Post-traumatic epilepsy: an overview

Abstract

Post-traumatic seizures (PTS) and post-traumatic epilepsy (PTE) are complications from traumatic brain injury (TBI). PTE refers to recurrent and unprovoked PTS that occur at least 1 week after TBI. Seizures during the first week after TBI are considered provoked, an acute complication from head injury, while seizures occurring 1 week after TBI are considered a manifestation of PTE and if only a single seizure occurs it is known as late PTS. EEG and neuroimaging help in the diagnosis of PTE. Predictors for PTE include TBI severity, presence of intracranial bleeding and early PTS. Several clinical trials have demonstrated that antiepileptic drugs are effective in reducing the frequency of acute PTS, but do not appear to alter the natural history of late PTS or PTE.

Late Post-traumatic Epilepsy in Children and Young Adults: Impropriety of Long-Term Antiepileptic Prophylaxis and Risks in Tapering

“…While correcting for the above confounders, we confirmed also in our study population that the antiepileptic prophylaxis they received is not protective against PTE when at maintenance doses, and we documented for the first time that its tapering at 6 months from trauma increases the risk of PTE. These results are consistent with previous reports from the literature [34][35][36] and provide further warning against the unconditional use of long-term prophylaxis for PTE. Still, the lack of a treated group who did not taper antiepileptic prophylaxis leaves an uninvestigated issue; it is unknown whether the extension of antiepileptic prophylaxis for more than 6 months is connected with the same issues we documented, or whether at later time points antiepileptic prophylaxis could acquire a protective role or its tapering could be safe.…”

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

“…After the stroke, scar formation and expression of proteoglycans might impede neurite outgrowth and inhibit structural and functional recovery (Cregg et al, 2014; Silver and Miller, 2004). Glial scars represent powerful barriers for re‐growth of axons, also in the case of mechanical trauma where astrogliosis is seen as a contributor to post‐traumatic epilepsy (Robel, 2016; Verellen and Cavazos, 2010). The triggers of glial transformation and activation in stroke or trauma remain elusive.…”

Neurodegeneration exposes firing rate dependent effects on oscillation dynamics in computational neural networks

“…The return of activity to a damaged network using STDP is reminiscent of how homeostatic plasticity allows a healthy network to gravitate towards a target activity rate (53). Interestingly, homeostatic plasticity may play a very different and destabilizing role in networks after either focal or more diffuse deafferentation of neurons (27), leading these networks into brief bursts of activity the resemble interictal discharges that appear in posttraumatic epilepsy (54,55). However, this rebalancing of networks with STDP has its limits, as the relative success of recovering initial dynamics is not complete at the highest injury levels.…”