Posttraumatic epilepsy: long-term follow-up of children with mild traumatic brain injury

Abstract

<jats:sec><jats:title>OBJECTIVE</jats:title><jats:p>Posttraumatic epilepsy (PTE) is a known complication of traumatic brain injury (TBI). The true incidence of PTE in children is still uncertain, because most research has been based primarily on adults. This study aimed to determine the true incidence of PTE in a pediatric population with mild TBI (MTBI) and to identify risk factors for the development of epileptic events.</jats:p></jats:sec><jats:sec><jats:title>METHODS</jats:title><jats:p>Data were collected from electronic medical records of children 0–17 years of age, who were admitted to a single medical center between 2007 and 2009 with a diagnosis of MTBI. This prospective research consisted of a telephone survey between 2015 and 2016 of children or their caregivers, querying for information about epileptic episodes and current seizure and neurological status. The primary outcome measure was the incidence of epilepsy following TBI, which was defined as ≥ 2 unprovoked seizure episodes. Posttraumatic seizure (PTS) was defined as a single, nonrecurrent convulsive episode that occurred &gt; 24 hours following injury. Seizures within 24 hours of the injury were defined as immediate PTS.</jats:p></jats:sec><jats:sec><jats:title>RESULTS</jats:title><jats:p>Of 290 children eligible for this study, 191 of them or their caregivers were reached by telephone survey and were included in the analysis. Most injuries (80.6%) were due to falls. Six children had immediate PTS. All children underwent CT imaging; of them, 72.8% demonstrated fractures and 10.5% did not demonstrate acute findings. The mean follow-up was 7.4 years. Seven children (3.7%) experienced PTS; of them, 6 (85.7%) developed epilepsy and 3 (42.9%) developed intractable epilepsy. The overall incidence of epilepsy and intractable epilepsy in this cohort was 3.1% and 1.6%, respectively. None of the children who had immediate PTS developed epilepsy. Children who developed epilepsy spent an average of 2 extra days in the hospital at the time of the injury. The mean time between trauma and onset of seizures was 3.1 years. Immediate PTS was not correlated with PTE.</jats:p></jats:sec><jats:sec><jats:title>CONCLUSIONS</jats:title><jats:p>In this analysis of data from medical records and long-term follow-up, MTBI was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population.</jats:p></jats:sec>

Posttraumatic epilepsy in intensive care unit–treated pediatric traumatic brain injury patients

“…In our cohort, approximately 10% of patients with mild TBI (GCS 13‐15) developed PTE. In comparison, a previous study on pediatric patients with mild TBI reported a PTE rate of 4% 29 . The difference is probably explained by a higher rate of abnormal brain imaging findings in our cohort (more intracranial hemorrhages and signs of brain edema).…”

Management of Concussion and Mild Traumatic Brain Injury: A Synthesis of Practice Guidelines

“…There may be no significantly increased risk following uncomplicated mTBI (concussion) 97 but likely more than a 2-fold increased risk in children and adults with cerebral contusions, hemorrhage, or skull fracture. [98][99][100] Concussive convulsion, in which brief posturing or other seizure-like activity is observed immediately after impact (in 1%-2% of cases), is thought to result from a transient loss of cortical inhibition (ie, have a nonepileptogenic cause) and is not associated with prolonged recovery from mTBI or the development of posttraumatic epilepsy. 101,102 Routine seizure prophylaxis is not recommended in any mTBI clinical practice guideline.…”

The clinical value of long - term electroencephalogram (EEG) in seizure - free populations: implications from a cross-sectional study

“…Proinflammatory cytokines, such as interleukin (IL)-1a and IL-1b, are implicated in the molecular cascade leading to neuronal injury after brain trauma. These patients are prone to have focal glial hyperplasia after 3 months or more [25][26][27]. Therefore, epileptiform discharges are induced, leading to drug-resistant epilepsy [28].…”