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[Preventive prophylactic treatment in posttraumatic epilepsy]
A Oliveros-Juste1, V Bertol, A Oliveros-Cid
1Servicio de Neurología, Policlinica Sagasta, Zaragoza, 50006, Espańa. aoliveros@hmservet.insalud.es
Insights
Posttraumatic epilepsy (PTE) affects 2-3% of epilepsy cases. Current antiepileptic drugs show limited prophylactic efficacy for PTE, necessitating research into novel treatments like neuroprotectors and receptor blockers.
Area of Science:
- Neurology
- Neuroscience
- Epileptology
Context:
- Posttraumatic epilepsy (PTE) arises from traumatic brain injury (TBI).
- Early seizures post-TBI, while not strictly epileptic, are risk factors for developing PTE.
- PTE affects 5-20% of TBI patients, particularly those with severe injuries.
Purpose:
- To evaluate the prophylactic efficacy of antiepileptic drugs (AEDs) for PTE.
- To explore novel therapeutic targets beyond traditional AEDs for PTE prevention.
- To recommend a risk-factor-based strategy for PTE management.
Summary:
- Classic AEDs (Phenobarbital, Phenytoin, Carbamazepine, Valproate) lack confirmed prophylactic efficacy against the 'kindling' effect in PTE.
- Emerging strategies involve lipid peroxidation inhibitors, neuroprotectors (antioxidants), glutamic and NMDA receptor blockers, and apoptosis modulators.
- A tailored approach, considering individual risk factors and focusing on AEDs with proven partial seizure efficacy and good tolerability, is advised.
Impact:
- Highlights the limitations of current AEDs in PTE prophylaxis.
- Identifies promising new drug classes for future PTE therapeutic development.
- Advocates for personalized medicine in managing PTE risk and treatment.
Abstract:
Posttraumatic epilepsy (PTE) represents about 2 3% of all the etiologies of epilepsy. The so called early seizures , which appear in the first week after the traumatic brain injury (TBI), are related to the severity of the injury; they do not have an strictly epileptic mechanism, but they become a risk factor to the development of PTE. PTE appears in 5% of all the patients suffering from all TBI, and in 15 20% of the patients suffering from a severe TBI. However, the endpoint uses to be to use antiepileptic drugs (AEDs) as prophylactic treatment in all well established PTE. The efficacy of classic antiepileptic drugs (Phenobarbital, Phenytoin, Carbamazepine, Valproate acid) to control the kindling effect has not been confirmed yet as a prophylactic treatment for PTE. Prophylactic efficacy of other drugs, like lipid peroxidation inhibitors, neuroprotectors (especially antioxidants), glutamic receptor blockers, NMDA receptor blockers, and drugs that modulate apoptosis via caspasas inhibition; however, they constitute new ways of therapeutic investigation with a strong experimental basis. Our recommended therapeutic strategy is not to administrate AEDs indiscriminately, but analyzing risk factors, designing a careful prevention for late seizures using AEDs with proven efficacy in partial seizures and with the best achievable tolerability; being also attentive to the possible use of new drugs in the future, like lipid peroxidation inhibitors, and drugs designed to inhibit other excitotoxic, ionic or oxidative processes.