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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In systemic lupus erythematosus (SLE), neurological involvement has been reported to occur with frequencies ranging from 14% (severe cases) to 83% (mild forms included). In spite of early diagnosis and aggressive treatment, neuropsychiatric SLE may represent a serious problem of management. We describe three cases, one with acute transverse myelitis, one with hemiparesis, and one with signs of focal and diffuse cerebral dysfunction, in whom improvement following intrathecal therapy with methotrexate and dexamethasone was observed.
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PMID:Central nervous system involvement in systemic lupus erythematosus: a new therapeutic approach with intrathecal dexamethasone and methotrexate. 771 11

Two cases of primary antiphospholipid antibody syndrome are reported. One patient presented multiple abortions and epilepsy. The second patient was affected by a brain vascular accident, with a residual hemiparesis. Both cases showed livedo reticularis in arms, NMR evidence of diffuse lesions of the white matter, high serum levels of anticardiolipin antibodies and cardiopathy. Lupus anticoagulant was also found in the serum of the first patient, and cortisone and antiaggregants enabled her to reach term in a fifth pregnancy after four miscarriages. In the other case histological examination of specimens of skin, peripheral nerve and skeletal muscle revealed occlusive, non arteriosclerotic vasculopathy and an absence of inflammatory lesions. Histological study has rarely been performed in primary antiphospholipid syndrome but suggests that the mechanism of thrombosis is not vascular; in our subjects it revealed findings similar to those in Sneddon syndrome.
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PMID:Primary antiphospholipid syndrome: two case reports, one with histological examination of skin, peripheral nerve and muscle. 799 67

Delayed neurological symptoms and signs following herpes zoster ophthalmicus (HZO) such as "Delayed contralateral hemiplegia with HZO" are supposed to be due to ipsilateral intracranial angiitis and ischemic disorder. We experienced a rare case with ipsilateral cerebral hemorrhage following HZO. Under the diagnosis of cerebral angiitis associated with HZO, we treated her conservatively and observed sequential change of angiography for four months. A 54-year-old female, who had been treated for systemic lupus erythematosus (SLE), developed HZO on left ophthalmic nerve area. Seven weeks after the onset of HZO, she complained of headache, mild right hemiparesis, and disturbance of consciousness. Computed tomography revealed subcortical hemorrhage at the left temporo-occipital lobe. Cerebral angiography showed vascular irregularities such as segmental narrowing and sausage-like dilation on proximal portion of the ipsilateral anterior, middle and posterior cerebral arteries. Same findings were seen on peripheral portions of the posterior cerebral artery on the same side. Moreover sequential angiograms showed appearance of an aneurysm in the left middle cerebral artery (M2 potion). Under the diagnosis of cerebral angiitis associated with HZO, she was treated with antiviral agents, antiplatelet drugs, steroid and stellate ganglion block. Those irregularities were found to diminish on the sequential angiograms, and the aneurysm disappeared four month later.
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PMID:[Sequential change of cerebral angiography in a case of cerebral angiitis following herpes zoster ophthalmicus]. 799 42

Antiphospholipid antibody syndrome is a newly-defined clinical entity of arterial thrombosis, venous thrombotic events, recurrent spontaneous abortion and thrombocytopenia in the presence of antiphospholipid antibodies. We have experienced a 23-year-old male SLE patient with positive anticardiolipin antibody who presented with left hemiparesis and paresthesia. The clinical and laboratory findings were compatible with the criteria for SLE and he was found to have anticardiolipin antibody, thrombocytopenia, prolonged partial thromboplastin time and cerebral thrombosis. Initially, he was treated with high dose steroid and warfarin and now he is being followed up with warfarin and steroid.
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PMID:A case of cerebral infarction associated with positive antiphospholipid antibody in a systemic lupus patient. 803 46

We describe a 36-year-old man with antiphospholipid antibody syndrome complicated by cerebral hemorrhage. In December 1991 he was brought to another hospital with sudden onset of left hemiparesis and status epilepticus. He had been well previously. A CT scan and MRI showed a cerebral hematoma located in the right frontoparietal region. Twelve days later he was transferred to our hospital. Although a CT scan, MRI, and cerebral angiography were repeated, they did not reveal any abnormality regarding an etiology. Only persistently abnormal finding in laboratory studies was positive for lupus anticoagulant and anticardiolipin antibody, i.e. antiphospholipid antibodies. There was no serological evidence of SLE or other autoimmune diseases. Stereotactic biopsy of the hematoma wall and scalp artery showed no abnormality. Based on above findings we conclude that antiphospholipid antibodies have played an important role for the hemorrhage. Antiphospholipid antibody syndrome should be considered in a case of an unexplained cerebral hemorrhage especially in a young and normotensive patient.
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PMID:[Cerebral hemorrhage in a case of antiphospholipid antibody syndrome]. 832 20

We describe the clinical presentation and course of two girls with cerebrovascular disease and mixed connective tissue disease. One developed rapid onset hemiparesis and aphasia secondary to left internal carotid artery occlusion. She experienced a complete recovery after treatment with prednisone and cyclophosphamide. The other patient was diagnosed as having mixed connective tissue disease but had acute neurologic deterioration. She died due to an intracerebral hemorrhage. Autopsy demonstrated small-vessel fibrinoid necrosis. Although cerebrovascular disease secondary to central nervous system vasculitis is a manifestation of systemic lupus erythematosus, this is the first description of cerebrovascular disease as a primary sign in mixed connective tissue disease. These cases demonstrate the range of cerebrovascular disease observed in children with mixed connective tissue disease.
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PMID:Stroke and mixed connective tissue disease. 840 68

A 47-year-old woman affected by systemic lupus erythematosus (SLE) presented with headache, fever, splenomegaly and edema of the lower extremities. CT showed diffuse low density in the cerebral white matter and marked splenomegaly in the abdomen. T2-weighted MR images showed diffuse high intensity lesions in the white matter. After immunosuppressive therapy with prednisolone, there was marked improvement in the cranial CT and MR appearances. The underlying pathological process was probably edema secondary to a lupus microangiopathy. SLE can be complicated by a widespread abnormality of the white matter with marked radiological changes but few neurological signs. In the present case, only an episodic mild hemiparesis for 3 weeks without seizure and psychiatric disturbance was found neurologically during the whole clinical course.
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PMID:Unusual neuroradiological findings in systemic lupus erythematosus. 844 Feb 78

We report a patient with medial medullary infarction who showed deep sensory impairment as his prominent neurological manifestation. A 54-year-old man with a history of hypertension was admitted to our hospital with numbness of the bilateral upper and lower extremities, followed by dysarthria and right hemiparesis. Physical examination revealed no abnormalities except for high blood pressure. He hiccuped continuously. On neurological examination, he exhibited dysarthria, mild dysphagia and right hemiparesis without facial or lingual paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and thromboxane synthetase inhibitor. His hiccups stopped within two weeks, and his right hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive lupus anticoagulant. MRI showed bilateral infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities. Neurological manifestations of our patient are not typical of medial medullary infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable hiccups to the bilateral medial medullary lesions, and emphasize the importance of lupus anticoagulant as one of the risk factors in brainstem infarction.
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PMID:[A case of medial medullary infarction with prominent deep sensory impairment]. 892 33

A 36-year-old female with a history of recurrent pregnancy loss experienced sudden onset of disturbance in consciousness, with right hemiparesis and total aphasia. Computed tomography revealed a massive hemorrhage in the left frontal lobe, and angiography showed occlusion of the anterior two-thirds of the superior sagittal sinus. Laboratory investigations detected the presence of lupus anticoagulant, elevation of the anticardiolipin beta 2-glycoprotein I complex antibody level, and a decreased protein S activity level. There were no underlying conditions, such as connective tissue disorders, malignancies, infectious diseases, and drug-induced disorders, so the diagnosis was primary antiphospholipid syndrome. Primary antiphospholipid syndrome should be considered in the evaluation of patients with "idiopathic" or "primary" sinus and cerebral venous thrombosis.
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PMID:Superior sagittal sinus thrombosis associated with primary antiphospholipid syndrome--case report. 954 Mar 31


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