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 76-year-old woman was transferred to our facility for acute right middle cerebral artery (MCA) stroke. She initially presented with headache, left sided weakness, intermittent fever, and generalized malaise. She also developed laceration on the back of head due to syncopal attack. Prior to presentation, she had fever, productive cough, and dyspnea and was treated with antibiotics for pneumonia. Her past medical history included hypertension, atrial fibrillation, congestive heart failure, and chronic obstructive lung disease.\nAt an outlying facility emergency room (ER), her physical exam was concerning for altered mental status, left-sided weakness, and mild respiratory distress. No meningeal signs were observed. Her laboratory findings included mild leukocytosis. All cultures remained negative. Head and chest imaging were unrevealing. A lumbar puncture (LP) could not be performed because of her elevated international normalized ratio (INR) due to regular warfarin use for atrial fibrillation. She was treated empirically with acyclovir, ceftriaxone, and vancomycin. Her mental status worsened. A repeat computed tomography (CT) scan demonstrated a stroke within the medial right temporal lobe. She was transferred immediately to our tertiary care for urgent magnetic resonance imaging (MRI) and a higher level of care.\nAt the time of presentation to our hospital, she was found to have an altered mental status with left-sided hemiparesis. She was febrile, tachypneic, and tachycardiac with elevated blood pressures. A repeat CT scan showed an acute right middle cerebral artery (MCA) infarct associated with significant gyral swelling, causing a left midline shift of 4 millimeters (mm) (Figure ). A brain magnetic resonance imaging (MRI) (Figure ) confirmed CT findings. Computed tomography angiography (CTA) did not show any acute intracranial arterial abnormality. Tissue plasminogen activator (TPA) was not administered as the patient was out of the thrombolytic window.\nOur working differentials included acute ischemic stroke and herpes encephalitis. Due to the patient's atypical presentation of altered mental status, headache, left-sided weakness, syncopal episode, and radiographic findings of stroke, an electroencephalogram (EEG) was performed, which showed a high epileptogenic potential in the right hemisphere with poor localization. Hypertonic saline was started to reduce brain edema, along with IV acyclovir 10 mg/kg thrice a day and levetiracetam. As the edema subsided and INR normalized, an LP was performed. Polymerase chain reaction analysis of CSF was positive for herpes simplex virus (HSV) type one, supporting the diagnosis of herpetic encephalitis.\nA video EEG to check therapeutic and prognostic response after treatment was done. On the fifth day, the patient showed significant clinical improvement.