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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous system involvement in systemic lupus erythematosus (SLE) is typically diagnosed on the basis of clinical psychiatric and/or neurologic syndromes (NPSLE). Neuropsychological tests can be used to assess nervous system integrity even in the absence of major NP syndromes. Their application has uncovered significant cognitive dysfunction, ranging from mild to severe, in a sizeable proportion of SLE patients irrespective of clinical NP status. Cognitive dysfunction has now been accepted as a bona fide manifestation of NPSLE. The heterogeneity of clinical NPSLE manifestations is paralleled by the diversity of cognitive deficits reported in different studies and within different patients. The success of attempts to explain these deficits on the basis of potential pathogenetic mechanisms, such as antibrain antibodies and proinflammatory cytokines, has been uneven. To date, the most robust findings have emerged in relation to antiphospholipid antibodies, which carry with them important therapeutic implications.
Lupus 2003
PMID:Cognitive dysfunction and antiphospholipid antibodies in systemic lupus erythematosus. 1471 6

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

As many as 66% of systemic lupus erythematosus (SLE) patients have been reported to have cognitive deficits. These deficits are often associated with information processing speed and working memory. Similarly, processing speed and working memory impairments are the hallmark of cognitive dysfunction in multiple sclerosis (MS). The Paced Auditory Serial Addition Test (PASAT) places high demands on processing speed and working memory. Fisk and Archibald, however, demonstrated that the total score of the PASAT does not accurately reflect impairments in these cognitive processes. They found that MS patients used a chunking strategy to obtain correct responses and reduce the cognitive demands of the task. In the present study, PASAT performance was examined for 45 SLE patients and 27 controls using alternative scoring procedures. Although the total number of correct responses did not differ between SLE and controls at the 2.4 or 2.0 s presentation rates, SLE patients had fewer dyads (correct consecutive responses) than controls at the faster rate, and more chunking responses than controls at both rates. Disease activity, disease duration, depression, fatigue, and corticosteroids could not account for these differences. The findings suggest that SLE patients, like MS patients, chunk responses more often than controls, and that this scoring procedure may better reflect the working memory and processing speed deficits present in SLE.
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PMID:Working memory and processing speed deficits in systemic lupus erythematosus as measured by the paced auditory serial addition test. 1475 Oct 5

Systemic lupus erythematosus is a multifactorial autoimmune disease of complex etiology, which may be associated with cognitive dysfunction, seizures, and headache. The authors present an unusual presentation of systemic lupus erythematosus complicated by global cerebral edema and subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm. The complicated patient management issues are discussed.
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PMID:Global cerebral edema and subarachnoid hemorrhage in a patient with systemic lupus erythematosus. 1502 Dec 88

Among the rheumatic diseases, systemic lupus erythematosus (SLE) reveals the highest frequency of central nervous symptoms. Psychiatric abnormalities are present in over 90% of the patients, if very mild cognitive impairment is included. The psychiatric syndromes listed by the American College of Rheumatologists encompass cognitive syndromes, including the acute confusional state, anxiety disorders, depressive symptomatology and psychosis. Associations between cognitive impairment and demographic and disease variables, i. e. disease severity, have not been clearly identified so far. The same holds true for the evolution of depressive symptoms. Reactive depression in coping with a chronic disease is, however, a psychologically plausible factor in addition to specific cerebral lesions. Therapeutic interventions in SLE should consist of a combined pharmacological and nonpharmacological treatment. Corticosteroid drugs, however, may be effective in alleviating mild psychiatric symptoms as well.
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PMID:[Psychiatric disorders in rheumatic diseases, as exemplified by systemic lupus erythematosus (SLE)]. 1511 90

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

Patients with lupus (SLE) experience progressive cognitive loss without evidence of CNS vascular disease or inflammation. SLE patients produce anti-DNA antibodies that crossreact with NMDA receptors and are capable of mediating excitotoxic death. We now show that mice induced by antigen to express these antibodies have no neuronal damage until breakdown of the blood-brain barrier occurs. Following administration of lipopolysaccharide (LPS) to immunized mice, antibodies gain access to the brain. They bind preferentially to hippocampal neurons and cause neuronal death with resulting cognitive dysfunction and altered hippocampal metabolism on magnetic resonance spectroscopy. Memantine, an NMDA receptor antagonist, given prior to LPS administration, prevents neuronal damage. Thus, systemic immune responses can cause cognitive impairment in the absence of an inflammatory cascade, implicating the immune system in yet another arena of human pathobiology. Furthermore, NMDA receptor antagonists prevent antibody-mediated damage and may constitute a new approach to therapy in SLE.
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PMID:Cognition and immunity; antibody impairs memory. 1530 99

Cognitive dysfunction represents one of several neurological and psychiatric complications of Systemic Lupus Erythematosis (SLE). Additional manifestations of nervous system involvement subsumed under the term neuropsychiatric SLE (NPSLE) include cerebrovascular disorder, seizures, psychosis, acute confusional state, anxiety and mood disorders. Neuropsychological investigations have facilitated the identification and description of cognitive impairment in SLE and NPSLE. Salient findings from studies of SLE-related cognitive dysfunction are reviewed with respect to neuroimaging procedures, indices of disease activity, and potential moderator variables. Data on cognitive functioning are also discussed in reference to other disease aspects including fatigue, sleep disturbance, and impact on health-related quality of life (HRQL). To date, neuropsychological functioning has been studied extensively, albeit separately from other commonly reported SLE-related symptoms. Future research may profit from investigating relationships between cognitive impairment, sleep disturbance and fatigue and their collective impact on functional capacity and quality of life.
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PMID:Factors influencing cognitive function, sleep, and quality of life in individuals with systemic lupus erythematosus: a review of the literature. 1559 65

The objective of this study was to examine psychological processes in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients in relation to measures of life stress, coping styles, social support and cognitive ability. Fifty-two SLE patients without overt neuropsychiatric symptoms, 29 RA patients and 27 healthy controls completed measures of depression, mood, disease activity, perceived health, stressful life events, coping, and social support. Variables entered into the multiple regression analysis following principal component analysis were: group, major difficult event, major life threatening event, disengaging coping, emotional coping, social support, and cognitive impairment. Depressive symptoms were associated with SLE group status (P < 0.001), major life-threatening events (P < 0.01), disengage coping (P < 0.001) and emotional coping (P < 0.05). SLE group status (P < 0.05), disengage coping (P < 0.05) and emotional coping (P < 0.05) were associated with current distressed mood. SLE patients without overt, major neuropsychiatric symptoms had greater psychological distress compared to RA and control subjects. Increased depressive symptoms and distressed mood state in SLE patients were related to use of disengaging and emotional coping styles. These findings are limited to SLE patients with no overt neuropsychiatric illness and low disease activity, suggesting the need for future studies with a greater variety of SLE patients. Interventions aimed at improving active coping and minimizing emotional response to stress may lower psychological distress in SLE patients with mild disease.
Lupus 2005
PMID:Major life stress, coping styles, and social support in relation to psychological distress in patients with systemic lupus erythematosus. 1593 36

Systemic lupus erythematosus (SLE) is an autoimmune disease that may involve the central nervous system (CNS) resulting in neuropsychiatric manifestations. The associated psychiatric disorders include depression, psychosis, mood disorders, anxiety, cognitive dysfunction, and delirium/ encephalopathy. Several autoantibodies may play a role in the pathogenesis of psychiatric complications of SLE, particularly antibodies against ribosomal P-proteins (anti-P) and possibly antibodies against endothelial cells (AECA). The reported prevalence of anti-P is highly variable in SLE patients and is dependent on different ethnic backgrounds, sensitivity and specificity of the assays employed for autoantibody detection, and the time at which sera were analysed in relation to the clinical event. Controversial data exist on the association of anti-P with psychiatric manifestations of SLE. These autoantibodies have been suggested to be specific markers of the psychiatric manifestations of SLE, particularly of the psychosis and depression, and the antibody level varied with the clinical activity of the disease. Some studies have confirmed the hypothesis of an association of anti-P antibodies with psychiatric manifestations of neuropsychiatric SLE (NPSLE) while others have disputed this relationship. This review summarizes the recent studies about relationship between anti-P antibodies and psychiatric manifestation of SLE.
Lupus 2005
PMID:Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: myth or reality? 1617 27


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