Treatment and outcome
With the consideration of CNS vasculitis, the patient started high-dose dexamethasone which resulted in a progressive improvement of his GCS to 15/15. His seizure was well-controlled, and he fully regained his motor function. He was then discharged from the hospital and improved. He had a follow-up at our hospital four months after the discharge date and was back to his daily routine activities.
.
Discussion
Herpes Simplex Encephalitis is a destructive inflammatory condition that typically impacts the cortex and the underlying white matter found in the temporal lobe. (1) A delay in treatment significantly increases the potential for axonal spread of the infection (2) The diverse clinical symptoms, delayed diagnosis, and persistent alterations in brain structure following treatment can all contribute to the illness and death associated with HSV encephalitis. In cases of suspected viral encephalitis, the decision to start antiretroviral therapy is based on clinical assessment. Serological testing should not cause a delay in treatment initiation which was true, as well in our patient; he was started on Acyclovir until a CSF sample was sent for serologic study. In our patient, the clinical presentation, imaging, laboratory evidence, and initial clinical response to Acyclovir provided strong support for the diagnosis of HSV-1 encephalitis
Magnetic resonance imaging is more significant in the early detection of HSV encephalitis compared to computed tomography scans, (3). Early finding on MRI usually occurs in the cingulate gyrus and medial temporal lobe(3). In the reported case, the Initial Brain CT scan shows hypo-density in the right capsule and median temporal lobe with minimal white matter edema characteristic of HSV encephalitis. There are no EEG findings pathognomonic for HSV encephalitis, but certain EEG features can be helpful in the diagnosis, including the presence of focal or lateralized abnormalities (4). In our patient, the EEG (Image 1) performed within 24 hours supported the diagnosis.
Cerebrovascular disease can develop as a complication of various central nervous system (CNS) infections (5) even though HSV is one of the least recognized causes. Since the early 1970s, it has been acknowledged that Herpes Simplex Encephalitis (HSE) can, in some cases, manifest with a cerebral infarction (6). An epidemiological study of HSE conducted in the USA reported that ischemic complications occurred approximately twice as frequently, at a rate of 5.6%, compared to hemorrhagic complications (7). This complication can occur regardless of early initiation of antiviral therapy. Our patient has both clinical and brain MRI worsening after an initial brief improvement with acyclovir treatment. Though vascular imaging is not done in this patient, taking into account the course of the patient and bilateral MCA territorial area of worsening on the imaging, we considered HSV-1-associated vasculitis with bilateral ischemic stroke. The exact pathophysiology underlying infectious vasculopathy has not been fully elucidated. Even if the presence of vasculitis and seizure are markers of poor prognosis in a patient with HSE(7) our patient’s neurological status returned to their baseline after treatment.