Systemic Lupus Erythematosus and Psychiatric co morbidities

Volume 3 Issue 5 May, 2013

Consultation Liaison Psychiatry Focus: Rheumatology

Systemic Lupus Erythematosus (SLE) is a multisystem disease with protean manifestations and these are a result of circulating pathogenic autoantibodies, deposition of immune complexes and presence of circulating inflammatory cytokines. Psychiatric symptoms are common in SLE and the prevalence shows a great variability ranging from 17 to 75 %. Neuropsychiatric SLE (NPSLE) manifestations occur as single or multiple events even during periods of no non‐nervous system disease activity. 40% of NPSLE manifestations develop before diagnosis of SLE and 63% occur within first year of diagnosis.

NPSLE syndromes in SLE may manifest in 19 different ways in the central and peripheral nervous system ranging from acute confusional state to plexopathy and polyneuropathy. What makes NPSLE so complex and heterogeneous is the multiplicity of proposed pathogenic mechanisms. Three mechanisms are currently described: autoantibodies, vascular abnormalities, and inflammatory mediators. Autoantibodies include antiribosomal P, antineuronal, antiglutamate, anti NMDA receptor and antiphospholipid antibodies

A psychiatric disturbance due to CNS lupus is a diagnosis of exclusion; all other possible causes of the observed symptoms must therefore be considered, including infection, electrolyte abnormalities, renal failure, drug effects, mass lesions, arterial emboli, and primary psychiatric disorders (such as bipolar disorder or severe stress disorder resulting from a chronic and life‐threatening disease). Controversy exists concerning the factors responsible for psychiatric manifestations as the pathophysiological process may be compounded by iatrogenic effects of corticosteroids and psychosocial stressors related to chronic disease.

The diagnosis of NPSLE can be made only on a case‐by‐case basis. Select autoantibodies, CSF analysis, neuroimaging, and neuropsychological testing may be used. If clinically indicated, echocardiograms and carotid Doppler ultrasonograms should be obtained to rule out atheroembolic disease to the brain, which is accelerated in active SLE.

The management of patients with NPSLE is multimodal and continues to be a major therapeutic challenge due to the broad spectrum of the NPSLE manifestations and limitations in diagnostic testing. Glucocorticoids are one of the primary therapeutics and other medications can range from nonsteroidal anti‐inflammatory drugs for symptomatic relief, anticoagulation for thrombotic diseases, to the immunosuppressives for inflammation such as cyclophosphamide, azathioprine, mycophenolate mofetil, and methotrexate. Evidence for the efficacy of these therapies is limited to uncontrolled clinical trials and anecdotal experience. Adjunctive symptomatic treatment complements these therapies by targeting mood disorders, psychosis, cognitive impairment, seizures or headaches. Psychotropic medications (antidepressants, anxiolytics, and atypical antipsychotics) may have an important adjunctive role in SLE patients with affective disorder or psychosis. There is no standardized treatment in lupus psychosis. The treatment includes a combination psychotropic medications and glucocorticoids to control underlying disease activity. Most psychiatric episodes resolve within 2–4 weeks and only 20% of SLE patients develop a chronic psychotic disorder of lesser severity. Close liaison with psychiatry is beneficial for treating clinician in the management of SLE.

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