A 49-year-old male with past medical history of type-1 diabetes mellitus, hepatitis B, chronic hepatitis C, intravenous drug abuse, and traumatic brain injury sustained after fall 2 years prior to presentation (with left hemisphere encephalomalacia) with no history of gastrointestinal bleed (not on aspirin or any anticoagulation treatment at home) presented to the emergency department (ED) with headache, altered mental status, and fever for 2 days' duration.\nOn arrival, patient was febrile with temperature of 102 F, pulse rate of 112 beats per minute, blood pressure of 143/80 mmHg, and respiratory rate of 20 breaths/minute with saturation of 100% on room air. Physical exam revealed a well-built and nourished gentleman, awake and orientated to person and place with Glasgow coma scale of 15. Fundoscopic exam revealed no papilledema. He was able to move all four extremities but had positive meningeal signs. Laboratory tests showed white blood cell (WBC) count of 9100/mm3 (72% polymorph nuclear (PMN) leukocytes and 19% lymphocytes). Patient had a lumbar puncture done and cerebrospinal fluid (CSF) analysis showed WBC count of 45 cells/mL (72% PMN leukocytes and 24% lymphocytes); protein of 78 mg/dL; and glucose of 201 mg/dl. Noncontrast computed tomography (CT) head showed an old left hemisphere encephalomalacia without any acute intracranial pathology ().\nPatient was treated empirically for meningoencephalitis (pending cultures) with vancomycin, ceftriaxone, and acyclovir plus first dose of dexamethasone prior to initiation of antibiotics and droplet precaution. Subsequently noncontrast magnetic resonance imaging (MRI) of the brain showed right temporal lobe involvement suggestive of HSV encephalitis (). Electroencephalography (EEG) showed slowing in the right frontoparietal area with no electrographic seizures. Patient's CSF cultures came back negative for both bacteria and HSV deoxyribonucleic acid (DNA) by polymerase chain reaction. But based on the patient's initial clinical presentation, EEG and MRI highly suggestive of HSV encephalitis, antibiotics were discontinued and acyclovir was continued. In the next days, fever subsided and neurological status improved so patient was discharged home on acyclovir treatment.\nTwelve days from the initial presentation, patient was brought back to the ED due to acute worsening of mental status. There was no trauma or fall as per family. He was confused, alert but disoriented to person, time, and place, and not following commands. Physical exam did not show any signs of trauma. Laboratory tests showed platelets count 343 × 103/mm3, partial thromboplastin time (PTT) 29.1 seconds, prothrombin time (PT) 14.3 seconds, and international normalized ratio (INR) 1.1. Noncontrast CT of the brain demonstrated interval development of acute hemorrhage within medial right temporal lobe, a rare complication of herpes simplex encephalitis. Computed tomography angiography (CTA) done at the same time was negative for any underlying vascular lesion (). Neurosurgery team was consulted and patient was treated conservatively. Subsequent CT scans done showed gradual improvement of the hematoma. Patient was continued on IV acyclovir and was discharged. Patient was followed up over the next 2 years and he returned to his baseline neurological status.
A previously healthy 34-year-old Korean female was admitted to a regional hospital for fever, myalgia and severe headache that had started 2 weeks ago. Brain MRI showed a high T2 signal intensity change and diffuse swelling of the right temporal lobe, insula and hippocampus (Fig. ). Lumbar puncture showed lympho-dominant pleocytosis. The patient was started on intravenous (iv) dexamethasone and acyclovir under a high suspicion of viral encephalitis.\nShe was transferred to our institution 4 days later due to persistent headache despite treatment. A noncontrast computed tomography (CT) brain scan taken at our institution showed a hemorrhagic transformation of the right temporal lobe, which was not observed on the initial MRI (Fig. ). Follow-up lumbar puncture showed 510 white cells per mm3 (82% lymphocytes), 144 mg/dL protein and 61 mg/dL glucose. CSF culture studies were negative for bacteria, fungi and tuberculosis. PCR of the CSF confirmed the presence of HSV1. The patient was free of neurological symptoms, with a Glasgow Coma Scale of E4M6V5, and was admitted for close observation and continuation of iv acyclovir. Corticosteroid treatment was discontinued upon her admission. On day 3 of hospitalization, the patient presented with a sudden onset of vomiting and severe headache. Brain CT showed an increased amount of temporal lobe hemorrhage and a leftward shift in the midline (Fig. ). Mannitol was administered but did not seem to have a significant effect. The patient became increasingly drowsy, and her right pupil became dilated. She underwent emergency right decompressive craniectomy, expansile duraplasty and ICP monitor insertion. Postoperative brain CT showed alleviation of midline shifting (Fig. ). The patient recovered fully 5 days after the surgery. Apart from mild intermittent headache and dizziness, she did not show any other significant clinical symptoms, including neuropsychological problems. There were no significant neurologic deficits upon neurological examinations performed by the attending neurosurgeon and neurologist. The patient was discharged after completion of 2 weeks of acyclovir and returned 2 months later for cranioplasty. She was followed up 3 more times after cranioplasty. She was stable, without any neuropsychological problems or neurologic deficits, and was able to successfully return to work as a public official.