A 74-year-old woman presented with refractory Epilepsia Partialis Continua from HSV-1 encephalitis that was initially obscured by severe hyponatremia (Na 117 mmol/L) and alcohol withdrawal.
Case Report (n=1)
Persistent or lateralizing Epilepsia Partialis Continua should prompt urgent MRI and empiric acyclovir initiation for HSV-1 encephalitis, even when alternative metabolic explanations like severe hyponatremia are present.
Abstract Introduction Epilepsia Partialis Continua (EPC) is a rare manifestation of HSV-1 encephalitis frequently misattributed to metabolic or toxic etiologies. Misdiagnosis delays initiation of antiviral therapy, resulting in poor outcomes.1 We report a case of EPC from HSV-1 encephalitis masked by hyponatremia and alcohol withdrawal, illustrating the diagnostic complexity of this disease process. Case Description A 74-year-old woman with alcohol use disorder presented with acute left-sided weakness and confusion. During transport, she developed continuous left facial clonic jerks consistent with EPC, refractory to benzodiazepines and levetiracetam. Initial CT head was nondiagnostic, and CTA head and neck revealed a chronic right internal carotid occlusion without acute ischemic changes, suggesting a non-stroke etiology. Laboratory evaluation showed severe hyponatremia (Na 117 mmol/L), and hypertonic saline therapy was initiated. The patient subsequently developed aspiration pneumonia, necessitating intubation for airway protection. Despite correction of serum sodium to 132 mmol/L, focal seizures persisted. Due to ongoing seizure activity, a delayed MRI brain was performed, demonstrating right anterior and mesial temporal diffusion restriction, while EEG revealed right frontotemporal slowing. Cerebrospinal fluid analysis showed lymphocytic pleocytosis with HSV-1 PCR positivity, confirming HSV-1 encephalitis. Acyclovir was initiated, but the patient’s neurologic status progressively declined. The family ultimately chose comfort care. Discussion This case highlights the diagnostic complexity of EPC as an early manifestation of HSV-1 encephalitis, particularly when coexisting metabolic or toxic factors obscure recognition. EPC occurs in approximately 5 to 10% of HSV-1 encephalitis cases and may precede the development of classic encephalitic features.2 HSV-1 shows a predilection for the mesial temporal and limbic cortex, resulting in focal cortical hyperexcitability that manifests clinically as EPC.3 Delayed recognition and treatment with acyclovir lead to irreversible neuronal damage and worse neurological outcomes.4Consequently, persistent or lateralizing EPC should prompt urgent MRI and empiric acyclovir initiation, even when alternative metabolic explanations appear sufficient. In critically ill patients with focal, refractory seizures, early neuroimaging and prompt antiviral therapy remain essential for optimizing neurologic outcomes. References: 1. Hughes PS, Jackson AC. Delays in initiation of acyclovir therapy in herpes simplex encephalitis. Can J Neurol Sci. 2012;39(5):644-648. 2. Cianfoni A et al. Epilepsia partialis continua as a presentation of HSV-1 encephalitis. Neuroradiology. 2013;55(9):1129-1138. 3. Misra UK, Kalita J. Mechanisms of viral encephalitis-related seizures and epileptogenesis. J Neurol Sci. 2021;429:118066. 4. Mailles A et al. Long-term outcome of patients presenting with acute infectious encephalitis of various causes in France. Clin Infect Dis. 2012;54(10):1455-1464. This abstract is funded by: None
Anand et al. (Fri,) conducted a case report in Epilepsia Partialis Continua from HSV-1 encephalitis (n=1). Acyclovir was evaluated. A 74-year-old woman presented with refractory Epilepsia Partialis Continua from HSV-1 encephalitis that was initially obscured by severe hyponatremia (Na 117 mmol/L) and alcohol withdrawal.