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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of the literature regarding central nervous system side effects of the nonsteroidal anti-inflammatory drugs (NSAIDs) revealed three general categories: aseptic meningitis, psychosis, and cognitive dysfunction. Aseptic meningitis is found most commonly in patients with lupus treated with ibuprofen, but it should be considered in any patient with meningitis if the patient has used NSAIDs. Psychosis, although infrequently reported with NSAIDs, should be suspected in an elderly patient started on a regimen of indomethacin who acutely develops disorientation, paranoia, or hallucinations. Finally, there appears to be some potential for memory dysfunction and attention deficits in elderly patients treated with NSAIDs. Until further studies are available on the incidence and severity of these cognitive changes, physicians should use low doses of NSAIDs in the elderly and remain alert to the possibility of such adverse side effects.
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PMID:Central nervous system side effects of nonsteroidal anti-inflammatory drugs. Aseptic meningitis, psychosis, and cognitive dysfunction. 206 81

The pathogenesis of neuropsychiatric lupus (NP-SLE) is unclear, but may involve vasculopathy, antibodies against nervous system tissue, or both. A major difficulty in determining the significance of antineuronal antibodies in NP-SLE has been lack of consistent clinical diagnostic approaches. By utilizing a new clinical classification of NP-SLE, neuropsychological assessments, and an assay for IgG antineuronal antibodies, we have found a significant association between antibody-positivity and cognitive impairment or nonfocal NP-SLE. These observations indicate that antineuronal antibodies may play a role in NP-SLE and emphasize the clinical importance of cognitive function in patients with SLE.
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PMID:Neuronal antibodies and cognitive function in systemic lupus erythematosus. 382 39

Hyperbaric oxygen has been used in patients with rheumatic disease for many years without reports of untoward or unusual complications for a variety of non-rheumatic indications. Recent evidence that hyperbaric oxygen inhibits the actions of certain cytokines, acts as an immune modulator and may help cognitive dysfunction has resulted in a re-examination of its potential role in rheumatic diseases. A case report of a lupus/scleroderma crossover patient is presented whose cognitive dysfunction improved after hyperbaric oxygen therapy. The history of hyperbaric oxygen and its physiology are related, along with a focused review of its effects on the immune and central nervous systems. Areas which might warrant further consideration by rheumatologists are outlined, as well as areas of concern.
Lupus 1995 Jun
PMID:Use of hyperbaric oxygen in rheumatic diseases: case report and critical analysis. 864 34

Neuropsychological assessments of adults with SLE have shown cognitive impairment, sequential processing deficits, memory loss, increased incidence of left handedness, learning disabilities and emotional distress compared with healthy individuals or subjects with other medical conditions. Neuropsychological testing regarding these variables in children and adolescents with SLE has been infrequently reported. For this study, eight children with SLE (age 9-17 years at diagnosis) were assessed with neuropsychological testing at a median of 10.5 months (range 1 week to 30 months) after diagnosis. Tests included Wechsler Intelligence Scale for Children-Revised or Wechsler Adult Intelligence Scale-Revised, Wide Range Achievement Test-Revised, Standard Binet Intelligence Scale Fourth Edition Memory Subtests or Wechsler Memory Scale (all mean = 100 +/- 15) and Gates MacInitie Reading Comprehension Test, Achenbach Child Behavior Checklist and Achenbach Youth Self Report. Mean intellectual scores were in the low average range (Wechsler Full Scale mean = 85.0 +/- 11.9, Verbal Scale mean 85.2 +/- 13.9, Performance Scale mean = 88.0 +/- 13.9). Academic achievement was globally depressed (reading recognition mean = 79.5 +/- 22.0, spelling mean = 78.9 +/- 23.5), especially in arithmetic (mean = 70.5 +/- 14.9). Children with SLE averaged 5 years behind grade placement in reading comprehension. Visual memory was also depressed in patients with SLE. Behavior ratings failed to demonstrate any significant aberrations in the test subjects.
Lupus 1995 Jun
PMID:Neuropsychological assessment of children and adolescents with systemic lupus erythematosus. 765 93

What have we learned about CNS lupus in recent years? An enormous amount of knowledge on pathophysiology of antiphospholipid antibodies, in particular, has been gathered. Although hard evidence of a direct pathogenetic role of these antibodies in cerebral lupus is still lacking, it is generally felt that the multiple microinfarctions found in the brains of lupus patients are related to their presence. Better understanding of the pathogenesis of cerebral lupus will come from the study of experimental models, as it has been possible to develop an antiphospholipid antibody syndrome in mice. Because no specific laboratory test for CNS lupus is yet available, diagnosing the condition remains a challenge to every clinician. Techniques including neuropsychometric testing, quantitative EEG, and SPECT scans have taught us more about cognitive dysfunction and psychosis in patients with SLE. These categories remain the most difficult to define. The concept of hypercoagulability in SLE patients has diverted the direction of therapy from immunosuppression towards anticoagulation. It is of utmost importance that randomised trials are commenced in order to determine the optimal mode of anticoagulation for various groups of lupus patients. It will be necessary to conduct such trials under strict inclusion criteria, based on well defined patient categories. Such an enterprise will require international co-operation of investigators.
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PMID:Controversies in lupus: nervous system involvement. 774 11

Poor performance on cognitive testing is common in SLE but it is not progressive in the majority of patients and may fluctuate or resolve without specific treatment. Cognitive impairment in patients without overt CNS-SLE may result from generalised disease activity or psychiatric disorder which reduce speed, concentration and motivation. This emphasises once again the importance of recognising and treating psychiatric disorder in these patients. Although mean cognitive scores are lower in SLE patients with overt CNS involvement than those without, an individual's cognitive score is a poor predictor of the presence of CNS involvement because of considerable overlap between groups. It has been suggested that the pattern of cognitive impairment, rather than simply whether it is present or absent, may be more helpful in identifying patients with CNS involvement but this requires further investigation in prospective studies. Cognitive impairment at one point in time is not predictive of future CNS events during 1 or 2 years of follow-up. Routine cognitive testing in SLE does not therefore appear to be helpful either for identifying patients with current CNS involvement or for identifying those at future risk of this complication. In the absence of double-blind randomised controlled trials, treatment of neuropsychiatric SLE is based on clinical experience and anecdotal case reports. Aggressive immunosuppression with high-dose corticosteroids in conjunction with either azathioprine or cyclophosphamide may be indicated in patients with life-threatening CNS-SLE but, on the basis of current evidence, is not justified in those with lone subtle cognitive abnormalities.
Lupus 1994 Jun
PMID:Psychiatric disorder and cognitive impairment in SLE. 795 Dec 98

Nervous system involvement in SLE encompasses a wide array of clinical manifestations which may reflect multiple etiologic factors including autoantibodies to nervous tissue antigens. The aim of the present study was to examine the association between autoantibodies to a wide range of brain antigens and cognitive abnormalities in an unselected population of 70 SLE patients. Using a battery of standardized neuropsychological tests, cognitive impairment was identified in 15/70 (21%) SLE patients compared with 1/25 (4%) patients with rheumatoid arthritis and 1/23 (4%) healthy subjects (P = 0.04). Integral membrane proteins were isolated from dissociated brain cells by temperature-induced phase separation with Triton X-114. Synaptosomes were isolated by differential centrifugation and membrane enriched fractions were prepared by lectin affinity chromatography. Western blotting identified IgG reactivity to a wide range of proteins (MW 22-52 K) in SLE patients. The proteins identified were distinct from well-characterized intracellular antigens including ribosomal P proteins. There was no significant difference in the prevalence of anti-brain antibodies between SLE patients who were cognitively impaired and those who were not impaired. Furthermore, there was no association between the presence of autoantibodies and subsets of cognitive dysfunction. These results suggest that circulating autoantibodies to brain antigens are not responsible for the abnormalities in cognitive function in SLE patients.
Lupus 1994 Jun
PMID:Brain reactive autoantibodies and cognitive impairment in systemic lupus erythematosus. 795 5

Antimalarials are under-utilized, disease-modifying agents that are useful in the management of lupus erythematosus. Antimalarials can promote a remission in non-organ-threatening lupus and decrease its risk of dissemination. They are especially useful for cutaneous and inflammatory joint disease and have modest actions in improving serositis, fatigue, and cognitive dysfunction. As agents that do not depress the bone marrow or promote opportunistic infections, antimalarials have potential applications in combination with other antilupus medications and with each other.
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PMID:Antimalarial agents and lupus. 815 1

Several independent studies have now demonstrated the presence of significant cognitive impairment in SLE patients. Such impairment, whether it precedes or follows overt NP events, suggests compromise of the neural substrate, irrespective of overt clinical NP symptomatology. The association between cognitive impairment and brain cross-reactive autoantibodies suggests one mechanism for CNS involvement in SLE that warrants further study; the data relating specific cognitive deficits to the presence of specific antibodies raise the intriguing possibility of system- or structure-specific immune-mediated involvement in the CNS. Whatever the mechanism, cognitive impairment in SLE may have significant implications for daily functioning of some lupus patients and requires the selection of appropriate psychosocial and somatic treatment strategies.
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PMID:Cognitive deficits in systemic lupus erythematosus. 826 24

In a cross-sectional study, 62 patients with systemic lupus erythematosus were assessed using standardized psychiatric and psychological methods; systemic disease activity was scored using the British Isles Lupus Assessment Group and the Lupus Activity Criteria Count indices. IgG and IgM anti-P antibodies were measured by ELISA using a synthetic 22 amino acid peptide as the relevant antigen. IgG and IgM anti-P antibodies were significantly associated with neuropsychiatric disorders (psychiatric and neurological) but failed to distinguish patients with psychiatric disorders from those with neurological disorders. These antibodies were not associated with cognitive impairment or systemic disease activity.
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PMID:Anti-P antibodies are associated with psychiatric and focal cerebral disorders in patients with systemic lupus erythematosus. 846 21


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