T69. Continuous Electroencephalogram (CEEG) as a biomarker for progression of Herpes Simplex Virus Encephalitis (HSE)

Abstract

Introduction HSE is the most common cause of sporadic fatal encephalitis worldwide and remains a devastating disease despite antiviral therapy. Clinically, it is often characterized by fever, headache, seizures and focal neurologic signs. EEG can be an important tool in the diagnosis of HSV. In the acute stage, EEG can show different EEG patterns, commonly including lateralized periodic discharges (LPDs), sharp waves, focal or generalized slowing. As such, EEG can be used to monitor the progression of the disease in patients with treatment refractory HSE. Methods Case report of a patient with HSE who was monitored on CEEG throughout course of her disease. Results A 62-year old female with no history of neurologic disease, who presented with generalized weakness and lethargy for 2 weeks and rapidly deteriorated with encephalopathy, fever, and seizures. Lumbar puncture demonstrated elevated protein and WBC with positive HSV DNA. CEEG initially showed right prefrontal 2-Hz LPD’s. Over the next 48 h, these evolved into focal right prefrontal status epilepticus. After a period of iatrogenic burst suppression, the CEEG showed right frontotemporal LPD’s which evolved into right frontotemporal electrographic seizures. As the CEEG progressed, the right sided seizures appeared to have a more posterior temporal focus. Later, there was additional independent semi-rhythmic 2–4 Hz delta over the left frontotemporal region which was on the ictal-interictal continuum but did not clearly evolve into seizures. As the recording continued, there were left frontal LPD’s more than right-sided ones. The final CEEG demonstrated bilateral independent sharp waves and generalized periodic discharges (GPD’s) with triphasic morphology with resolution of electrographic seizures. As the CEEG revealed evolution of the underlying disease, treatment was escalated with a 21 day course of acyclovir, multiple anti-epileptic agents, including suppressing medications (i.e., midazolam and ketamine), as well as use of plasma exchange and steroids given the refractory seizures. MRI was obtained at three points during hospital stay and confirmed what CEEG heralded. Initially, there was diffusion restriction of the bilateral (right > left) insular cortices and right hippocampus/amygdala. Repeat MRI showed diffusion normalization with T2-weighted and FLAIR hyperintensity in the right > left insula and new involvement of the right temporal lobe. The final MRI demonstrated involvement of the bilateral inferior frontal regions and left temporal lobe, consistent with evolution from the prior studies and with new findings seen on CEEG, suggesting spread of HSE to these regions. Conclusion We report the case of a patient with HSE who was monitored on CEEG and propose that CEEG can be used as a marker for progression of disease and thus may prompt escalation in therapy. While imaging studies may confirm spread of disease, using CEEG may prevent the delay of treatment and lead to more rapid therapy in cases of refractory HSE.