Velíšková lab · Cell Biology & Anatomy, New York Medical College · STAR program · 2019
Traumatic stress at the moment of brain injury and the risk of post-traumatic epilepsy
Post-traumatic epilepsy arrives late. Between the injury and the first unprovoked seizure lies epileptogenesis — neuronal loss, mossy-fiber sprouting, and a shift toward excitation in the hippocampus. Clinically, TBI rarely happens calmly, and severe stress at the time of injury is associated with worse progression. No one had delivered both insults together in an animal and watched what happened.
Status. Presented as a poster through the STAR program at New York Medical College, 2019, under Dr. Jana Velíšková.
The question
Does a severe stress event at the moment of cortical contusion increase seizure susceptibility during the epileptogenic period?
How it is being done
- Adult male rats were submerged for 45 seconds — a life-threatening stressor — immediately before controlled cortical impact. Controls swam freely before the same impact.
- Open-field and elevated-plus-maze testing confirmed the stress manipulation had worked, rather than assuming it.
- Seizure susceptibility was measured in a flurothyl chamber at five and ten days after injury — two points inside the epileptogenic window.
What it shows so far
- At five days the two groups were indistinguishable.
- By ten days the stressed animals had a significantly lower threshold for tonic-clonic seizures (p = 0.02) and spent longer seizing.
- The interaction therefore emerges during epileptogenesis rather than at the moment of injury — consistent with stress acting on the process that builds epilepsy, not on the injury itself.
Materials
This page grows as the work does.