POST TRAUMATIC SEIZURES FOLLOWING HEAD INJURY
What is Post Traumatic Epilepsy and Post Traumatic Seizures?[edit | edit source]
- The terms post traumatic seizures and post traumatic epilepsy are used to describe the same entity.
- Post-traumatic epilepsy (PTE) is defined as a recurrent seizure disorder secondary to brain injury following head trauma.
- The term Post-traumatic epilepsy as per latest definition is used when a person has had two or more unprovoked seizures following head trauma .
Pathophysiology of Post traumatic Seizures[edit | edit source]
- Traumatic brain injury (TBI) is divided into two phases based on the different physical factors leading to the injury.
- Primary injury phase or acute phase is due to the damage caused by the external mechanical forces
- Secondary injury phase happens after the direct injury and results mainly from the immune response, neuronal cell death and oxidative stress, as well as augmented neurogenesis and neuroplasticity .
- Neuroinflammation and seizure activity are closely linked which has been shown in studies that there is demonstrable immune activation in the epileptic foci of brain tissue from patients with epilepsy .
- Role of inflammatory cytokines and chemokines has been suggested in increasing the regional hyperexcitability and subsequent seizure susceptibility .
Types of Post Traumatic Seizures[edit | edit source]
Posttraumatic seizures (PTS) following head injury are divided into 3 types depending upon time of seizure episode after the injury:
- early (≤ 7 days)
- late (> 7 days)
In the Early seizure category, seizures occurring within a few minutes to hours after a head injury is called Immediate Post traumatic seizures
About one-third of early PTE occurs within the first hour, one-third between 1 and 24 hours, and the rest between 1 and 7 days after injury
Focal seizures account for most of all early seizures (from 50 to 80%), with the remaining being primarily generalized tonic clonic (25–50%).
Most early focal seizures are focal motor seizures
Immediate concussive convulsions are thought to be due to brief traumatic functional decerebration that results in loss of cortical inhibition.
The incidence of PTS is higher with penetrating head injuries than with closed head injuries (occurs in 50% of penetrating trauma cases
Early PTE is an indication of an increased risk for development of late PTE, being approximately 25%
Management of Post Traumatic Epilepsy[edit | edit source]
Anticonvulsants (AEDs) may be used to prevent early posttraumatic seizures (PTS) in patients at high risk for seizures
Prophylactic AEDs do NOT reduce the frequency of late PTS
Discontinue AEDs after 1 week except for cases meeting specific criteria
No treatment studied eﬀectively impedes epileptogenesis (i.e., neuronal changes that ultimately lead to late PTS)
Taper AEDs after 1 week of therapy except in the following high risk cases:
- penetrating brain injury
- development of late PTS
- prior seizure history
- patients undergoing craniotomy
For high-risk cases give AEDs for 6-12 months, get an EEG done to rule out presence of a seizure focus before discontinuing AED
High risk criteria for Post Traumatic Epilepsy[edit | edit source]
- acute subdural, epidural, or intracerebral hematoma (SDH, EDH or ICH)
- open-depressed skull fracture with parenchymal injury
- seizure within the first 24 hrs after injury
- Glasgow Coma Scale score< 10
- penetrating brain injury
- history of significant alcohol abuse
- ± cortical (hemorrhagic) contusion on CT
Article Written By: Dr Sandeep Moolchandani MS, MHA, DrNB Neurosurgery
- Post-traumatic epilepsy: An overview – https://doi.org/10.1016/j.clineuro.2005.09.001
- Sharma R, Leung WL, Zamani A, O’Brien TJ, Casillas Espinosa PM, Semple BD. Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets. Brain Sciences. 2019; 9(11):318. https://doi.org/10.3390/brainsci9110318
- de Vries, E.E.; van den Munckhof, B.; Braun, K.P.; van Royen-Kerkhof, A.; de Jager, W.; Jansen, F.E. Inflammatory mediators in human epilepsy: A systematic review and meta-analysis. Neurosci. Biobehav. Rev. 2016, 63, 177–190. https://dx.doi.org/10.1016/j.neubiorev.2016.02.007
- Webster, K.M.; Sun, M.; Crack, P.; O’Brien, T.J.; Shultz, S.R.; Semple, B.D. Inflammation in epileptogenesis after traumatic brain injury. J. Neuroinflamm. 2017, 14, 10. https://www.ncbi.nlm.nih.gov/pubmed/28086980
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