Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Lupus 2003
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

MULTIPLE OBSTACLES: There are many and various difficulties and obstacles during the medical treatment of epilepsy. They may create major stumbling blocks and largely jeopardize the control of this type of disease. POOR COMPLIANCE: Particularly frequent (30 to 50% of epileptics), it is one of the principle causes of pseudo-pharmaco-resistance. THE SIDE EFFECTS OF DRUGS: These are also frequent (15 to 30% of cases). Whatever their severity, they may be an important obstacle to the success of the treatment. Some of these effects are idiosyncratic, dose-independent, whereas others, non-idiosyncratic, are dose and time-dependent. THE AGGRAVATION OF EPILEPSY WITH ANTIEPILEPTIC AGENTS: This is possible and is usually due to an error in diagnosis, either in the type of seizure or the type of epilepsy in cause and which leads the physician to select an inappropriate treatment. Pregnancy may aggravate the progression of epilepsy in around a quarter of cases. Strict monitoring of the treatment is required. Intercurrent diseases and/or their treatment may have an impact on the epilepsy and its treatment. The diseases may be common affections or bacterial infections, psychiatric problems, lupus erythematosus or HIV infection. Likewise, the possible impact of commonly prescribed drugs such as those for gastric ulcers, asthma, cardiovascular diseases or even immunosuppressor treatments should be known. Renal failure and hepatic diseases often have a negative impact on antiepileptic treatments.
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PMID:[Difficulties and obstacles during medical treatment of epilepsies]. 1287 Apr

Antiphospholipid antibody syndrome (APS) may present with neurological syndromes. Cerebrovascular disease, chorea/ballismus, epileptic seizures, headache, cognitive impairment, transverse myelopathy, Devic's syndrome and multiple sclerosis-like presentations feature among others. Cerebrovascular disease is one of the most common presenting symptoms of APS, second only to deep vein thrombosis, and accounts for half of neurological manifestations in patients with APS; accelerated atherogenesis and cardioembolism are the most likely mechanisms implicated. Though infrequent, chorea is consistently associated with APS; the pathogenetic role of antiphospholipid antibodies (APLab) in this case might be routed through cerebrovascular disease in some cases and through purely immunological pathways in others. Both ischemic and immunological mechanisms have been demonstrated in the pathogenesis of epileptic seizures, which may account for 7% of neurological manifestations in APS. Although frequent in APS, a causative link between APLab and most common types of headache (migraine and tension-type headache) is more than dubious. Cognitive impairment may derive from a well-defined clinical tableau of multi-infarct dementia. Nevertheless, (highly frequent) less severe cognitive impairment has also been associated with the presence of APLab in the absence of magnetic resonance findings. A relationship between APS and transverse myelopathy seems likely but small numbers in the studies published to date preclude definite statements; routinely testing for APLab patients with neurological manifestations suggestive of multiple sclerosis seems to be unrecommended at the present time.
Lupus 2003
PMID:APS and the brain. 1471 5

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.
Lupus 2003
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.
Lupus 2004
PMID:Recent advances and future perspective in neuroimaging in neuropsychiatric systemic lupus erythematosus. 1511 42

A 52-year-old previously healthy woman was admitted to our hospital for status epilepticus in November 1999. She had not taken oral contraceptives. After treatment with intravenous diazepam and phenytoin, she did not develop seizures anymore. When she became alert, there was a mild left hemiparesis. Lumbar puncture showed an opening pressure of 145 mm H2O, and the cerebrospinal fluid was acellular. Cranial MR imaging demonstrated thrombosis of the superior sagittal sinus and fresh infarction in the right frontal lobe. Plasma fibrinogen, fibrin degradation product, and prothrombin fragment 1 + 2 levels were elevated. Proteins S and C activities and anti-thrombin III levels were within the normal range. Lupus anticoagulant and anti-cardiolipin antibody were negative. She was treated with continuous heparin infusion for ten days and with oral warfarin thereafter. Six months after the first admission, platelet count became more than 400 x 10(3)/microliter. In July 2002, she developed slowly progressive monoplegia of the left arm. Cranial MR imaging demonstrated patent superior sagittal sinus, fresh infarction in the right parietal lobe, and old small infarction in the right corona radiata. The patient was maintained on warfarin and 100 mg of aspirin thereafter. In September 2002, platelet count was 737 x 10(3)/microliter. Bone marrow examination showed increased megakaryopoiesis with normal erythroid and myeloid series and no chromosomal aberrations. Serum C-reactive protein and iron levels were in the normal range. An abdominal ultrasound demonstrated mild splenomegaly. Thus, we made a diagnosis of essential thrombocythemia (ET). ET causes thrombotic events in the course of the disease at a rate of 7% per year. Cerebral infarction is not uncommon, but occurrence of cerebral sinus thrombosis has been rarely reported. Recently, several cases have been reported in which cerebral infarction was the first manifestation of ET even with platelet counts lower than 600 x 10(3)/microliter. To our knowledge, there have been no reported cases of ET presenting with cerebral venous sinus thrombosis. Platelet count should be monitored in the patients with venous sinus thrombosis of undetermined etiology.
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PMID:[Superior sagittal sinus thrombosis as first manifestation of essential thrombocythemia]. 1519 36

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.
Lupus 2004
PMID:Systemic lupus erythematosus in Pakistan. 1554 May 18


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