POSITRON EMISSION TOMOGRAPHY AND MAGNETIC-RESONANCE-IMAGING FOR CEREBRAL INVOLVEMENT IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS

Citation
M. Sailer et al., POSITRON EMISSION TOMOGRAPHY AND MAGNETIC-RESONANCE-IMAGING FOR CEREBRAL INVOLVEMENT IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS, Journal of neurology, 244(3), 1997, pp. 186-193
Citations number
48
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
03405354
Volume
244
Issue
3
Year of publication
1997
Pages
186 - 193
Database
ISI
SICI code
0340-5354(1997)244:3<186:PETAMF>2.0.ZU;2-Q
Abstract
Central nervous system (CNS) involvement in systemic lupus erythematos us (SLE) remains difficult to diagnose, particularly since structural abnormalities may not be revealed by magnetic resonance imaging (MRI). Glucose utilisation was measured by positron emission tomography (PET ) in 35 SLE patients to detect signs of CNS involvement. The patients were examined by a standardised neurological examination, a battery of tests to evaluate neuropsychological performance and MRI. Antineurona l antibodies were determined to investigate their putative role in CNS involvement in SLE. Twenty patients had distinct neurological (17) an d/or psychiatric (3) symptoms. Ten patients had pronounced cognitive i mpairment. Neurological and cognitive deficits were thus found to be u nrelated disorders in SLE. Global glucose utilisation of SLE patients did not differ significantly from that of normal controls, nor were di fferences found between SLE patients with or without neurological or c ognitive abnormalities. On MRI of the brain, the number and size of wh ite matter lesions correlated with the presence of neurological defici ts but were unrelated to the severity of cognitive impairment. Within the normal range, lower global glucose utilisation tended towards lowe r values with increasing number and size of white matter lesions. Pati ents with lesions larger than 8 mm also showed distinctly increased Ig G anticardiolipin antibody titres, whereas measuring antineuronal anti bodies did not reveal any relation to the variables investigated. We c onclude that the demonstration of CNS lesions by MRI can contribute co nfirmatory evidence for CNS involvement in SLE, but PET or the presenc e of antineuronal antibodies adds little if any information beyond tha t obtained by clinical examination, neuropsychological testing, and MR I.