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)

Hearing loss in an uncommon symptom in multiple sclerosis (MS). In nine patients with MS, seven with unilateral hearing loss and two with bilateral impairment, accompanying symptoms and signs included facial numbness, hemifacial paresis or spasms, ipsilateral limb ataxia, nystagmus, vertigo, tinnitus, and spastic-ataxic gait. Central auditory dysfunction was suggested by audiometric findings and/or by brainstem auditory evoked potentials in all nine patients. Clinical improvement in two was accompanied by return toward normal in the results of audiometric or electrophysiologic studies. Hearing impairment should be sought in patients with MS and appropriate studies pursued.
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PMID:Hearing loss in multiple sclerosis. 684 85

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

Movement disorders following midbrain haemorrhage are infrequently encountered in rehabilitation, and are uncommonly corrected by pharmacologic means. This report describes a 20 year-old male with a prior history of cocaine abuse who presented with a 4 day history of dysarthria and blurred vision following methamphetamine abuse. Physical examination demonstrated hypertension, left facial hemispasm, bilateral upward gaze paresis and ataxic gait. Magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) showed multifocal parenchymal haematomas in the mesencephalic tegmentum, subcortical left front region and right anterior thalamus consistent with cavernous angiomas. The patient was transferred to rehabilitation on hospital day 5. The following day, he developed choreoathetoid movements, dystonia, and aphasia, secondary to an extension of the midbrain haemorrhage. Cogentin was initiated with slight improvement in choreoathetoid movements. The patient began intensive multidisciplinary rehabilitation therapy but after 18 days of therapy, the patient remained totally dependent in activities of daily living (ADLs), transfers, mobility and was unable to communicate in any manner. A trial of Sinemet was initiated, with resultant steady improvement in functional ability over the next month. By discharge, the patient was independent in ADLs and ambulation. By 9 months post discharge follow-up, the patient was fully independent with normal cognition, and had self tapered all medications without ill effect. Dopamine agonist trials of appropriate duration appear indicated in cases of movement disorder (paucity or excess) following midbrain lesions.
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PMID:Pharmacologic management of movement disorder after midbrain haemorrhage. 965 26

A 65-year-old man presented with a rare case of cavernous malformation with hemorrhage located within vestibular schwannoma. He had suffered hearing impairment for 20 years, and was admitted to our hospital with vertigo and ataxic gait. Neurological examination revealed hearing loss, facial nerve paresis, and left cerebellar ataxia. Magnetic resonance imaging demonstrated a left vestibular schwannoma 35 mm in diameter, as well as a heterogeneous area associated with hypointense rim within the tumor, indicating intratumoral hemorrhage. Subtotal removal of the tumor together with the fibrously encapsulated hematoma was performed through a left retrosigmoid craniotomy. Histological examination of the surgical specimen revealed cavernous malformation within vestibular schwannoma. Immunohistochemistry for matrix metalloproteinase (MMP)-2 and -9, and tissue inhibitors of metalloproteinase-2 showed strong expression in the endothelial cells of the cavernous malformation, but not in the interstitial structures. His symptoms significantly improved after surgery and he underwent gamma-knife therapy for the residual tumor. Cavernous malformations may show dynamic characteristics such as repeated hemorrhage and de novo formation. MMP-2 and -9, which are implicated in angiogenesis and hemorrhage, may be upregulated in such tumors.
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PMID:Association of cavernous malformation within vestibular schwannoma: immunohistochemical analysis of matrix metalloproteinase-2 and -9. 1803 6

The study aimed to evaluate the correlations between the clinical and paraclinical data in the lateral bulbar infarction, benefiting from the access to the semiologic characteristics of a group studied and the MRI angiography, without a contrast agent, through the 3D TOF technique combined with MIP, as an imaging technique for the evaluation of the arterial lesion. The study group included 20 patients with lateral bulbar infarction, 14 men, and 6 women aged between 21 and 80 years, the mean age being 56, 9 years, who were enrolled in the study in the period 2012 and 2014, following the admission in the National Institute of Neurology and Neurovascular Diseases. All the patients enrolled in this stage study, performed brain MRI - in the Medinst laboratory, which included the following sequences T1, T2, Flair, DWI, MRI angiography without contrast agent (3D TOF combined with MIP). The study was retrospective. Following the analysis of the 3D TOF sequences combined with MIP, it was found that in the group studied, 8 patients had damage at the level of the vertebral artery, 2 at the level of the posterior inferior cerebellar artery and 10 patients presented mixed lesions of both the vertebral artery and of the PICA artery. In terms of the mechanism involved, most of the lateral bulbar infarctions were generated by arterial dissection (9 cases) and 6 cases had atheroma as etiology. Regarding the risk factors, dyslipidemia and smoking predominated in the studied group and the most common signs and symptoms were gait abnormalities, the ataxia of the limbs, dysphonia, and Horner syndrome. Abbreviations: 3D TOF = 3D time of flight angiography, MIP = maximum intensity projection, MRI = magnetic resonance imaging, CT = computed tomography, FLAIR = fluid attenuated inversion recovery, DWI = diffusion weighted imaging, HTA = hypertension, DZ II = diabetes mellitus, VA = vertebral artery, PICA = posterior inferior cerebellar artery, VG = vertigo, NT = nystagmus, N/ E = nausea/ emesis, DP = dysphagia, PVP = pharyngeal/ vocal cord paresis, HS = Horner syndrome, PTH = pain/ temperature hypesthesia, LA = ipsilateral limb ataxia, GA = Gait ataxia, C-R-F = Cardiovascular risk factors, L = left, R = right.
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PMID:Correlations between the semiologic changes and the imaging aspects in the lateral bulbar infarction. 2797 32