MRI of the mind and CT check of the top performed after indicator onset was steady from a recently available hospital discharge six months earlier [ Figure 2 ]. Open in another window Figure 2. CT mind at most latest hospital discharge almost a year prior (A) compared to CT mind upon readmission for behavioral adjustments (B). diseases from the anxious system, central anxious system viral diseases, central nervous system infections, encephalitis, central nervous system infections, neuroimmunology, clinical specialty Introduction A significant association is identified between Herpes Simplex Virus-1 encephalitis (HSVE) and a post-infectious autoimmune encephalitis mediated by autoantibodies, most significantly N-methyl-D-aspartate receptor (NMDAR) antibodies.1-3 It is shown that 10-30% of patients with HSVE will later develop anti-NMDA receptor antibodies in the serum and CSF.2-4 In a mouse model, 4 of 6 mice inoculated with HSV-1 later develop serum antibodies to NMDAR and decreased expression of NMDAR in the hippocampus.5 The exact pathophysiology underlying this phenomenon remains ill-defined, but evidence suggests that HSV-mediated neuroinflammation exposes host NMDARs to the immune system, triggering CNS autoimmunity.2,3,6,7 Auto-antibodies detected in the post-infectious period must be interpreted within the context of clinical presentation. Importantly, a small proportion of patients without suspected autoimmune encephalitis will also develop auto-antibodies following central nervous system infection.1,3,8 In 1 prospective cohort trial, neuronal surface auto-antibodies were detected in either the serum or CSF of 30% (11/34) of patients following HSVE without clinical signs of encephalitis.1 Studies have also shown that a percentage of patients will test positive for more than 1 auto-antibody following infection,1,3,8,9 posing the GS-9451 question of which, if any, of these auto-antibodies are truly pathogenic. It remains unknown if neuronal auto-antibodies in patients with atypical clinical presentations represent a wide phenotypic range or may be incidental in a subset of patients. Here we present a challenging case of post-HSV NMDARE in a patient with comorbid psychiatric disease, extensive structural damage from her initial infection, and a nebulous timeline of symptom onset. Case Presentation A 19-year-old female with GS-9451 significant psychiatric comorbidities presented to a local hospital with altered mental status and seizures. Her past medical history was notable for psychiatric disease; including generalized anxiety disorder, panic attacks, agoraphobia, claustrophobia, self-mutilation behaviors, and depression. Her parents described behavioral and verbal disinhibition since a young age. She was withdrawn from school due to debilitating anxiety, but was not known to have cognitive deficits. There was no history of hallucinations, psychosis, or manic episodes. The patients presenting examination was notable for agitation, but otherwise non-focal and without meningismus. Her hospital course was complicated by fevers, headache, seizures, and progressive altered mental status. MRI of the brain showed partially enhancing FLAIR/T2 hyperintensities in the frontal and temporal lobes with right to left midline shift and diffuse leptomeningeal enhancement [ Figure 1 ]. She was intubated and empirically prescribed broad spectrum antibiotics, acyclovir, and intravenous antiepileptic medications for potential non-convulsive status epilepticus. She was then transferred to our GS-9451 hospital for further care. Open in a separate window Figure 1. MRI at initial presentation demonstrated FLAIR hyperintensities in the right frontal, temporal, and parietal lobes with subsequent right to left midline shift and mild uncal herniation (A). There was high signal on DWI in these areas, which (B) most likely represented T2 shine-through, based on lack of ADC drop out (C). There was diffuse right greater than left leptomeningeal enhancement, demonstrated here on coronal (D) and axial (E) post-contrast images. FLAIR= fluid-attenuated inversion recovery; DWI= diffusion weighted imaging; ADC = Apparent diffusion coefficient; T1 post= T1 weighted image after contrast administration. Upon transfer, lumbar puncture (LP) revealed an opening pressure (OP) of 55 cm H2O, 629 WBC /uL (70% lymphocytes, 17% Monocytes), 18 RBC /uL, glucose 54 (serum glucose 101) mg/dL, and protein 109 mg/dL; BioFire Diagnostics Inc. FilmArray Meningitis/Encephalitis PCR panel (M/E panel) was positive for HSV-1. All other infectious and inflammatory CSF studies returned negative; NMDAR antibodies were not tested at that time. After weaning of sedation, she had persistently poor mental status and intermittent loss of brainstem reflexes despite ICP management and acyclovir. Repeat imaging revealed herniation and she underwent emergent hemicraniectomy. Following the procedure, she was intermittently able to follow simple commands, had Rabbit Polyclonal to GCNT7 intact cranial nerves/brainstem reflexes, but had developed left hemiplegia. This improved with time, but her mental status continually fluctuated. EEG showed generalized slowing and left rhythmic delta activity without seizures or epileptiform discharges while on levetiracetam monotherapy. Imaging several days into her course showed interval development of bilateral frontal lobe infarcts. CT angiogram demonstrated right.