A 79-year-old right-handed woman, with a history of hypertension, hyperlipidemia, and prior TIA, currently prescribed clopidogrel, was taken to an outside hospital with acute onset aphasia and right sided weakness. The time she was last known well was at 21:30 h. Her NIHSS score was documented as 10 at 23:47, within the three-hour intravenous TPA window, and her initial computed tomography (CT) head was negative for intracranial haemorrhage. However, her systolic blood pressure was documented as 195–217 mmHg, and she received several boluses of intravenous labetalol, totaling 40 mg, without a decrease below the 185 mmHg threshold to receive TPA. TPA was withheld, and she was transferred to our institution for possible endovascular intervention.\nOn arrival, at 01:30 h the following morning and now 4 h from symptom onset, her blood pressure was 137/79 and her heart rate was 91 beats per minute and regular. Her temperature was 97.1°F (36.2°C). Her neurological exam was significant for global aphasia, left sided gaze deviation, right sided face, and arm and leg weakness. Her NIHSS score had increased to 15, with the following point distribution: level of consciousness (0), orientation (2), commands (2), gaze (1), visual fields (0), facial symmetry (1), left arm motor (0), right arm motor (2), left leg motor (0), right leg motor (3), ataxia (0), sensory (0), language (2), dysarthria (2), and extinction (0).\nA stat CT perfusion and CT angiogram were obtained (Figures and ). There was no evidence of decreased blood flow or volume, and no evidence of a proximal vessel occlusion, which was unexpected given the density of her neurological findings on clinical exam. She was admitted to the acute stroke intermediate intensive care unit. Additionally, she was started on 3% hypertonic saline at 30 cc/h empirically in anticipation of cerebral edema, given the significance of her physical findings. She later developed a fever, with a temperature of 101.4°F (38.6°C), now approximately 11 h after symptom onset. A chest X-ray demonstrated bibasilar atelectasis (not shown), and admission lower extremity Doppler ultrasound showed no evidence of thrombus. Urine analysis demonstrated pyuria with moderate bacteria, and admission examination of her peripheral blood count demonstrated leukocytes totaling 10.2 × 103/μL. Two sets of blood cultures were obtained and she was started on broad spectrum antibiotics. Her temperature peaked on hospital day 2 at 103.3°F (39.6°C), now 22.5 h after symptom onset.\nAn MRI brain was obtained on hospital day 2, which demonstrated no evidence of restricted diffusion suggestive of a stroke (). Additionally, FLAIR imaging, although slightly motion degraded, showed only nonspecific white matter hyperintensities in the periventricular white matter, suggestive only of microangiopathy ().\nThe patient continued to demonstrate aphasia and right hemiparesis on hospital day 2. She was immediately loaded with intravenous valproic acid at 20 mg/kg and continued at 250 mg every eight hours thereafter. Additionally, the patient was empirically started on intravenous acyclovir at 10 mg/kg every eight hours. Furthermore, her antibiotics were broadened to include CNS penetrating fourth-generation cephalosporin. A stat EEG was ordered.\nThe family gave additional history of several prior lumbar spine injections for back pain, with the most recent approximately two months prior. As a result, empiric antifungal coverage was added with amphotericin B.\nCSF examination on hospital day 2 demonstrated clear, colorless CSF, with an opening pressure of 29 cm H2O, CSF protein of 61 mg/dL (normal 15–55), CSF glucose of 89 mg/dL, and a CSF pleocytosis (in cells/μL) consisting of 84 RBC and 7 WBC in tube 1 and 39 RBC and 11 WBC in tube 2, with a differential of 57% neutrophils and 19% lymphocytes in tube 4.\nEEG on hospital day 2 demonstrated focal slow waves and focal sharps, which were periodic at times in the left frontotemporal and midtemporal regions, and slowing of the alpha rhythm (). These abnormalities normalized by hospital day 3, with a reemergence of a posterior dominant rhythm of 8-9 Hz ().\nAdditionally, the patient's physical exam began to improve; by hospital day 3, she was to move the right upper extremity against gravity. By hospital day 6, she was alert and oriented to person, place, and time, with 4/5 strength in the right upper extremity.\nOn hospital day 6, the CSF PCR returned positive for HSV type 1. On hospital day 7, the patient was transferred to an acute inpatient rehabilitation facility. She was to complete a 21-day course of acyclovir via peripherally inserted central catheter, and she was instructed to follow up in four weeks. However, she failed to return to the clinic for her follow-up appointment.
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.