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

Apoplexy of the heart can be responsible for sudden and for recurring instability of cardiac rhythm and conduction, and for the clinical counterparts of syncope and sudden death. Every pathophysiological mechanism which produces cerebral apoplexy has its counterpart in apoplexy of the heart. Among the mechanisms documented are thrombosis, embolism and rupture of those special vessels supplying the sinus node, atrioventicular (A-V) node and His bundle. Apoplexy of the heart can occur either with or without significant or recognizable ventricular myocardial infarction. Acute vascular accidents within the critical centers of cardiac impulse formation and conduction deserve more frequent consideration in the explanation of unusual cases of "epilepsy", of seizure disorders of the elderly, of neurologic manifestations (which may be secondary as well as primary) of systemic diseases such as lupus erythematosus or thrombotic thrombocytopenic purpura, and indeed of every case of otherwise unexplanined syncope or sudded death at any age.
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PMID:De subitaneis mortibus. XXVIII. Apoplexy of the heart. 61 31

Systemic lupus erythematosus (SLE) developed in as 23-year-old woman with psoriasis during treatment with psoralen-ultraviolet-A (PUVA). The connective tissue disease was characterized by an erythematous rash, hair loss, nephritis, splenomegaly, seizures, and coma. Serum antinuclear antibodies were present in high titer, and hypocomplementemia developed. Antibodies to native or ultraviolet-irradiated DNA were not demonstrated. While the association of psoriasis and lupus may have been fortuitous, the temporal relationships suggest that PUVA treatment in this case may have been of pathogenetic importance in the development of the connective tissue disease.
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PMID:Systemic lupus erythematosus: association with psoralen--ultraviolet-A treatment of psoriasis. 76 Jun 58

A patient with a hereditary deficiency of the second component of complement and discoid lupus erythematosus with features of systemic lupus erythematosus was studied. The propositus had a 9-year history of rash and arthralgia. Transient renal disease had completely resolved; there was a history of seizures. Examination of his serum disclosed antinuclear antibodies but no total haemolytic complement activity. C2 was absent. Serum concentrations of C1s, C3, C5 and C9 were elevated; other complement components were present in normal concentration, including C3 pro-activator. The patient's C3 pro-activator was electrophoretically converted by inulin and four of five lipopolysaccharides, but was poorly converted by aggregated human IgG. Two separate turnover studies with radiolabelled C3 showed fractional catabolic rates of 3-03 and 2-48% of the remaining plasma pool/hr (range of three normals: 1-62-2-18%/hr); and estimated C3 synthetic rates of 2-74 and 2-31 mg/kg/hr (range of three normals: 0-89-1-40 mg/kg/hr). Serum complement profiles of the patient's family demonstrated that the C2 deficiency was inherited as an autosomal codominant. One sibling, homozygous for C2 deficiency, and three other siblings, both parents and one daughter, all heterozygous for C2 deficiency, are in good health. Immunofluorescent studies of the patient's diseased skin exhibited substantial deposits of IgG, IgM, C1q, and C4 but not of later acting complement components, properdin, or C3 proactivator. These studies do not support the notion that inflammation in C3-deficient individuals with lupus erythematosus is mediated by the alternative complement pathway.
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PMID:C3 metabolism in a patient with deficiency of the second component of complement (C2) and discoid lupus erythematosus. 108 39

CNS involvement is a rare manifestation of collagen disease. But in three patients with lupus erythematosus (L.E.) the disease was from its onset characterized by CNS signs: epileptic seizures, cerebellar ataxia, and organic psychosis. The combination of epilepsy or organic psychosis with inflammatory joint disease should make one consider L.E. in the differential diagnosis, even if there is no close time relationship between the occurrence of these signs. Muscle biopsy, EEG recordings and CSF examinations may be of diagnostic value in addition to serological and immunological studies.
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PMID:[Early CNS manifestations in lupus erythematosus (author's transl)]. 118 35

The most frequent neurological lesions found on Cranial Computerized Tomography (CT scan) in patients with Systemic Lupus Erythematosus (SLE) are cortical atrophy (psychosis, although in general atrophy is not associated with a particular clinical presentation), infarcts and haemorraghes (strokes). We describe a patient diagnosed of SLE who developed a psychotic clinical picture followed by generalized epileptic seizures within a context of diffuse lupus encephalopathy. On the neurological examination, she presented cortical blindness, generalized piramidalism and extrapiramidal rigidity. Various electroencephalographic recordings showed signs of diffuse cerebral involvement predominantly in posterior regions. Cerebrospinal fluid analysis showed a slight increase of IgG without oligoclonal bands and a positive anti-DNA antibody with an homogeneous pattern. Sequential CT images were carried out demonstrating hypodense areas initially in the occipital regions that extended progressively to the temporal, parietal and finally to the frontal lobes, with a moderate mass effect on the lateral ventricles and with no contrast enhancement. The images of the lesions on the CT disappeared completely with the adequate treatment as the symptomatology resolved. A MRI and cerebral angiography were performed when the patient recovered. Both MRI and angiography showed no alterations. We consider that this neuroradiological finding is exceptional, because of its total resolution. Nevertheless, more observations will be necessary to determine the exact meaning of these abnormalities.
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PMID:[Atypical neuroradiologic manifestation of systemic lupus erythematosus]. 149 82

Central nervous system (CNS) dysfunction in patients with systemic lupus erythematosus (SLE) is highly variable, although it is often described under a single heading of "neuropsychiatric" or "CNS" SLE. To clarify these CNS abnormalities, we studied 91 lupus patients, 63 of whom had CNS symptoms or signs, over 599 patient years. By placing patients in relatively homogeneous clinical groups (stroke, seizure, suicide attempt, hallucination, confusion, decreased alertness) we detected significant (but variable among groups) correlations with other manifestations of SLE, suggesting separate mechanisms for each CNS disorder. These correlations were lost if all "CNS-SLE" was considered as a single group. Patients with decreased alertness often had undetected systemic infections and had a high death rate from infection, rather than from CNS-SLE. The understanding of the pathogenesis and potential treatment of CNS disorders in lupus will depend on classifying the patients into homogeneous groups.
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PMID:Central nervous system disease in patients with systemic lupus erythematosus. 151 50

We tested sera of patients with various autoimmune rheumatic diseases for the presence of antibodies against sulphatide (an acidic glycosphingolipid), identified as a target antigen for antibodies against the liver cell membrane. Thirty-five percent (7/20) of patients with lupus in the active stage possessed anti-sulphatide antibodies, whereas 10% (2/20) of those in the inactive stage and 20% (4/20) of those in the stationary stage possessed such antibodies. Moreover, 10% (3/29) of patients with other autoimmune rheumatic diseases also possessed anti-sulphatide antibodies. The level of anti-sulphatide antibodies was significantly correlated with the levels of anti-double-stranded (ds) DNA antibodies (r = 0.634, P less than 0.001) and dextran sulphate-binding IgG (r = 0.407, P less than 0.001). The serum levels of antibodies against sulphatide were correlated with a history of seizures or psychosis in patients with autoimmune rheumatic diseases. Gels coupled with polyanionic dextran sulphate, monoanionic sulphanilic acid and DNA were shown effectively to adsorb anti-sulphatide antibodies in the sera of patients with active systemic lupus erythematosus (SLE) and autoimmune chronic active hepatitis (AI-CAH). These results suggest that the observed reactivity with sulphatide is due to the presence of antibodies capable of reacting with various anionic molecules in the sera of patients with autoimmune rheumatic diseases as well as those with AI-CAH.
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PMID:Antibodies against sulphatide in sera from patients with autoimmune rheumatic diseases. 154 28

Reported is the case of a 24-year-old Finnish woman who developed malignant hypertension while taking an oral contraceptive (OC) that contained 30 mcg of ethinyl estradiol. She presented with blurred vision, but reported no other remarkable signs or symptoms during the 5 months in which she had been using OCs. Laboratory tests at admission revealed incomplete systemic lupus erythematosus (SLE) with DNA antibodies and high levels of antiphospholipid antibodies. Her blood pressure was 220-140 mmHg. OC use was discontinued and antihypertensive treatment initiated, with good results. 2 years later, however, the patient developed epileptic seizures and an area of local atrophy in the cerebellum was identified through computerized tomography. In the 4-6th years after initial presentation, the patient experienced 3 miscarriages, all at 7-8 weeks of gestation. 1 year after presentation, the patient satisfied 4 of the criteria for SLE (positive DNA and antiphospholipid antibodies, thrombocytopenia, leukopenia, and proteinuria). At present, the patient's symptoms are being controlled with carbamazepine and metroprolol. The patient's older sister, who had never used OCs, had SLE. It appears that high levels of antiphospholipid antibodies are an additional risk factor for the development of vascular complications in OC users but are not induced by OCs. Similarly, while OCs are not believed to cause SLE, they can exacerbate the disease or unmask a lupus diathesis.
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PMID:Malignant hypertension and antiphospholipid antibodies as presenting features of SLE in a young woman using oral contraceptives. 174 6

A prospective study of the neurological manifestations in all patients with systemic lupus erythematous (SLE) was conducted between February 1985 to January 1989. Excluding herpes zoster infection of peripheral or cranial nerves, post-herpetic neuralgia and migraine, 36 neurological episodes occurred in 33 patients. The presenting symptoms were mental confusion (10), psychosis (five), seizures (six), focal neurological deficit (three), coma (two), headache (five), blurring of vision (three), neuropathy (one) and myelopathy (one). Of these manifestations, only eight episodes were due to primary involvement by SLE: psychosis (two), seizure (two), multiple cerebral infarcts (one), papillitis (one), neuropathy (one) and myelopathy (one). Infection was the most common secondary cause of neurological episodes: all 10 episodes of mental confusion (fungal seven, pyogenic two, tuberculous one, nocardial one); two of six seizures (tuberculous one, pyogenic one); all five headaches (tuberculous meningitis three, cryptococcal meningitis two). The other secondary causes included steroid psychosis (two), hypertensive encephalopathy with seizure (one) and hypertensive retinopathy (one). Three of five cases of focal neurological deficit were due to macrovascular disease rather than to vasculitic infarction. We concluded that cerebral psychosis was a relatively rare presentation in our patients with SLE. In patients who presented with a neurological problem, especially mental confusion, efforts should be made to ascertain the underlying cause, especially if this may be an infection.
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PMID:Neurological manifestations of systemic lupus erythematosus: a prospective study. 180 Oct 58

The central nervous system (CNS) is clinically involved in approximately 40% of all systemic lupus erythematosis (SLE) patients. Minor psychiatric symptoms and abnormalities on neuropsychological testing are being detected with increasing frequency. This review summarizes current thinking concerning the diagnosis and pathogenesis of CNS lupus. The main symptoms of CNS lupus can be diffuse (generalized seizures, psychosis) or focal (stroke, peripheral neuropathies). Neuropsychiatric symptoms often occur in the first year of SLE, but are rarely the presenting symptoms of the disease. In studies on the pathology of CNS lupus, vasculopathy, infarcts and haemorrhages are often observed, whereas vasculitis is rare. Endocardial lesions and mural thrombi have also been reported in 33-50% of CNS lupus patients. In diagnostic imaging of the CNS, magnetic resonance imaging (MRI) scans often provide evidence for edema or small infarcts, both in focal and diffuse CNS lupus, whereas computerized tomography (CT) scans only show gross abnormalities. The first reports on position emission tomography (PET) scans in CNS lupus patients show decreased glucose uptake in the brain. The cerebral blood flow decreases during active diffuse and focal CNS lupus. The blood-brain barrier is somewhat more frequently impaired in diffuse CNS lupus. Intrathecal IgG and IgM production is observed in 25-66% of all CNS lupus patient. Various specificities of autoantibodies have been observed in CNS lupus. Of these, anticardiolipin (ACA) antibodies show a well-documented association with focal involvement of the CNS in SLE. These antibodies could cause thrombosis by interfering with the protein C pathway of fibrinolysis. In addition, they are associated with endocardial and valvular heart disease, which is often observed in SLE and which could cause embolism. The relation between ACA and diffuse CNS lupus is not yet clear. Low-avidity anti-DNA antibodies are also found in CNS lupus, possibly because of their cross-reaction with cardiolipin. Antineuronal antibodies and lymphocytotoxic antibodies have been associated with diffuse CNS lupus and abnormalities on neuropsychological testing. However, the population of these antibodies is rather heterogeneous and it has not been possible to assess a common target antigen. Therefore, it is still obscure whether there is also a second immune-mediated mechanism responsible for the development of the diffuse form of CNS lupus.
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PMID:Diagnosis and pathogenesis of CNS lupus. 186 69


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