Psychosis in a Case of Japanese Encephalitis With Comorbid Systemic Lupus Erythematosus: A Rare Presentation

Japanese encephalitis (JE) virus, a flavivirus, is transmitted through the bite of the Culex mosquito. Like other mosquito-borne viral diseases, such as dengue and chikungunya, JE is also associated with neuropsychiatric sequelae.^1–3 A minority of infected patients (1%) develop encephalitis with symptoms such as fever, headache, weakness, cognitive impairment, disorientation, seizures, and coma.⁴ Psychiatric symptoms include affective instability, behavioral problems, personality changes, catatonia, and obsessive-compulsive symptoms.⁵ The literature on neuropsychiatric presentations of JE in cases with comorbid systemic lupus erythematosus (SLE) is sparse.

Case Report

A 25-year-old woman with SLE and on hydroxychloroquine 200 mg for the last 6 years presented to a health center with fever with chills and rigor, along with vomiting, decreased verbal output, memory impairment, and 1 episode of urinary incontinence. Around 2 weeks after the onset of symptoms, she had also developed repetitive involuntary movements of the extremities along with suspiciousness and fearfulness. She was admitted to the hospital, where she received supportive care and a short course of methylprednisolone injection (250 mg/day for 5 days), which was around 4 weeks after the onset of symptoms. Given the incomplete improvement in symptoms, she was referred to our center around the sixth week of symptom onset. The patient’s hemoglobin level was 13.2 g/dL, total leukocyte count was 8,910/µL, and platelet count was 298,000/µL. Renal function tests revealed a urea level of 11.4 mg/dL and creatinine of 0.48 mg/dL. Liver function tests showed total bilirubin level of 0.77 mg/dL, alanine aminotransferase of 58 U/L, and aspartate aminotransferase of 34 U/L. Her sodium level was 136 mmol/L, while potassium was 4.1 mmol/L. Her erythrocyte sedimentation rate was 22 mm/h, and C-reactive protein level was 1.5 mg/L. Thyroid profile, vitamin B₁₂, and infectious markers were checked and found to be within normal limits. Serum antinuclear antibody and antibodies to U1 ribonucleoprotein were positive. The patient’s anti–double-stranded DNA level was 22 IU/mL, and complement levels C3 and C4 were 115 mg/dL and 62 mg/dL, respectively, all within normal laboratory limits. The cerebrospinal fluid (CSF) examination revealed protein and glucose levels of 57 mg/dL and 54 mg/dL, respectively. Her white blood cells were elevated (15/µL), and oligoclonal bands were not detected. Autoimmune encephalitis and paraneoplastic panels were negative. Electroencephalography revealed no abnormalities, while serum and CSF immunoglobulin M (IgM) were positive for JE. Other infective causes were ruled out.

Magnetic resonance imaging of the brain showed subtle symmetric hyperintensities in the bilateral thalami on T2/fluid-attenuated inversion recovery imaging, suggestive of encephalitis sequelae. Psychiatric evaluation revealed that 2 weeks after the onset of initial symptoms, the patient had developed behavioral changes in the form of suspiciousness, fearfulness, and hallucinatory behavior with a firm belief that unknown people were trying to harm her, and she would not be convinced otherwise when her family members tried to reassure her. On mental status examination, the patient exhibited hallucinatory behavior, anxious affect, and delusion of persecution in thought content; however, she denied any perceptual abnormalities. At the same time, she had developed repetitive, involuntary, distal-predominant upper-extremity movements (right > left) and orofacial movements. The patient also developed foot drop and difficulty walking. On neurological examination, there were jerky, rhythmic movements of the distal extremities. Motor power was 4/5 in bilateral upper and lower limbs, while tone was normal. In reflexes, there was ill-sustained clonus (3+) in the left ankle, while other reflexes were within normal limits. No significant sensory deficits were detected. A nerve conduction study was done, which revealed left common peroneal axonopathy. SLE disease activity index-2000 (SLEDAI-2K) was 16 (psychosis and peripheral neuropathy). She was started on trihexyphenidyl 4 mg along with 250 mg/day of methylprednisolone injection for 5 days and a single dose of intravenous cyclophosphamide 800 mg in the seventh week after the onset of initial symptoms (fever with chills and rigor). There was improvement in involuntary movements and memory impairment. However, her psychiatric symptoms persisted. A provisional diagnosis of secondary psychotic syndrome (6E61) was made as per the International Classification of Diseases, Eleventh Revision.⁶ Olanzapine was started at a dose of 2.5 mg in the eighth week after the onset of initial symptoms and optimized to 5 mg. Subsequently, the patient had a significant improvement in psychotic symptoms, which was sustained in outpatient follow-up in the next month.

Discussion

Our patient developed decreased verbal output, memory impairment, involuntary orofacial and hand movements, foot drop, and difficulty walking. In the available literature, commonly reported neurological sequelae of JE include cognitive impairment, motor neuron symptoms, and cranial nerve symptoms such as dysphagia, speech difficulty, and vision and hearing loss.⁷ Our patient also demonstrated psychiatric symptoms in the form of hallucinatory behavior and delusion of persecution. It has been reported that psychiatric symptoms (forced crying/laughing and disturbance in consciousness) are common during the convalescent phase of JE, similar to the current case.³ Psychotic symptoms, particularly persecutory delusions, are relatively less common.⁸ In a study by Sarkari et al,⁸ of 453 JE cases, only 6 patients had persecutory delusions (1.3%).

This case also demonstrates a diagnostic dilemma. The patient had been known to have SLE for the last 6 years, and neuropsychiatric SLE may present with neurological and psychiatric symptoms, including psychosis.⁹ However, the patient had been on stable treatment, and psychiatric symptoms started 6 years after the diagnosis of SLE.⁹ Neuropsychiatric SLE (NPSLE) manifests early in the course of the illness, and common presentations include mood disorders, anxiety disorders, and cognitive dysfunction, while psychosis is relatively rare.⁹ In the current case, the psychotic symptoms occurred 6 years after the diagnosis of SLE, and there was no improvement in psychotic symptoms despite optimization of SLE treatment.

There was a temporal correlation between the onset of acute presentation of JE and psychiatric symptoms, which had started around 2 weeks after the initial presentation of fever with chills and rigor. Based on history, examination, and detailed evaluation, including positive serum and CSF IgM for JE and neuroimaging consistent with JE, it is possible that the psychotic symptoms could be secondary to JE. However, considering the history of SLE with a SLEDAI of 16, neuropsychiatric SLE remains a plausible explanation for these symptoms. Moreover, the case presentation could involve possible confounding by steroids. In conclusion, the current case underscores the importance of considering viral encephalitis as a differential diagnosis for acute neuropsychiatric presentations associated with fever, particularly in patients residing in endemic areas.

Article Information

Published Online: June 2, 2026. https://doi.org/10.4088/PCC.25cr04132
© 2026 Physicians Postgraduate Press, Inc.
Prim Care Companion CNS Disord 2026;28(3):25cr04132
Submitted: November 3, 2025; accepted February 13, 2026.
To Cite: Afroz O, Ramawat RB, Ahmed S, et al. Psychosis in a case of Japanese encephalitis with comorbid systemic lupus erythematosus: a rare presentation. Prim Care Companion CNS Disord 2026;28(3):25cr04132.
Author Affiliations: Department of Psychiatry, All India Institute of Medical Sciences, New Delhi, India (Afroz, Ahmed, Patil); National Drug Dependence Treatment Centre, All India Institute of Medical Sciences, New Delhi, India (Ramawat).
Corresponding Author: Vaibhav Patil, MD, Department of Psychiatry, 4th Floor, Teaching Block, All India Institute of Medical Sciences, New Delhi, India 110029 ([email protected]).
Financial Disclosure: None.
Funding/Support: None.
Patient Consent: Consent was obtained from the patient to publish the case report, and information has been deidentified to protect anonymity.
ORCID: Omar Afroz: https://orcid.org/0009-0001-8303-8260; Raja Babu Ramawat: https://orcid.org/0000-0002-3719-3438; Vaibhav Patil: https://orcid.org/0000-0002-2204-8625