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Neurological involvement in systemic lupus erythematosus
1Royal Cornwall Hospitals Trust, Truro, UK.
Current Opinion in Neurology
|June 27, 1998
Summary
Neurological involvement in systemic lupus erythematosus (SLE) has uncertain causes, possibly involving retroviruses and specific antibodies like antiribosomal P and antiphospholipid antibodies. Cognitive impairment is a key manifestation, with imaging and treatment showing limited but evolving progress.
Area of Science:
- Neurology
- Immunology
- Rheumatology
Background:
- The etiology of neurological involvement in systemic lupus erythematosus (SLE) remains largely uncertain.
- Recent reports suggest potential links to retrovirus activity in human and mouse models.
- Specific autoantibodies, including antiribosomal P and antiphospholipid antibodies, are implicated in SLE pathogenesis and neurological manifestations.
Purpose of the Study:
- To review the current understanding of neurological involvement in SLE.
- To explore the role of specific autoantibodies in SLE-related neurological disease.
- To discuss diagnostic imaging techniques and current/future treatment strategies for neurological SLE.
Main Methods:
- Literature review of recent reports on retrovirus activity in SLE.
- Analysis of the association between antiribosomal P antibodies and psychiatric disease.
- Examination of the role of antiphospholipid antibodies and anti-Beta 2 glycoprotein I antibodies in neuronal tissue.
- Evaluation of neuroimaging techniques such as PET and SPECT in active SLE.
- Review of current treatment approaches and experimental therapies for neurological SLE.
Main Results:
- Antiribosomal P antibodies are specific to SLE and associated with psychiatric disease.
- Antiphospholipid antibodies may directly affect neuronal tissue beyond causing thrombosis.
- Cognitive impairment is an increasingly recognized neurological manifestation of SLE.
- SPECT imaging shows sensitivity in active SLE, though it remains nonspecific.
- Current treatments for neurological SLE are disappointing, with limited controlled trials.
Conclusions:
- The precise mechanisms underlying neurological involvement in SLE require further elucidation.
- Specific autoantibodies play a significant role in the pathogenesis of neurological SLE.
- While imaging techniques have limitations, they offer insights into disease activity.
- Future experimental approaches hold promise for improved therapeutic outcomes in neurological SLE.