1410 - Herpes Simplex Meningocephalitis with Subsequent Right MCA Stroke, Subarachnoid Hemorrhage, and NMDA-R Encephalitis - A 22-year-old’s Complex Rehabilitation Journey: A Case Report

Friday, February 20, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

BV

Brian Vu, MD

resident physician
Casa Colina Hospital
Chino Hills, California, United States
AC

Alvin Chang, MD

resident physician
Casa Colina Hospital
Pomona, California, United States
XY

Xinyi Ye, MD

resident physician
Casa Colina Hospital
Pomona, California, United States

Submitter(s)

BV

Brian Vu, MD

Casa Colina Hospital
Chino Hills, California, United States

Case Diagnosis: 22-year-old male with Herpes simplex meningoencephalitis (HSE) developing subsequent right middle cerebral artery stroke (MCA), subarachnoid hemorrhage (SAH), and NMDA receptor encephalitis (NMDARE).

Case Description: The patient presented multiple times to the emergency department with persistent headaches and vomiting, but was discharged due to unremarkable imaging. New onset weakness, fever, and altered mentation prompted acute admission. CT head revealed SAH in the bifrontal and right temporal lobes. Subsequent MRI brain confirmed a right MCA infarct. CSF and PCR analysis identified HSE as the etiology. Upon acute rehabilitation transfer, initial exam showed cognitive deficits, gait dysfunction, and weakness. Methylphenidate was trialed to support cognitive recovery. By discharge, he achieved greater independence and mobility, but cognitive deficits persisted. Within three months, he was rehospitalized for NMDARE. Initial outpatient therapy evaluations noted regression in prior functional gains. Neuropsychological evaluation revealed impairments in processing speed, visual attention, and initiation - limiting ability to work or drive. Methylphenidate was restarted for cognition and behavior. Outpatient therapy and acquired brain injury program enrollment allowed the patient to progress towards post-rehabilitation levels.

Discussions: HSE likely triggered a cascade leading to right MCA stroke and subarachnoid hemorrhage, manifesting functional deficits requiring acute rehabilitation. HSV induces inflammation and vasculitis, which contributes to vessel damage, narrowing, and thrombosis. This predisposes vessels for ischemic and hemorrhagic compromise leading to cerebral vascular events. The subsequent NMDARE posed rehabilitation challenges due to regression in functional progress. It’s possible that NMDA receptor (NMDAR) antigen exposure during the innate immune response created autoantibodies against NMDAR over weeks to months. The clinical course highlights the importance of longitudinal, multidisciplinary outpatient rehabilitation. Moreover, this case adds treatment examples to the current literature for this phenomena.

Conclusions: HSE may cause stroke and delayed onset NMDARE, requiring close monitoring by a longitudinal, multidisciplinary rehabilitation team after acute infection.