Abstracts

Rationale: Post-traumatic epilepsy (PTE) in children after a traumatic brain injury (TBI) occurs in 10-20 % of children following severe head trauma (Ratan et al., 1999; Barlow et al., 2000). The presence of two or more unprovoked seizures defines PTE (Annegers et al., 1980). Epileptic spasms (ES) in infants and children are characterized by a sudden, symmetric or asymmetric flexion or extension of the axial and/or proximal limbs, and associated with poor outcome. Etiologies for the development of ES include genetic, metabolic, and symptomatic causes but the pathophysiology of ES remains unclear despite development of various animal models. The incidence of ES in PTE in children is unknown. The aim of this study is to recognize epileptic spasms (ES) as a seizure type after traumatic brain injury (TBI), accidental or nonaccidental, in infants and children. Since ES following TBI is an acquired form of ES in a previously normal child, we hypothesized that understanding its epidemiological and clinical characteristics may provide some insight into mechanisms of epileptogenesis in ES. Methods: A retrospective electronic chart review was performed at Children's Hospital of Michigan from years 2002 to 2012. Charts of 321 patients were reviewed for the evidence of post-traumatic epilepsy. Various clinical variable were collected including age at TBI, mechanism of trauma, severity of brain injury, electroencephalography/neuroimaging data and seizure semiology. All patients seen in both inpatient and outpatient settings were followed in the clinics for the development of PTE. Diagnosis of epilepsy was invariably confirmed with EEG and/or video EEG during the initial or subsequent evaluation(s). Semiological classification of seizures was used based on history, and when available, video EEG data (Lders et al., 1998). This study excluded patients who had subclinical seizures in the pediatric intensive care unit, neonates with hypoxic ischemic injury at birth, or patients with history of provoked or unprovoked seizure prior to TBI. Also, patients who only had one seizure within the first week of head injury and without any additional unprovoked seizures before the cutoff time period were excluded. Results: Six (12.8%) of the 47 patients diagnosed with post-traumatic epilepsy (PTE) had ES plus at least one other seizure type. Follow up duration ranged from 9 months to 8 years 5 months. ES occurred between 2mo ?" 2 years after TBI. Spasms were never documented acutely post TBI. All patients with ES had multiple irritative zones manifesting as multifocal epileptiform discharges, unilateral or bilateral. Cognitive delay and epileptic encephalopathy were seen in all 6 patients, five of whom were free of spasms after treatment with vigabatrin or adrenocorticotropic hormone (Table 1). Conclusions: The incidence of epileptic spasms in children after severe TBI is approximately 13%. Nonaccidental head trauma is a risk factor of epileptic spasms. While posttraumatic epilepsy (not ES) may start 10 years after the head injury, ES starts within 2 years according to our small cohort. Patients with PTE and ES are a unique group that needs further investigation involving multiple centers. Pathophysiology of ES is unknown, however our data support a combination of previously proposed models in which the primary dysfunction is a focal or diffuse cortical abnormality, coupled with its abnormal interaction with the subcortical structures and brainstem at a critical maturation stage (Figure 1). Funding: none