2. Definition
Post-traumatic seizure (PTS) is defined as a seizure disorder which occurs following brain injury, and it
can be further classified as immediate (within 24 hours of injury onset), early (<1 week after injury) or
late (>1 week after injury).
PTS
Ding K, Gupta PK, Diaz-Arrastia R. Epilepsy after Traumatic Brain Injury. In: Laskowitz D, Grant G, editors. Translational Research in Traumatic Brain Injury. Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016. Chapter 14. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK326716/
3. Mechanism of PostTraumatic Seizures
Epileptogenesis is defined as the development and extension of tissue capable of generating
spontaneous seizures, including development of an epilepsy condition and progression after the
condition is established
TBI Focal
insults
Diffuse insults
Result in cicatrix in the cortex or subcortical regions, and the neighboring neural tissue
experiences inflammation, gliosis, and ultimately neuronal sprouting and neurogenesis
induce seizure / abnormal brain activity
Cerebral edema, intracranial hemorrhage, cerebral contusion or laceration, alterations in the
blood–brain barrier, changes in extracellular ions, excessive release of excitatory
neurotransmitters such as glutamate, damage to tissues caused by free radicals, and changes
in the way cells produce energy
Ding K, Gupta PK, Diaz-Arrastia R. Epilepsy after Traumatic Brain Injury. In: Laskowitz D, Grant G, editors. Translational Research in Traumatic Brain Injury. Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016. Chapter 14. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK326716/
4. Mechanism of PostTraumatic Seizures
TBI trauma mostly delivered into neocortex
Focal lesion may affects other cortical and subcortical structures
may change into diffuse alteration of brain
May cause Altered synaptic circuitry of cortical structure, include
: into hippocampus and dentate gyrus (important structure in
epilepsy)
Hunt, Robert F et al. “Neural circuit mechanisms of post-traumatic epilepsy.” Frontiers in cellular neuroscience vol. 7 89. 18 Jun. 2013, doi:10.3389/fncel.2013.00089
7. Anatomical Consideration of PTS
Hippocampus thought to be important structure of epileptogenesis,
and dentate gyrus is a structure susceptible to injured by TBI
(diffuse effects)
Rhoton : Atlas of Head, Neck , and Brain.
9. PTS Cellular Mechanism
A series of cellular and molecular events
occur following TBI that involve three
temporally overlapping responses in the
brain: primary and secondary injuries and
“self-repair” mechanisms
Hunt, Robert F et al. “Neural circuit mechanisms of post-traumatic epilepsy.” Frontiers in cellular neuroscience vol. 7 89. 18 Jun. 2013, doi:10.3389/fncel.2013.00089
Progression of cellular events following TBI.
10. Posttraumatic Seizures (PTS) Classification
Early PTS
1 ≤ 7 days after head trauma
Late PTS
2 > 7 days after head trauma
Immediate PTS
3 Within minutes to an hour or
so
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
11. Posttraumatic Seizures (PTS) Classification
Early PTS
1 ≤ 7 days after head trauma
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
30% incidence in
severe head injury and
≈ 1% in mild to
moderate injuries.
Early
PTS
May precipitate adverse events as a result of
elevation of ICP, alterations in BP, changes in
oxygenation, and excess neurotransmitter
release
12. Posttraumatic Seizures (PTS) Classification
Late PTS
2 > 7 days after head trauma
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
Estimated incidence 10–
13% within 2 yrs after
“significant” head
trauma for all age
groups
Late
PTS
Less Frequent in children. Risk of developing
late PTS may be higher after repeated head
injuries.
2
13. PTS and PenetratingTrauma
PenetratingTrauma
The incidence of PTS is higher with penetrating head injuries than
with closed head injuries.
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
14. Treatment
Drug of Choices :
PTS
Phenytoin
Carbamazepi
ne
PHT early administration could prevent early PTS. Regiments : 20 mg/kg loading
dose of PHT within 24 hrs of injury, administration after 1 week : no benefits. Adverse
effect : cognitive function reduction
Effective in reducing the risk of early PTS
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
PTS
Drug of Choices :
15. Initiation of Anti Epileptic Drugs
AED may be used (short term use) to prevent early
posttraumatic seizures (PTS) in patients at high risk for seizures
AED PTS
Begin AEDs (usually levetiracetam, phenytoin
or carbamazepine) within 24 hrs of injury in
the presence of any of the high risk
criteria
once epilepsy has developed, continued
AEDs reduce the recurrence of further
seizures
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
16. Discontinuation of AEDs
1. Taper AED after 1 week of
therapy except in the following
cases
a) Penetrating brain injury b) development of
late PTS (i.e., a seizure > 7 days following head
trauma) c) prior seizure history d) patients
undergoing craniotomy
2. for patients not meeting the criteria to discontinue AEDs after 1
week
a. maintain ≈ 6–12 mos of therapeutic AED levels
b. recommend EEG to rule out presence of a seizure focus before discontinuing
AEDs for the following: repeated seizures, presence of high risk criteria
Greenberg, Mark S. (2019). Handbook of Neurosurgery. Thieme, New York. Ch. 13, 243 – 252
