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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous system involvement in systemic lupus erythematosus (SLE) occurs in 24%-50% of all patients in the United States at some time during the course of their illness. Lupus cerebritis with associated headache, seizures, stroke, and chorea is just one of a wide array of central nervous system disorders SLE patients can develop. It also is one of the most difficult manifestations of lupus to diagnose. Advances in imaging and laboratory analysis have contributed to an earlier and more specific diagnosis of lupus cerebritis. Despite improvements in the ability to treat SLE, management of nervous system manifestations remains unsatisfactory. Controversy exists as to the best approach for treatment. Newer combination therapies based on anecdotal evidence are suggested.
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PMID:Lupus cerebritis: a case study. 1219 58

Involvement of the central nervous system in systemic lupus erythematosus (SLE) has been well described. It usually includes psychiatric disturbance, seizures, and cranial nerve disorders. Movement disorders are less common, chorea being the one most frequently described. A parkinsonian syndrome may be an extremely rare manifestation of cerebral lupus. We report on a case of juvenile parkinsonism as a manifestation of SLE and review the literature.
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PMID:Juvenile parkinsonism as a manifestation of systemic lupus erythematosus: case report and review of the literature. 1246 77

Pancreatitis is a well-established but unusual complication of thrombotic thrombocytopenic purpura (TTP). It is also an unusual complication of systemic lupus erythematosus (SLE). However, TTP occurring as a consequence of acute pancreatitis in a patient with SLE has never been reported. We report a 24-year-old African American woman with active systemic lupus (SLE) who developed thrombotic thrombocytopenic purpura (TTP) following an episode of acute pancreatitis. The TTP was manifested by low-grade fever, microangiopathic hemolytic anemia, renal insufficiency, altered mental status, seizures and thrombocytopenia. The patient was initially treated with pulse corticosteroids with inadequate response and subsequently with daily plasmaphresis, leading to full remission. This case represents first report of pancreatitis leading to TTP in a patient with systemic lupus erythematosus.
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PMID:Pancreatitis leading to thrombotic thrombocytopenic purpura in systemic lupus erythematosus: a case report and review of literature. 1263 Jul 59

The purpose of this case report is to describe the clinical, electroencephalographic and neuroimaging findings from a woman with systemic lupus erythematosus presenting with complex partial status epilepticus (CPSE) of neocortical temporo-parieto-occipital origin. The patient experienced complex visual hallucinations that initially were attributed to treatment with corticosteroids; however, an electroencephalogram (EEG) demonstrated the epileptic aetiology of her symptoms. CPSE should be considered as a possible cause of altered mental status in lupus. An urgent EEG is essential to make an accurate diagnosis.
Seizure 2003 Jun
PMID:Complex partial status epilepticus of extratemporal origin in a patient with systemic lupus erythematosus. 1276 74

Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) is common and results in different clinical manifestations. Several pathogenic mechanisms have been suggested to play a role in determining such a variety of clinical symptoms. The thrombophilic state associated to the presence of antiphospholipid antibodies has been suggested to be responsible for a noninflammatory vasculopathy which causes clear ischaemic events as well as alterations of the cerebral microcirculation that are likely associated to seizures, cognitive dysfunction or psychosis. Although less frequent, a true vasculitic process affecting cerebral circulation has also been reported. In both cases, brain endothelium does represent the target of the pathogenic mechanisms. Brain endothelial cells display peculiar functional and phenotypical characteristics in comparison with endothelial cells from other anatomical districts, raising the possibility that this might be the reason for its susceptibility in lupus disease. We review and present data suggesting that a higher and firmer expression of beta 2 glycoprotein I on endothelial cell membranes can be responsible for a selective damage/activation by circulating anti-beta 2 glycoprotein I, and that antiendothelial cell antibodies crossreact with brain endothelium and in some cases, specifically bind brain endothelial cells only in lupus patients with central nervous involvement.
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PMID:Endothelium and the brain in CNS lupus. 1471 12

Involvement of the central nervous system (CNS) is one of the most important complications of systemic lupus erythematosus (SLE), occurring in 14-75% of SLE patients. Neurological and psychiatric involvement is mainly manifested as cerebrovascular disease, seizures, cognitive impairment, headaches and psychosis. However, diagnosis of brain involvement in SLE (i.e., neuropsychiatric lupus: NPSLE) as well as understanding of pathogenetic mechanisms still remains a difficult challenge. Although a wide range of neurodiagnostic tools have been used in the last decade to assess CNS involvement, no single technique has proven to be definitive or reliable. Since neurometabolic impairment, neurochemistry and perfusion abnormalities in NPSLE may precede anatomic lesions, new functional techniques such as magnetic resonance spectroscopy, diffusion and perfusion weighted imaging, and magnetization transfer imaging may be useful in order to indentify pathologic changes unrevealed by conventional imaging. So these new diagnostic tools could modify diagnostic and therapeutic approaches to this major unsolved problem, also shedding some light on the physiopathology of CNS disease in SLE.
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PMID:Recent advances and future perspective in neuroimaging in neuropsychiatric systemic lupus erythematosus. 1511 42

Phenytoin (diphenylhydantoin; Dilantin), ALZA Corp.) is a highly effective and widely prescribed anticonvulsant agent used in the treatment of focal and tonic clonic generalised seizures. The side effects of phenytoin can occassionally engender significant morbidity. Phenytoin can induce generalised eruptions that include: a maculopapular exanthem, Stevens-Johnson syndrome, generalised exfoliative dermatitis, toxic epidermal necrolysis, vasculitis and fixed drug eruptions. Phenytoin is linked to a hypersensitivity syndrome that manifests with fever, rash and lymphadenopathy. Patients receiving phenytoin may develop pseudolymphoma or, rarely, malignant lymphoma and mycosis fungoides-like lesions. Rarer cutaneous side effects include drug-induced lupus, purple hand syndrome, pigmentary alterations and IgA bullous dermatosis. Phenytoin can effect clotting function and alter vitamin and mineral levels. Prenatal exposure to phenytoin may result in a spectrum of structural, developmental and behavioural changes, known as the fetal hydantoin syndrome. Patients who use phenytoin in the long-term commonly manifest with gingival hyperplasia, coarsening of the facies, and hirsutism.
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PMID:Impact of phenytoin therapy on the skin and skin disease. 1550 Apr 23

Clinical features of systemic lupus erythematosus (SLE) have been described from different geographical regions in the world, with some clinical differences among different racial groups. Although data on the characteristics of SLE in Pakistan is scarce, it is not uncommon in the South East Asian region. The purpose of this study was, therefore, to delineate the clinical pattern and disease course in Pakistani patients with SLE and to compare it with international data on lupus patients. A total of 196 patients with SLE fulfilling the clinical and laboratory criteria of the American Rheumatism Association admitted to the hospital between 1986 and 2001 were studied by means of a retrospective review of their records. Demographically, it was seen that SLE is a disease predominantly of females in their third decade, which is consistent with worldwide data. The mean age of presentation was 31 years (range 14-76) and the mean duration of follow up was 34 (4-179) months. Generally, there was less cutaneous (46%), arthritic (38%), serositis (22%) and renal involvement (33%) but more neuropsychiatric symptoms (26%) in our population. Eighty-six percent of patients were ANA positive, whereas anti dsDNA was positive in 74% of patients. Infections, renal involvement, seizures and thrombocytopenia were associated with poor prognosis (P < 0.05). This study is the first of its kind in Pakistan. The clinical and laboratory characteristics of SLE patients in our study place our population in the middle of a spectrum between the Caucasians and other Asian populations. It has shown that the clinical characteristics of SLE patients in this country may be different to those of its neighbors.
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PMID:Systemic lupus erythematosus in Pakistan. 1554 May 18

We report on a 14 year old boy who presented with the symptoms abdominal pain, fever and proteinuria. A hematoma in the region of the right pararenal space was diagnosed. Prothrombin time and activated partial thromboplastin time were prolonged, lupus anticoagulant and anticardiolipin antibodies were positive and serum cortisol was normal. Ten days after admission the boy suddenly suffered generalized seizures due to low serum sodium. As well, the patient developed hemolytic anemia, acute elevated liver enzymes, hematuria and increased proteinuria. At this time a second hemorrhage of the left adrenal gland was documented. Adrenal function tests revealed adrenal insufficiency. We suspected microthromboses in the adrenals and secondary bleeding and treated the boy with hydrocortisone, fludrocortisone and phenprocoumon. CONCLUSION: Adrenal failure is a rare complication of APS in children with only five cases reported to date. As shown in our patient, this syndrome can manifest in a diverse set of simultaneously occurring symptoms.
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PMID:Adrenal failure followed by status epilepticus and hemolytic anemia in primary antiphospholipid syndrome. 1583 93

Neurological disturbances frequently emerge in antiphospholipid syndrome (APS). One hundred and twenty four patients (100 women, 24 men, mean age 37.5 +/- 11.3 years) with primary APS (PAPS), including 76 patients with Sneddon's syndrome and positive antibodies to phospholipids (aPL), have been studied. A structure of neurological disturbances was as follows: ischemic lesions of cerebral blood flow (LCBF) which comprised stroke and transient LCBF (91%); thrombosis of brain venous sinuses (3%); epileptic seizures (24%); headache (65%); chorea (15%); visual neuropathy (9%); peripheral neuropathy (6%); multiple-sclerosis-like syndrome (10%); myasthenia syndrome (1%); syndrome of parkinsonism of non-vascular genesis (1%) and psychotic disorders (2%). 84% patients had main systemic APS symptoms (fetal loss, thrombosis), which preceded neurological appearances in 78% cases. All the patients had aPL: aPL to cardiolipin (aCL) and/or lupus coagulant (LC) and/or aPL to phosphatidyl serine, phosphatidyl inositol, phosphatidyl ethanolamine. In some patients, aCL titres ranged from positive to negative values and LC was not consistently detected. Thus, the presence of clinical symptoms of PAPS including neurological disturbances demands an investigation of different aPL types as well as a replicate study for immunological confirmation of PAPS.
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PMID:[Neurological appearances of primary antiphospholipid syndrome]. 1598 22


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