The aetiology of neurological involvement in systemic lupus erythemato
sus (SLE) still remains largely uncertain, but there are some recent r
eports of retrovirus activity linked to human and mouse models of SLE.
Antiribosomal P antibodies appear specific to SLE and tend to be asso
ciated with psychiatric disease, but not exclusively so. The role of a
ntiphospholipid antibodies in the pathogenesis of SLE may not be solel
y to cause thrombotic events, but also to act directly on neuronal tis
sue. The importance of another group of antibodies, those against Beta
2 glycoprotein I, a phospholipid binding protein, is now being recogn
ized. Amongst the many neurological manifestations of SLE, cognitive i
mpairment is becoming increasingly recognized and appears not to be si
mply a response to chronic disease or its treatment. Of the newer imag
ing techniques applied to SLE, positron emission tomography has proved
inconsistent and somewhat disappointing but single photon emission co
mputed 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 neurologica
l disease have been published to date but a number of experimental app
roaches do offer hope for the future, Curr Opin Neurol 11: 247-251. (C
) 1998 Lippincott-Raven Publishers.