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)

Clinical and neuropathological findings in a case of an unusually protracted encephalitis have been described. The patient was a 44-year-old man who experienced mental deterioration, right abducens and facial paresis, right and, subsequently, left hemiparesis, and consciousness disturbance with an intermittent low grade fever and occasional headache during one year and three months. Electroenphalograms showed periodic lateralized epileptiform discharges. Virus titers including herpes simplex virus were all normal. Neuropathological examinations revealed marked atrophic changes in the right temporal lobe, insular lobe and hippocampus with minimal inflammatory signs. The distribution of the lesions was almost identical with that of acute necrotic encephalitis or herpes simplex encephalitis despite its unusually protracted course.
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PMID:An autopsy case of protracted necrotic encephalitis with marked atrophy of unilateral temporal lobe. 47 90

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70

In the past five years, the authors have performed stereotactic evacuation of hypertensive thalamic hematoma using Komai's CT-stereotactic apparatus in 44 cases. Liquefied hematoma was aspirated through a stereotactic cannula, and solid hematoma difficult to aspirate was dissolved by a plasminogen activator (Urokinase) and drained out through a silastic catheter. The mean ratio of the total volume of evacuated hematoma to the estimated volume by CT image was 83.8%. The recovery from motor paresis and consciousness disturbance was observed during the early postoperative days in most patients. Functional outcome (ADL) at 3 months after operation was as follows: 24 cases (54.5%) recovered to a full or partial (self-cared) social life, 15 (34.1%) required partial care at home and 2 (4.5%) remained bedridden. Although 3 patients died within 1 month after operation, the cause of death in these patients was admitted to have no direct relation to operative procedure or to rebleeding due to the Urokinase injection. Postoperative functional prognosis was not affected by the timing of the operation. The important factors affecting ADL were preoperative neurological grade and CT classification. This stereotactic method apparently exceeded the conventional craniotomy method in the functional outcome.
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PMID:[Stereotactic evacuation of hypertensive thalamic hematomas using plasminogen activator (urokinase)]. 351 66

Bilateral simultaneous hypertensive intracerebral hemorrhages (HICH) are a rare occurrence. Computed tomography (CT) enables us to diagnose such a condition which is difficult to recognize clinically. In the series, six patients (2.6%) from a series of 553 HICH cases had suffered from simultaneous rehemorrhage in the contralateral hemisphere. It comprised four males and two females. Their ages ranged from 54 to 64 years with a mean age of 58 years. The clinical symptoms were excessively sever and were characterized by severe consciousness disturbance (semicoma to coma, 6 cases), aphasia (5 cases) and bilateral paresis (3 cases). CT density profiles were identical, implying that the hematomas were of similar age but located areas; two were bilateral basal ganglia, one was bilateral specular thalamus, pontine-ganglia (right), thalamo (left)-ganglia (right) and occipito (right)-thalamus (left) individually. All of the hematomas had ruptured into the ventricles. The predominant sites of hemorrhage were in the putamen (50%, 6/12) and the thalamus (33%, 4/12). Two patients received emergency craniotomy for evacuation of the hematomas. However, they died soon after the operations. In the remaining four non-surgical cases, two died of central failure, another died of pneumonia and the remain one survived but retained hemiplegia sequelae. The serious surgical results and outcome in bilateral HICH was compared that of unilateral HICH. Hemodynamically, poor cerebral blood flow and diaschisis phenomenon may contribute to the poor prognosis in these patients.
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PMID:Bilateral simultaneous hypertensive intracerebral hemorrhages. 834 Sep 50

An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs.
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PMID:Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation--case report. 1048 40

We report a 48-year-old chronic alcoholic man, who developed consciousness disturbance, oculomotor paresis, and flaccid tetraplegia. His dietary habit was very poor since one month prior to the present admission and he was drinking alcoholic beverage. On admission on April 19, 1999, he showed disturbance of consciousness, tetraparesis without sensory disturbance, gaze paresis, and vertical nystagmus on downward gaze. His blood thiamine level was 12 ng/ml (normal range: 23.8-45.9). MRI demonstrated symmetric hyperintense lesions in the motor and premotor cortices bilaterally, in addition to other changes indicating Wernicke's encephalopathy. His motor weakness and oculomotor disturbance improved after treatment with intravenous thiamine. His cortical MRI also normalized. We believe that his cortical abnormality was responsible for his motor paresis and this is an unusual and unique finding for Wernicke's encephalopathy.
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PMID:[Unusual MR findings of Wernicke encephalopathy with cortical involvement]. 1121 34

Two rare cases of dissections which involve the anterior cerebral artery (ACA) are reported. A 58-year-old woman presented with a ruptured dissecting aneurysm manifesting as sudden onset of severe headache and consciousness disturbance followed by aphasia, right hemiparesis, paresis of the left lower extremity, and choreoathetotic movements of the upper arms and face. Computed tomography and angiography revealed subarachnoid hemorrhage due to a dissecting aneurysm at the left A1 segment. The dissecting aneurysm was trapped surgically on the day of onset. Her neurological deficits disappeared within a month. A 39-year-old woman experienced continuous dull headache from the day before onset, and then suffered right hemiparesis. Magnetic resonance (MR) imaging revealed cerebral infarction at the left globus pallidus. Angiography and MR imaging revealed a dissecting aneurysm at the left A1 segment and occlusion of the left Heubner's artery. She received conservative treatment and her neurological findings were improved. Dissections or dissecting aneurysms involving the ACA can be classified into three types: Extension of a dissection to the ACA from the internal carotid artery, dissection at the A1 segment, and dissection at the A2-A4 segments. These types of dissection have distinct uniform clinical features.
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PMID:Dissecting aneurysms at the A1 segment of the anterior cerebral artery--two case reports. 1139 8

A 51-year-old woman had developed fever and consciousness disturbance at 47 years of age. Brain magnetic resonance imaging (MRI) revealed acute disseminating encephalomyelitis (ADEM)-like lesions without gadolinium enhancement (GDE). One year later, she had an episode of bilateral optic neuritis and cerebellar ataxia. Speech deficit and right hand weakness occurred at the age of 51 years. Neurological examination showed motor aphasia, finger agnosia, right-left disorientation, and right hand paresis. Neuromyelitis optica (NMO)-IgG was seropositive. Cerebrospinal fluid examination showed negative results for myelin basic protein and oligoclonal IgG band. The IgG index was normal. Brain MRI revealed a tumefactive lesion in the left temporo-parietal region and conglomerate ovoid lesions in the pericallosal regions. No GDE was found in the brain lesions. Visual evoked potential test showed bilateral prolongation of P100 latencies. She was treated twice with methylprednisolone pulse therapy followed by oral prednisolone, but the motor aphasia did not respond to steroid treatment. She had no prior history of myelitis and was diagnosed as NMO spectrum disorder (NMOSD). Similar to previous studies of NMO-IgG seropositive extensive brain lesions, this patient with NMOSD indicated no GDE in tumefactive lesions at two episodes of encephalopathy. Compared to multiple sclerosis (MS), a high frequency of non-enhancing tumefactive lesions is reported in patients with NMO or NMOSD. The absence of GDE in tumefactive lesions could help to differentiate between NMO and MS.
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PMID:Repeated non-enhancing tumefactive lesions in a patient with a neuromyelitis optica spectrum disorder. 2153 34

Introduction. Familial hemiplegic migraine (FHM) is a rare disorder characterized by migraine attacks with motor weakness during the aura phase. Mutations in CACNA1A, ATP1A2, SCN1A, and PRRT2 genes have been described. Methods. To describe a mutation in ATP1A2 gene in a FHM case with especially severe and prolonged symptomatology. Results. 22-year-old woman was admitted due to migraine-type headache and sudden onset of right-sided weakness and aphasia; she had similar episodes in her childhood. Her mother was diagnosed with hemiplegic migraine without genetic confirmation. She presented with fever, decreased consciousness, left gaze preference, mixed aphasia, right facial palsy, right hemiplegia, and left crural paresis. Computed tomography (CT) showed no lesion and CT perfusion study evidenced oligohemia in left hemisphere. A normal brain magnetic resonance (MR) was obtained. Impaired consciousness and dysphasia began to improve three days after admission and mild dysphasia and right hemiparesis lasted for 10 days. No recurrences were reported during a follow-up of two years. We identified a variant in heterozygous state in ATP1A2 gene (p.Thr364Met), pathogenic according to different prediction algorithms (SIFT, PolyPhen2, MutationTaster, and Condel). Conclusion. Prolonged and severe attacks with diffuse hypoperfusion in a FHM seemed to be specially related to ATP1A2 mutations, and p.T364M should be considered.
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PMID:Familial Hemiplegic Migraine with Severe Attacks: A New Report with ATP1A2 Mutation. 2781 13