Neurological involvement in systemic lupus erythematosus

The aetiology of neurological involvement in systemic lupus erythematosus (SLE) still remains largely uncertain, but there are some recent reports of retrovirus activity linked to human and mouse models of SLE. Antiribosomal P antibodies appear specific to SLE and tend to be associated with psychiatric disease, but not exclusively so. The role of antiphospholipid antibodies in the pathogenesis of SLE may not be solely to cause thrombotic events, but also to act directly on neuronal tissue. The importance of another group of antibodies, those against Beta 2 glycoprotein I, a phospholipid binding protein, is now being recognized. Amongst the many neurological manifestations of SLE, cognitive impairment is becoming increasingly recognized and appears not to be simply a response to chronic disease or its treatment. Of the newer imaging techniques applied to SLE, positron emission tomography has proved inconsistent and somewhat disappointing but single photon emission computed tomography in active disease appears more sensitive compared to MRI, although it still remains a nonspecific technique. The treatment of SLE remains disappointing and no controlled trials for neurological disease have been published to date but a number of experimental approaches do offer hope for the future.