain stem lesion in six rabbits (50%). The rabbits with the brain stem lesions, in which neurological signs were very severe, died within 6 days. Lesions in the cerebellar hemisphere and/or vermis were noted in four rabbits (33%) that survived more than 1 month. To better understand the pathogenesis of VT2 in these brain lesions, we examined the deterioration of the blood-brain barrier and cerebrospinal fluid-brain barrier by using horseradish peroxidase as a tracer. The tracer was detected by electron microscopy both in the subendothelial layer, including the basal lamina, and throughout the cytoplasm of the ependymal cell layer covering the ventricle after intravenous or intrathecal treatment with horseradish peroxidase. We also determined the localization of VT2 by immunoelectron microscopy and found that it was localized on edematous endothelial cells of capillaries, ependymal cells, and myelin sheaths. The present study suggests that VT2 was conveyed from the endothelial and ependymal cell layers and caused edematous changes in the rabbit brain.
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PMID:Magnetic resonance imaging and histopathological study of brain lesions in rabbits given intravenous verotoxin 2. 894 46


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