Psychosis in Patients with Systemic Lupus Erythematosus

Abstract

Neuropsychiatric manifestations in systemic lupus erythematosus (SLE) are common; however, psychosis per se is bit uncommon. They may be cognitive deficit, lupus headache, psychoses, seizures, peripheral neuropathy, and cerebrovascular events. Psychiatric symptoms in SLE can be functionally independent psychiatric disorders. It can be due to drugs (steroids) used for SLE or secondary to SLE because of its brain involvement, which is termed as neuropsychiatric systemic lupus erythematosus (NPSLE). No single clinical, laboratory, neuropsychological, and imaging test can be used to differentiate NPSLE from non-NPSLE patients with similar neuropsychiatric manifestations. Presently we are discussing about three cases of SLE with psychosis and which had different clinical presentation. The present reports also depict the approach to case differential diagnosis and management of the same.

A clinical approach to new-onset psychosis associated with immune dysregulation: the concept of autoimmune psychosis

“…It also serves as a reminder not to overlook appropriate neurological workup, (such as neuroimaging, EEG testing, and CSF investigation), but rather to apply it more broadly to formulate accurate differential diagnostic considerations that entertain underlying autoimmune process among other organic etiologies. Examples of atypical psychotic presentations suggestive of organic causes [ 31 , 32 ] are (1) atypical age of onset; (2) predominance of particular symptoms such as confusion, disorientation, and language disintegration; (3) catatonia, given its diverse etiology; (4) predominance of visual or multi-modal hallucinations (visual and tactile); (5) olfactory hallucinations suggestive of mesial temporal lobe pathology; (6) predominance of specific delusions such as those related to misidentifications (Capgras syndrome); (7) antecedent or concurrent medical illness or systemic manifestations including significant weight loss; and (8) lack of predisposing risk factors for primary psychosis such as a strong family history of schizophrenia, a premorbid schizoid personality, or precipitating stress for mental disorder.…”

“…The clinical accompaniments [ 17 , 33 , 34 ] are (1) atypical psychotic presentation [ 31 , 32 ]; (2) neurological disturbances such as rapidly evolving encephalopathy, seizures including faciobrachial dystonic seizures pathognomonic for limbic encephalitis associated with leucine-rich-glioma inactivated 1 (LGI1) antibody, abnormal movements, autonomic instability, language disintegration, and reduced level of consciousness; (3) antecedent systemic symptoms or viral-like febrile illness suggestive of prodromal phase of autoimmunity; (4) unexplained soft or overt findings on neurological examination; and (5) strong personal or family history of autoimmune disorders.…”

“…The ancillary diagnostic abnormalities suggestive of underlying neuroimmune dysregulation [ 32 – 38 ] include the followings: (1) elevated serum levels of antibodies targeting synaptic and neuronal cell membrane proteins, or biomarker characteristic for comorbid autoimmune disorders such as systemic lupus erythematous and Hashimoto’s encephalopathy among many others; (2) CSF, neuroimaging, and EEG abnormalities after excluding other organic causes such as infectious etiologies: (a) CSF abnormalities include antibodies targeting synaptic and neuronal cell membrane proteins, lymphocytic pleocytosis, oligoclonal bands, elevated IgG index, and elevated neopterin level (a non-specific marker of T helper cell 1 activation-dependent immune response) [ 35 ]; (b) neuroimaging structural and functional abnormalities such as unilateral or bilateral hippocampal MRI FLAIR/T2 signal hyperintensities suggestive of autoimmune limbic encephalitis [ 33 ], as well as hyper-, hypo-, or heterogeneous cerebral glucose metabolism on FDG- positron emission tomography (PET) or altered cerebral blood flow on single photon emission computed tomography (SPECT) [ 33 , 36 , 37 ]; we suspect that FDG hypermetabolism, as opposed to hypometabolism, might be more indicative of inflammation after excluding alternative causes [ 38 ]; and (c) EEG abnormalities such as epileptiform discharges, delta brushes [ 33 ].…”

The role of neutrophils in the pathogenesis of systemic lupus erythematosus

“…currently-medications used for SLE-including corticosteroids, anti-malarials, cyclosporin, B cell depletion, and BAFF blockade-are not always effective in cases of severe disease 12 . These immunosuppressive medications often increase risk of infection and in the case of steroids, cause weight gain, osteoporosis, and in rare cases, steroidinduced psychosis 13 . The significant side effects of current therapies often lead to medication non-compliance in lupus patients, contributing to the elevated mortality in these individuals 14,15 .…”

Psychopharmacological Options in the Management of Lupus Cerebritis: A Case Report

“…Previous suggestions have been made through case reports regarding pharmacological management of neuropsychiatric systemic lupus erythematosus. One study recommended use of olanzapine and quetiapine in this group of patients (6). Good sense suggests that the same precautions and monitoring that is undertaken for the general psychiatric population should be employed when using psychotropic drugs in this patient category.…”