Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MRI findings of a 14-year-old boy with subdural empyema (SE) are reported and compared with those of serial CT-scan. He was admitted with fever, headache, right hemiplegia and facial palsy. Initial enhanced CT-scan revealed a slit left lateral ventricle and a shift in the mid-line structures, but failed to detect any SE. MRI at 10 days after admission clearly demonstrated SE as an area of low intensity on T1-weight (T1WI) and very high intensity on T2-weight (T2WI). Post-contrast enhanced MRI (CE-MRI), using Gd-DTPA, showed a contrast enhancement in the wall of SE. However, no definite parenchymal abnormal intensity areas were detected, suggesting that the diagnosis was made sufficiently early for timely treatment and good neurological outcome. CE-MRI proved to be a more powerful and better diagnostic procedure than enhanced CT-scan, and was very useful in determining the state and development of the disease.
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PMID:The efficacy of MR imaging in subdural empyema. 135 35

A 64-year-old right hemiplegic woman, who had been treated for hypertension for 15 years, was admitted to our hospital. Neurologic examination on admission disclosed right hemiplegia and motor aphasia; however, ophthalmoparesis, pupillary abnormality, and blepharoptosis were not evident. Excessive sweating on the right side of the body, which was most marked on the face, was observed. Amount of sweating on the left side of the body was normal. Unilateral hyperhidrosis persisted for more than 2 months. MRI revealed hemorrhagic infarctions in the left basal ganglia, internal capsule, thalamus, hypothalamus, and medial part of the cerebral peduncle. 123I-IMP SPECT disclosed hypoperfusion in the left striatum, thalamus, occipital cortex, and right cerebellar hemisphere. Cerebral angiography revealed arteriosclerotic changes in the basilar artery, but that the left posterior cerebral artery and its branches were not occluded. Unilateral persistent hyperhidrosis is rare after ischemic stroke. Hypothalamic lesion was thought to be responsible for the hyperhidrosis in this patient. As the hypothalamus receives its blood supply from the posterior cerebral artery, unilateral persistent hyperhidrosis may be an important sign of cerebral infarction in the posterior cerebral artery region.
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PMID:[Unilateral persistent hyperhidrosis after ischemic stroke]. 139 37

A 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
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PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
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PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

A 10-year-old girl had an infarction in the left brain during an acute viral meningoencephalitis. She initially showed seizure, unconsciousness and fever, and right hemiplegia gradually developed. She died at the 48th day of disease from respiratory disturbance and renal failure. Cranial MRI during the acute phase of the disease, when there was no clinical sign of right hemiplegia, showed a high intensity lesion in the left parietal and occipital areas on T-2 weight image. Autopsy disclosed the findings suggesting viral encephalitis, including multiple focal necrosis, perivascular round cell infiltration, proliferation of glial cells and spongy degeneration with some intranuclear inclusion bodies, and infarction in the left hemisphere. These findings suggest that T-2 high intensity lesion on MRI reflected infarction.
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PMID:[A case of brain infarction associated with viral encephalitis: MRI and pathological findings]. 193 Nov 68

A 58-year-old woman was admitted to our hospital with complaints of general fatigue, thirst and lumbago. A diagnosis of Cushing's syndrome was made on the basis of elevated serum levels of cortisol and adrenocorticotropic hormone (ACTH). Although Cushing's disease was most suspected, no evident image of pituitary adenoma could be found on brain CT scan and MRI. Therefore, treatment with oral Trilostane was started. Three months after admission, left hemiplegia was noticed and cerebral abscess in the right frontal lobe was demonstrated by brain CT scan. In spite of surgical removal of the abscess by total resection, she had a relapse in the same site and also developed a new lesion in the left lateral lobe. Surgical drainage was performed and Nocardia asteroides was isolated from the drained pus. An intensive chemotherapy with aminobenzylpenicillin (ABPC) and latamoxef (LMOX) in combination resulted in marked decrease in size of the lesion in the brain and subsequent improvement of left hemiplegia was achieved. Since approximately one month before when a diagnosis of cerebral abscess was made, there had been demonstrated a coin lesion in the right middle field on chest X-ray films. This lesion in the right lung disappeared concomitantly with the improvement of the lesions in the brain. This fact strongly suggests that the lesion in both brain and lung were of the same nature. Nocardia is known to make a primary lesion in the lung after being inhaled and then through hematogenous dissemination to make distant lesions in various sites, especially in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Cushing's syndrome associated with Nocardia cerebral abscess]. 206 9

A 67-year-old woman with medial medullary infarction is reported, including clinical manifestations, MRI and angiographical findings, and results of evoked potentials. She suffered from contralateral hemiplegia and disturbance of deep sensation. Motor paresis of the tongue was absent. Magnetic resonance imaging revealed a lesion in the medial portion of the medulla oblongata. The 17 cases previously reported with medial medullary infarction are reviewed. Only 3 cases had triad of medial medullary infarction, contralateral hemiparesis, deep sensory disturbance, and ipsilateral hypoglossal paresis. Therefore, lesion detection is necessary to diagnose medial medullary infarction. Most infarctions limited to the upper third of the medulla were caused by occlusions of vertebral arteries or their branches and prognosis was good. In contrast, infarctions in the lower two thirds were caused by occlusions of anterior spinal arteries and their branches and the prognosis was poor. Thus localization of the lesion using MRI plays an important role to predict the prognosis.
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PMID:[Medial medullary infarction demonstrated by MRI]. 218 65

A 64 year-old woman experienced, at 6 weeks' interval, two episodes of encephalitis with left hemiparesis, coma and signs of meningitis. Paraclinical examinations showed lymphocytic meningitis, right temporal hypodensity at CT and high titers for herpes simplex at blood serology. The spontaneous course was favourable with almost complete recovery. A third recurrence took place 2 months later with left hemiplegia, confusion and meningism. A tentative diagnosis of herpes simplex encephalitis was confirmed by major intrathecal synthesis of herpes virus specific antibodies and by highly suggestive MRI images. Treatment with acyclovir resulted in rapid regression of motor deficit and meningism, but neuropsychological disorders regressed more slowly with persistent visuo-constructive and memory disorders. During a fourth and milder recurrence, a stereotactic temporal brain biopsy was performed, which showed lesions of encephalitis and elevated titers for HSV1 in the temporal fluid. Another course of acyclovir followed by vidarabine produced complete remission. The possibility of recurrent types of herpes simplex encephalitis is discussed.
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PMID:[Recurrent herpetic encephalitis]. 220 90

We report the case of a patient affected by contralateral hemiplegia during herpes zoster ophthalmicus (HZO) evaluated both with serial CT scans and with MRI. We suggest that MRI examination of patients affected by HZO could be useful for the detection of early signs of cerebral arterial damage which are not yet clinically and radiologically apparent.
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PMID:MRI evaluation of a case of herpes zoster ophthalmicus with delayed contralateral hemiplegia. 238 2

We reported a 72-year-old male with ischemic oculopathy due to ophthalmic artery stenosis followed by ipsilateral border zone infarction due to internal carotid artery stenosis. The patient had history of hypertension and diabetes mellitus. He had severe headache and visual disturbance of the right eye. He was diagnosed right neovascular glaucoma and left diabetic retinopathy (simple type), and received diuretics, beta-blockade and other anti-hypertensive drugs. One month later, he noticed left mild hemiparesis in a morning, and he experienced progression of left hemiparesis over a week. He was admitted to our hospital on the 11th day. He showed left complete hemiplegia, left sensory disturbance, anosognosia and left unilateral spatial neglect. His right eye was diagnosed neovascular glaucoma but left eye was normal. The 5th days CT showed low density area in the right terminal zone and bilateral periventricular lucency. At the same area, the 46th days MRI showed high intensity area in the T2-weighted image and low intensity area in the T1-weighted image. Cerebral angiography performed on the 33rd day, disclosed severe kinking at the cervical segment and 50% stenosis at the intracavernous segment in the right internal carotid artery, and 90% stenosis and post-stenotic dilatation of the right ophthalmic artery. Left internal carotid artery had each 60% stenosis at the cervical segment and the intracavernous segment. Left ophthalmic artery had severe stenosis from its beginning to distal part. This infarction was considered berder zone infarction by it's localization (terminal zone) and internal carotid artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of ischemic oculopathy followed by border zone infarction]. 258 88


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