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| Author(s): |
Simone Appenzeller
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | Campinas, SP. |
| Institution: | Universidade Estadual de Campinas (UNICAMP). Faculdade de Ciências Médicas |
| Defense date: | 2006-12-08 |
| Examining board members: |
Lilian Tereza Lavras Costallat;
Eloisa Silva Dutra de Oliveira Bonfã;
Emilia Ioue Sato;
Sandra Regina Muchinechi Fernandes;
Manoel Barros Bértolo
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| Advisor: | Fernando Cendes; Lilian Tereza Lavras Costallat |
| Abstract | |
Central nervous system (CNS) manifestations in systemic lupus erythematosus (SLE) arecomplex. They may be directly caused by SLE disease activity or may be secondary to comorbities. Our objective was to determine CNS manifestations in SLE patients and to determine structural and functional neuroimaging abnormalities associated with its occurrence. Patients with four or more classification criteria for SLE, followed at the Rheumatology Unit of the State University of Campnas were included. We observed 11.6% of epileptic seizures in SLE patients. The occurrence of epileptic seizures was associated with the presence of stroke and antiphospholipid antibodies. Recurrence of seizures was rare and associated only with the presence of antiphospholipid antibodies. Migraine was more frequently observed in SLE patients than controls and was associated with disease activity, Raynaud¿s phenomenon and antiphospholipid antibodies. Pacients with past history of migraine had more frequently organ damage. We observed white and gray matter atrophy in SLE patients. Although both were associated with disease duration and past history of CNS involvement, only gray matter atrophy was associated with the total corticosteroid dose. Patients with cognitive impairment had more frequently corpus callosum and hippocampal atrophy. A transient axonal dysfunction, secondary to disease activity and not to CNS involvement, was observed in SLE. Our results suggest that structural and functional neuroimaging methods are useful in confirming CNS involvement, but also identify subclinical involvement in SLE patients (AU) | |