799: CONCUSSION AND SEIZURES A NOVEL PRESENTATION OF SECOND IMPACT SYNDROME

Abstract

Learning Objectives: Second impact syndrome (SIS) is sudden brain herniation due to recurrent brain injury while still symptomatic from a concussion. We describe a novel presentation of SIS with difficult-to-control seizures causing the second injury. Methods: A healthy 17-year-old male with intellectual disability presented 9 days after a concussion to the emergency department of a tertiary children’s hospital with generalized tonic-clonic seizures (GTCs). Imaging from the initial concussion was normal and he had no further injuries in the interim, but he required inpatient observation for 6 days due to prolonged encephalopathy. His seizures stopped with midazolam and fosphenytoin, and his electroencephalogram (EEG) showed mild slowing of the background. 3 days later he developed encephalopathy and recurrent GTCs, and for the next 3 days, he continued to have 2–3 seizures per day with bifrontal sharp waves on EEG. MRI of the brain showed diffuse edema, no herniation, and hyperemia consistent with recent seizures. Lumbar puncture was notable for an opening pressure of 31 cm H 2 O; cerebrospinal fluid studies were negative. A broad infectious, inflammatory, autoimmune, toxic, and metabolic work-up was negative. Treatment included multiple antiepileptic drugs (consistently within therapeutic, non-toxic ranges), broad anti-infective agents, intravenous immunoglobulin, and pulse-dose steroids. He was not started on an anesthetic for seizure control. 8 hours after his last seizure, the patient developed dilated, non-reactive pupils, lost brainstem reflexes and had no discernible electrocerebral activity on EEG. He was intubated and hyperosmolar therapy with strict neuroprotective measures was initiated. CT showed transforaminal herniation of the cerebellar tonsils, so a neurosurgical intervention was deemed futile. Technical support was withdrawn after brain death testing confirmed brain death. Results: Physiologic changes in the brain due to seizures, including edema, increased intracranial pressure, vascular damage, hypoxia, and others can contribute to clinical phenomena such as post-ictal confusion and/or paresis. In our case, these changes appear to have resulted in a unique presentation of SIS, with the second impact being difficult-to-control, although not overly long or frequent, seizures. 799