Neuropsychiatric lupus erythematosus, cerebral infarctions, and anticardiolipin antibodies.

Fields, Roderick A.; Sibbitt, Wilmer L.; Toubbeh, Hala; Bankhurst, Arthur D.

doi:10.1136/ard.49.2.114

Cited by 56 publications

(30 citation statements)

References 26 publications

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“…Moreover, placement of antibrain antibodies into the cerebrospinal fluid of normal animals produced recurrent epileptic activity (18). Nevertheless, the absence of aCL in the cerebrospinal fluid of 5 patients with positive serum aCL and acute CNS SLE, 3 of whom had seizures (19), makes a role for aCL as a direct antineuronal antibody unlikely.…”

Section: Discussionmentioning

confidence: 99%

Association between antiphospholipid antibodies and epilepsy in patients with systemic lupus erythematosus

Herranz¹,

Rivier

Khamashta

et al. 1994

Arthritis & Rheumatism

165

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Objective. To determine whether the occurrence of seizures is correlated with the presence of serum antiphospholipid antibodies (aPL) in systemic lupus erythematosus (SLE) patients.Methods. The study included 221 unselected patients with SLE. Of these, 21 patients with epileptic seizures not attributed to any cause other than SLE were identified. Epilepsy was diagnosed by clinical history and electroencephalography. Blood samples were tested for the presence of antibodies to cardiolipin (aCL, IgG and IgM isotypes) and lupus anticoagulant (LAC).Results. LAC was detected in 43.8% of the patients with epilepsy and in 20.8% of controls (P = 0.057). A statistically significant association was found between moderate-to-high titers of IgG aCL and the presence of seizures (P = 0.02). Brain computed tomography and/or magnetic resonance imaging scanning was performed in 14 patients. All patients with abnormal features found on these tests had positive aPL (P = 0.03). Nine patients (42.9%) had at least 1 of the classic features associated with the aPL syndrome. Conclusion. We confirmed that epilepsy as a primary neuropsychiatric event is significantly associated with moderate-to-high titers of IgG aCL in SLE

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Section: Discussionmentioning

confidence: 99%

Association between antiphospholipid antibodies and epilepsy in patients with systemic lupus erythematosus

Herranz¹,

Rivier

Khamashta

et al. 1994

Arthritis & Rheumatism

165

View full text Add to dashboard Cite

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“…17,18 Immulon I microtiter ELISA plates (Dynatech) were coated with 30 L (45 g/mL) of a standardized phospholipid antigen (Louisville aPL Diagnostics, Inc). The plates were blocked for nonselective binding with a 1% gelatin solution.…”

Section: Immunologic Testingmentioning

confidence: 99%

Neurometabolite Markers of Cerebral Injury in the Antiphospholipid Antibody Syndrome of Systemic Lupus Erythematosus

Sabet

Sibbitt

Stidley

et al. 1998

Stroke

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Background and Purpose-To determine the neurometabolic patterns of brain injury in systemic lupus erythematosus with antiphospholipid antibody syndrome (SLE-aPLS). Methods-Forty-nine SLE patients (12 SLE-aPLS) and 23 control subjects were studied using magnetic resonance imaging and spectroscopy. N-Acetylaspartate/creatine (NAA/Cre) and choline/Cre (Cho/Cre) were measured in normalappearing tissue. IgG and IgM antiphospholipid antibodies (aPL) were measured by enzyme-linked immunosorbent assay. Results-Stroke, epilepsy, and elevated IgG-aPL were more common in SLE-aPLS patients than in SLE patients (PϽ0.001). NAA/Cre was lower (PϽ0.05) and Cho/Cre higher (PϽ0.001) in SLE-aPLS patients than in SLE patients without aPLS. Regression models showed NAA/Cre was most related to injury seen by imaging (PϽ0.01), disease duration (PϽ0.05), and prior neuropsychiatric SLE (NPSLE) (Pϭ0.07). Reduced NAA/Cre was more closely related to IgG-aPL (PϽ0.01) than the presence of stroke or aPLS. When adjusted for all factors, Cho/Cre was most associated with the presence of aPLS (Pϭ0.05). Conclusions-SLE and SLE-aPLS are actually a clinical continuum describing brain injury in SLE, with SLE-aPLS beingcharacterized by increased aPL, NPSLE, stroke, epilepsy, and disturbed neurochemistry. An elevated IgG-aPL level is a potent risk factor for brain injury as measured by NAA/Cre in SLE that is independent of stroke and aPLS. However, thrombotic phenomena and the presence of aPL (aPLS) are most closely associated with increased Cho/Cre in SLE. These results suggest that aPLs exacerbate SLE, resulting in increased thrombotic and nonthrombotic brain injuries. Spectroscopy detects brain injury in SLE and may permit better understanding of the neurological consequences of SLE and SLE-aPLS. (Stroke. 1998;29:2254-2260.)

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“…Numerous studies link APA with stroke [2,3,32,72]. A direct pathogenic role of APA and stroke is, however, not established.…”

Section: Indirect Immune-mediated Effectsmentioning

confidence: 96%

Systemic lupus erythematosus: immunopathogenesis of neurologic dysfunction

Moore

Lisak

1995

Springer Semin Immunopathol

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Neurologic complications of systemic lupus erythematosus (neuro-SLE) are common. The most frequent manifestations of neuro-SLE are seizures, encephalopathy, and behavioral changes, but a wide variety of other neurologic abnormalities affecting the central and peripheral nervous system and muscle also occur. Although the prevalence of neuro-SLE is high, the diversity of clinical presentations, the multiple potential etiologies, and the absence of sensitive and specific diagnostic tests render diagnosis difficult. Recent advances in understanding mechanisms of neuronal dysfunction combined with advances in imaging techniques, including functional imaging, should help in diagnosis and management. The mechanisms of neurologic injury can be divided into three broad categories. First, neuronal dysfunction may result from direct effects of the immune system on brain cells such as autoantibody binding to cell surface, immune complex deposition with secondary inflammation, and effects of cytokines. Second, immune- mediated injury to supportive structures such as the vasculature may also affect the nervous system by producing ischemia. Finally, the neuraxis may be affected by any one of several immune and non- immune effects of infection, toxins, and metabolic disturbances.

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Neuropsychiatric lupus erythematosus, cerebral infarctions, and anticardiolipin antibodies.

Cited by 56 publications

References 26 publications

Association between antiphospholipid antibodies and epilepsy in patients with systemic lupus erythematosus

Association between antiphospholipid antibodies and epilepsy in patients with systemic lupus erythematosus

Neurometabolite Markers of Cerebral Injury in the Antiphospholipid Antibody Syndrome of Systemic Lupus Erythematosus

Systemic lupus erythematosus: immunopathogenesis of neurologic dysfunction

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