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 40-year-old left-handed Caucasian female with chronic headaches, along with a 20-pack-year smoking history, presented to an outside facility with one week of diffuse, generalized headache, fever, nausea, emesis, and photophobia. Her physical exam was without any focal neurological deficit. Initial cranial imaging was negative for hemorrhage. A lumbar puncture was performed and cerebrospinal fluid (CSF) studies demonstrated 558 white blood cells/mm3 with 100% monocytes, protein 115 mg/dL, and glucose 55 mg/dL. Polymerase chain reaction (PCR) of the CSF was positive for HSV-2. Taken together, the lymphocytic pleocytosis with elevated protein, along with CSF-PCR-positive staining for HSV, established the diagnosis of HSV-2 encephalitis.\nAcyclovir was initiated, and one week later while still hospitalized, she developed an acute altered mental status and left-sided weakness with cranial imaging showing a large right temporal lobe hemorrhage with significant midline shift. She was transferred to our facility where a computed tomography angiography (CTA), performed on arrival and shown in Figure , was negative for any underlying vascular lesion. There was again the demonstration of a large right temporal lobe intracerebral hemorrhage that was displacing the right middle cerebral artery superiorly as well as midline shift. Informed patient consent was waived due to her condition upon admission.\nShe was taken to the operating room for a decompressive unilateral (right) hemicraniectomy and temporal lobectomy. We had the operating room prepared for a possible vascular lesion despite the initial negative study. Figure -C demonstrates intraoperative images. A 15 x 12 cm (AP x lateral) craniectomy was measured out and performed, ensuring to stay within 2 cm off of the midline to avoid superior sagittal sinus bleeding []. The dura was opened in a cruciate fashion. A large red vein was noted superficially and coursed anterior-inferiorly toward the Sylvian fissure. A right temporal lobectomy was performed, measuring 5 cm posterior to the temporal tip. The parenchyma was noted to be very friable. The hematoma was removed, and there were no intraoperative complications. As the brain was decompressed, the red superficial vein normalized to the typical blue color commonly encountered. A postoperative angiogram was performed and demonstrated no vascular lesion as well as a normal alignment of the middle cerebral artery as is seen in Figure .\nPostoperative imaging is shown in Figure , which demonstrates good decompression and highlights the appropriate size of the craniectomy.\nHistopathological studies are shown in Figure and are consistent with herpes encephalitis, showing perivascular lymphocytic infiltrate, neuronophagia, and hemorrhage.\nShe had no postoperative complications and completed a three-week course of acyclovir. She was discharged to acute rehab with plans to return at a later date for cranioplasty.