Case Presentation: A 40 year-old female with previous out of state hospitalizations for MDD and bipolar disorder with psychotic features presented with disorganized thoughts, withdrawn affect and depression at the behest of her family. Psychiatric evaluation noted echolalia, negativism, withdrawal and poor PO intake. A diagnosis of severe depression with catatonic features was made and patient was admitted to inpatient Psychiatry. She started therapy with Ativan for catatonia with minimal improvement. Pt was noted to have thrombocytopenia and leukopenia which led to investigation. Given pain in the bilateral hands and wrists, rheumatologic work up was sent. ANA was 1:2560. She also had a positive autoantibody testing to double stranded DNA, Smith antibody, and ribonucleoprotein. Low complement levels along with elevated inflammatory markers were also present. MRI brain and spine were unremarkable. CSF revealed unremarkable testing for NMO/AQP4 antibodies. Patient met SLICC criteria for SLE and was diagnosed as likely having neuropsychiatric manifestations of the disease. She began treatment with high dose steroids and cyclophosphamide and had moderate improvement in her symptoms. She required ongoing treatment for catatonia with IV Ativan and eventually amantadine. With the combined therapy for catatonia and neuropsychiatric SLE, patient improved and was discharged with ongoing Psychiatric and Rheumatologic care.
Discussion: Neuropsychiatric manifestations of systemic lupus erythematosus (NPSLE) occur in around 50% of patients with Systemic lupus erythematosus (SLE). 1 Catatonia is a rare CNS manifestation of SLE.1-3 Catatonia is characterized by a range of motor abnormalities and altered mental states, has been sporadically reported in SLE patients. Causes of catatonia include schizophrenia, critical medical illness, infections, drugs and auto-immune diseases like SLE.1, 4Catatonia in SLE patients presents with many symptoms including: mutism, stupor, agitation, and stereotypic movements. These symptoms often mimic primary psychiatric disorders, leading to delayed diagnosis and treatment. Catatonia in SLE may result from immune dysregulation, neuro-inflammation, and cerebrovascular abnormalities, although the precise pathophysiological mechanisms remain unclear.4Neuropsychiatric SLE, presenting as catatonia is very uncommon, and treatment of this condition is not well defined. Previously the role of benzodiazepines, immunosuppression, plasma exchange, and electroconvulsive therapy (ECT) have been described in its management.2, 4
Conclusions: This clinical vignette illustrates the rare but clinically significant phenomenon of NPSLE contributing to catatonia. As seen in this case, there is an intricate interplay between catatonia and SLE. Collaboration between rheumatologists, internists and psychiatrists is essential for timely diagnosis and effective management.Considering SLE as a contributing factor in the diagnosis of catatonic symptoms is important, particularly when other organic causes have been ruled out. Understanding the relationship between catatonia and lupus can contribute to improved diagnosis and management of both conditions, ultimately enhancing clinical outcomes as in this case.
