A recent narrative review published in Clinics and Practice (MDPI) offers a reassessment of the risk of post-traumatic epilepsy (PTE) following mild and moderate traumatic brain injury (TBI) - a development with implications for insurers and those handling TBI claims.

Traditionally, PTE has been associated with severe TBI where the causal link between injury and subsequent seizures is more established. However, the review by Mavroudis et al. presents evidence that even mild and moderate TBIs can lead to epilepsy, sometimes months or years after the initial injury. As the authors note, “Although mild TBI represents the majority of cases in clinical practice, a subset of patients develop unprovoked seizures months or even years post-injury”. 

The study analysed 24 peer-reviewed investigations spanning nearly four decades, focusing on patients with mild (GCS 13–15) and moderate (GCS 9–12 or imaging-positive) TBI. While uncomplicated mild TBI carries a low risk of PTE (<1%), the risk increases significantly in cases involving early seizures, intracranial bleeding, or abnormal neuroimaging. Moderate TBI - particularly when accompanied by contusions or subdural hematomas - showed PTE incidence rates between 6–12%. “In moderate TBI, especially those involving temporal and frontal lobe contusions and subdural hematomas, the risk of PTE frequently exceeds 5–10%, particularly when accompanied by early seizures, prolonged loss of consciousness or midline shift” 

For insurers, the delayed onset of epilepsy introduces complex causation challenges. Claimants may present with seizures long after the initial trauma, and while this study suggests a potential link to the earlier mild or moderate TBI, it does not imply causation in every case. Crucially, the review identifies several predictive factors that can help assess whether there is a causal connection:

1. Early post-injury seizures (within seven days): “Among the most consistent predictors of PTE, early post-traumatic seizures… emerged as a dominant factor… with odds ratios ranging from 8 to 50” 

2. Neuroimaging findings: “SDH, intracerebral haemorrhage (ICH) and especially contusions in the temporal lobe were consistently associated with high risk of PTE” 

3. Psychiatric comorbidities, including depression and anxiety

4. History of prior TBI or neurosurgical intervention

5. EEG abnormalities, where available

From a defence perspective, the study presents both risk and opportunity. On one hand, it raises the threshold for what may once have been considered a “low-risk” brain injury, potentially increasing the volume and complexity of claims asserting long-term neurological sequelae. On the other hand, it provides a structured framework for rebutting such claims when predictive markers are absent or inconsistent with the alleged outcome.

The review also highlights the biological complexity of epileptogenesis. “The pathogenesis of PTE is multifactorial, involving excitotoxicity, neuroinflammation, gliosis, blood-brain barrier disruptions and maladaptive synaptic remodelling." This delayed pathology can also be used to challenge causation.

For insurers, the key takeaway is the continued need for an evidence-based approach when handling brain injury claims. Blanket assumptions that mild TBIs are low risk are no longer tenable. Instead, these claims should be assessed with reference to specific clinical indicators, neuroimaging, and medical history.

In conclusion, this study equips insurers with a deeper understanding of the evolving science around PTE and offers practical tools to assess causation. As litigation around brain injuries becomes increasingly sophisticated, so too must the strategies used to evaluate and defend such claims.