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 48-year-old man with known symptomatic epilepsy reported diarrhea and fever for some days. This was followed by a series of focally beginning secondary generalized seizures. Thus the emergency physician administered 7.5 mg midazolam intravenously and admitted the patient to the neurological department. On admission, the patient was sedated and presented residual aphasia. A meningeal irritation was not noted. The neurological signs and symptoms were interpreted as postictal. There were no visible injuries, therefore a series of seizures due to afebrile infection was presumed. The patient was observed under intermediate care aspects. The next 2 days the patient's condition improved, he was afebrile and no focal neurological deficits were present. The medication with levetiracetam was augmented to a dosage of 1500 mg/daily. Electroencephalography showed slightly slowed focal activity on the left temporal side on the background of normal alpha wave activity. The day before the planned discharge from inpatient care, the patient suffered with sudden onset of a series of epileptic seizures progressing to a convulsive status with high fever of 40°C. Oral intubation and mechanical ventilation became necessary in order to treat status epilepticus. As anticonvulsive agents phenytoin, levetiracetam, midazolam, and propofol were applied, the Cranial computed tomography (CCT) scan at this time revealed hyodensities in the right temporal lobe and the right insular cortex []. The left sided hypodensity is related to a former head injury. The following cerebrospinal fluid (CSF) analysis showed elevated lymphocytic cell count (27/μL; normal < 4) with normal glucose but elevated protein (699 mg/dl (normal < 450)), indicating an inflammatory CSF syndrome. Polymerase chain reaction (PCR) assay for HSV-1 was tested positive. A treatment regimen was implemented with acyclovir (10 mg/kg body weight) three times daily for 21 days. After 4 days of ventilation the patient could be extubated and improved clinically successful. Cranial magnetic resonance imaging (MRI) on day 10 showed extended encephalitic changes in the right frontal and temporal lobe []. After a rehabilitation program, follow-ups took place as an outpatient. Yet due to neuropsychological impairments he cannot work in his profession as a carpenter anymore. Under the current antiepileptic therapy (levetiracetam 1500 mg daily), the patient is seizure-free.