Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

This is a report of cerebral infarction and cerebral hemorrhage derived from systemic lupus erythematosus. A 49-year-old male was admitted to our hospital due to dysarthria and supranuclear facial palsy. He had been suffering from SLE and medicated incompletely since 9 years prior to admission. A CT scan showed a small infarction in the left parietal area. An angiography revealed a tapering stenosis of the left carotid siphon and an occlusion of the left vertebral artery at the cisternal portion. On the 13 days after the admission, he complained of a high fever and right hemiparesis. The CT scan disclosed newly multiple small infarctions in the left parietal area. The angiography showed the progressing of the tapering stenosis at the left carotid siphon, and demonstrated the narrowing of the left superior temporal artery and ophthalmic artery in addition to the disappearance of a left posterior communicating artery. High dose of steroid was given to him, but cerebral hemorrhage and huge left cerebral infarction were complicated. On the 26 days after the admission, his general condition was worsened and died. It was considered that the cerebral infarction and hemorrhage might be derived from the vasculitis of SLE.
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PMID:[A case of systemic lupus erythematosus associated with cerebral infarction and cerebral hemorrhage]. 757 35

We report a 46-year-old woman who extensively showed intracranial calcifications possibly due to neuropsychiatric systemic lupus erythematosus (NPSLE) and antiphospholipid syndrome (APS). She had been treated with oral prednisolone for SLE since age 15, and experienced two abortions due to APS at ages 28 and 35 respectively. After a convulsion attack due to NPSLE at age 30, she had been suffering from dysarthria and choreic movement in her extremities. On admission to our hospital brain CT demonstrated extensive and symmetrical calcifications bilaterally in basal ganglia, subcortical white matter of the frontal lobe and dentate nuclei. She was shown to have neither metabolic nor congenital disorders causing these intracranial abnormalities. In this patient both NPSLE and APS, therefore, might have contributed to the remarkable intracranial calcifications in a long clinical course.
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PMID:[Neuropsychiatric systemic lupus erythematosus associated with anti-phospholipid syndrome, showing massive intracranial calcifications]. 1463 17

Anti Phospholipid Syndrome (APS) is a relatively new conception of syndrome complex first noticed in 1983. It may be primary or secondary to other diseases like SLE, RA, Systemic sclerosis, behchet's syndrome, temporal arteritis, sjogren's syndrome psoriatic arthropathy etc. Clinical manifestations are consequences of vascular thrombosis and embolism like DVT, pulmonary embolism, stroke, TIA, complication of pregnancy with pregnancy loss. We report a 34 years married female housewife who presented with sudden onset of nausea, vomiting, vertigo, dysphagia, dysarthria and ataxia. She had a chronic leg ulcer. Neurological findings were consistent with lateral medullary syndrome due to stroke though she was normotensive, nondiabetic with normal lipid profile. She had history of two abortions in last three years. Investigations were done accordingly and she fulfilled the diagnostic criteria of APS. No secondary cause was detected after thorough clinical examination and laboratory investigations. She was treated symptomatically along with oral anticoagulation. She improved slowly but steadily.
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PMID:Anti phospholipid syndrome. 1918 54