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)

A 17 year old girl with chronic relapsing pancreatitis since the age of 11 developed focal seizures, leukopenia, anemia and thrombozytopenia, signs suggesting lupus erythematodes. All immunologic investigations, including tests for Anti-DNS-Antibodies were negative, however. Therapy with prednisone and azathioprine resulted in clinical remission. Reduction of the immunosuppression lead to a severe crisis, which was controlled by plasmaseparation and cyclophosphamide. Subsequent analysis of circulating immune complexes revealed bound anti-DNS-antibodies.
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PMID:[Acute recurrent pancreatitis as the main symptom of lupus erythematosus disseminatus in childhood]. 325 73

Cranial magnetic resonance imaging in 28 systemic lupus erythematosus patients who had experienced 30 acute neuropsychiatric events showed focal brain lesions in 16 of 30 events (53%) and low brain volume (atrophy) in 20 of 30 events (67%). Definite focal lesions were significantly more frequent in patients with clinically localized neurologic deficits (8 of 8, 100%), or seizures (5 of 6, 83%) than in patients without such localizing signs (3 of 16, 19%). Many of these lesions were occult on intravenous contrast-enhanced x-ray computed tomography. In 2 patients, lesions in gray matter resolved within 2 or 3 weeks, in association with clinical improvement. Magnetic resonance imaging is an important technique for detecting the extent of brain injury in cerebral lupus.
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PMID:Identification of brain lesions in neuropsychiatric systemic lupus erythematosus by magnetic resonance scanning. 334 21

Lacunar infarcts in the basal ganglia are known to cause various movement disorders, such as chorea, focal dystonia, and hemichorea-hemiballismus. We report here a case of putaminal lacunar infarction which presented with "painful tonic spasms" of the contralateral limbs. This consisted of paroxysmal brief, painful, flexor contractures of the upper, and occasionally the lower limb. These were not focal seizures but were controlled with carbamazepine, which has been used for the "painful tonic spasms" well-associated with multiple sclerosis. The putaminal infarct we describe is probably related to a lupus anticoagulant and systemic lupus erythematosus.
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PMID:Painful tonic spasms caused by putaminal infarction. 381 Jul 37

A 13 year old girl with catatonia resulting from cerebral lupus is described. She had concurrent minor epileptic status, but abolition of her seizure activity failed to influence her catatonic state. She recovered after treatment with corticosteroids and immunosuppressive agents. Cerebral lupus should be considered in the differential diagnosis in patients presenting with catatonia.
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PMID:Cerebral systemic lupus erythematosus presenting with catatonia. 402 63

Two patients with well documented systemic lupus erythematosus developed a syndrome resembling thrombotic thrombocytopenic purpura. Both had severe thrombocytopenia, microangiopathic hemolytic anemia, seizures, and renal dysfunction. Prothrombin time, partial thromboplastin time, thrombin time, and fibrinogen levels were normal; fibrin degradation products were minimally elevated. Histologic evaluation of renal biopsies in both patients confirmed the impression of intravascular thrombosis. Therapy with corticosteroids, other immunosuppressive drugs and splenectomy (in one case) proved unsuccessful. The infusion of fresh frozen plasma, with or without plasmapheresis, reversed the syndrome. This report indicates that patients with systemic lupus may develop a thrombotic thrombocytopenic purpura like syndrome which responds to fresh plasma infusion.
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PMID:Thrombotic thrombocytopenic purpura syndrome in systemic lupus erythematosus: treatment with plasma infusion. 404 Nov 34

Fifty-one sera from patients with systemic lupus erythematosus (SLE) were studied in order to evaluate the prevalence of anticardiolipin (ACA) and anti-mitochondrial antibodies (AMA) type M5, and also to explore their relationship with the main serological and clinical features of the disease. A group of 25 (49.0%) patients was found to be ACA positive (IgG or IgG and IgM); in this group we found a significantly higher prevalence of false positive VDRL (p less than 0.01), lupus-like anticoagulant (p less than 0.05), and AMA type M5 (p less than 0.01), but not of anti-ds or ss-DNA antibodies. Three sera positive for ACA, AMA-M5 and anti ss-DNA were absorbed with cardiolipin liposomes. Anti-DNA and AMA-M5 showed only a minimal decrease. Central nervous system involvement and especially seizure syndrome was demonstrated with a higher prevalence in ACA-positive groups (p less than 0.05). Despite the results of absorption experiments, the close relationship between AMA-M5 and ACA, false positive VDRL or lupus-like anticoagulant (LLAC) might justify a speculation on the antiphospholipid nature of this antimitochondrial activity.
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PMID:Anti-phospholipid and anti-mitochondrial type M5 antibodies in systemic lupus erythematosus. 408 63

The study of serum from a patient with C2 deficiency is described. The patient had an episode of pneumococcal meningitis at 5 mo of age with seizures and transient hemiparesis and apparent purpuric skin lesions. He was first admitted to the University of Minnesota Hospitals at 10 yr of age following the discovery of proteinuria accidentally by his mother. Since then he has been admitted repeatedly to this hospital with numerous clinical findings including arthralgia, recurrent abdominal pain, proteinuria, membranous nephropathy, malar butterfly rash, seizures, personality aberrations, and recurrent fever. In June 1971, the patient developed positive DNA and DNP antibodies and positive LE cells. When the C profile was studied before and after recognition of lupus, C1q, C1s, and C4 dropped. C3 levels were elevated as were C5, C6, and C7, C3 proactivator had been reduced in the patient even before he developed lupus. Also because of a traumatic renal biopsy leading to a perirenal hematoma, he required surgery and a blood transfusion. 1 h after blood transfusion, a C2 titer of 23 hemolytic units was detected. Almost immediately levels of C3, C5, C6, and C7 dropped, C8 and C9 remained elevated. The addition of C2 from normal blood permitted dramatic activation of C3. These findings support the view that the rare deficiency in production of C2 predisposes to serious susceptibility to infection, vascular and mesenchymal disease as well as to renal disease and a lupus syndrome.
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PMID:C2 deficiency. Development of lupus erythematosus. 457 55

Three cases are presented, in two of which the CNS lesions revealed the presence of systemic lupus erythematosus (SLE). The diagnosis of SLE was certain according to the criteria of the ARA, and it was further confirmed by results of renal needle puncture biopsy. Case 1: A 16-year-old adolescent developed choreic movements followed, one month later, by psychotic symptoms suggesting a mixed hebephrenic-catatonic schizophrenic affection. Cutaneous lesions and signs of renal insufficiency 3 months later established that these disorders were related to SLE. A favourable outcome was observed rapidly for the systemic signs, recovery from neuropsychic symptoms being obtained after 3 months only but then in a few days. This course suggests the diagnosis of a "functional psychosis" of lupus origin. Case 2: A 24-year-old woman developed left hemiparesis followed by febrile coma. The slowly favourable course of the disease led to the appearance of a progressive dementia, with numerous epileptic seizures. Although tests for antinuclear antibodies were negative and the ESR was normal, several minor biological anomalies were suggestive of a systemic disease and the diagnosis of SLE was finally established. Corticotherapy produced only slight transient improvement. This progression towards dementia with progressive cerebral atrophy is most probably related to cerebral lupus lesions, the initial coma in the absence of any other apparent cause possibly being the first sign. Case 3: A 47-year-old woman developed simultaneously or separately episodes of arthralgia and uveitis of unknown origin over a 12-year period, and attacks of regressive multilocular neurological deficiency over a 15-year period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central nervous system involvement in systemic lupus erythematosus]. 671 10

A 20-year-old patient with biologically-confirmed lupus developed a perirenal abscess following puncture biopsy of the kidney. Postoperative treatment included metronidazole at a mean dose of 2.5 g daily for 68 days (total dose : 165 g). Generalised convulsive seizures occurred on four occasions, associated with paresthesia of the four limbs, but without loss of motor or reflex activity, though some distal hypoesthesia was detected. An acute lupus attack was eliminated, the convulsive seizures not recurring after discontinuation of treatment, and the paresthesias diminishing progressively over a period of three months. Electrical investigations showed lack of motor anomalies but a marked reduction in sensory conduction. This is the 13th reported case of polyneuritis due to metronidazole, the 4th case of convulsive seizures, and the first case in which both manifestations occurred. The plasma concentration curve after oral administration of 1 g of the product to this patient demonstrated that the product was not being metabolised in a pathological manner.
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PMID:[Convulsive seizures and polyneuritis in a patient with lupus treated with metronidazole (author's transl)]. 731 7

The validity of the hypothesis that some of the neuropsychiatric manifestations of systemic lupus erythematosus (SLE) are mediated by the direct effects of antibody binding to neuronal cell membranes is dependent on the demonstration of antineuronal activity within the central nervous system of patients with active central nervous system disease. Using a radiolabelled staphylococcal protein A assay, we tested cerebrospinal fluid from 27 patients with SLE and central nervous system manifestations, and cerebrospinal fluid from 18 additional patients with SLE but free of central nervous system disease for antibody reactive with the cultured human neuronal cell line SK-N-SH. Cerebrospinal fluid from 20 of 27 patients with active lupus central nervous system disease had increased immunoglobulin G (IgG) antineuronal activity compared with cerebrospinal fluid from two of 18 patients with SLE without central nervous system disease. Ninety percent of the patients with psychosis, organic brain syndrome or generalized seizures had increased IgG antineuronal activity as compared with only 25 percent of the patients who presented with hemiparesis or with chorea/hemiballismus. Antineuronal activity per microgram of IgG was concentrated eightfold in the cerebrospinal fluid of patients with active central nervous system disease as compared with the serum activity. Patients with or without active central nervous system disease did not differ significantly in the amount of serum antineuronal binding activity. The results are consistent with the hypothesis that the more diffuse central nervous system manifestations of SLE are a direct result of the interaction of antibody with neuronal cell membranes.
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PMID:Cerebrospinal fluid antibodies to neuronal cells: association with neuropsychiatric manifestations of systemic lupus erythematosus. 746 11


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