A 51-year-old diabetic woman was admitted to hospital with fever and acute confusion. In the emergency department, no signs of meningeal irritation and focal neurological signs were detected. A CCT was unremarkable [] and lumbar puncture showed 1 cell/μL (normal < 4) and slightly elevated protein 646 mg/dl (normal < 450) with normal glucose. As blood glucose was high (351 mg/dl), an infection triggered diabetic disorder was suspected. Therefore the patient was treated by the internist. The following day the patient suffered from aphasia. Since aphasia persisted, a stroke of the left temporal lobe was assumed next. However, as fever continued and confusional symptoms predominated, a second lumbar puncture was performed. The result, this time, showed elevated cell count (31 cells/μL, normal < 4) and elevated protein 1157 mg/dl (normal < 450). HSV was tested positive in the first and second CSF sample by PCR. Despite virostatic therapy with intravenous acyclovir (10 mg/kg every 8 h for 21 days), the patient's condition deteriorated, making mechanic ventilation and intensive care necessary. Furthermore neuroradiologically severe left-hemispheric encephalitic changes could be observed []. After a prolonged rehabilitation program, the patient is at home, but needs professional care.
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.