there is a lot of info confirming Post Traumatic Epilepsy (PTE), but little on the exact causation, due to the mysterious nature of the causation of epilepsy.
There is much research supporting the link between brain injury and subsequent seizures, Post-traumatic epilepsy , including the onset of delayed seizures:
Traumatic brain injury (TBI) has been recognized as a cause of
epilepsy since antiquity, and it remains one of the most common and
important causes of acquired epilepsy today. Epidemiologic studies
have demonstrated a clear relationship between the severity of injury
and the likelihood of developing epilepsy, with the risk approaching
50% in TBI cases associated with direct injury to brain parenchyma.
Importantly, many TBI victims develop epilepsy months or years
following the initial injury, ...
Epilepsy after head injury: an overview.
Lowenstein DH. doi: 10.1111/j.1528-1167.2008.02004.x.
Posttraumatic seizures may not appear for as long as 20 years after an accident.
Stanford Epilepsy Center Robert S. Fisher, M.D., Ph.D.
Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring
Paul M. Vespa, M.D., et al
The risks of epilepsy after traumatic brain injury ☆
John F Annegers2, Sharon Pasternak Coan
The University of Texas Health Science Center at Houston, School of Public Health, USA
A Population-Based Study of Seizures after Traumatic Brain Injuries
John F. Annegers, Ph.D., et al
N Engl J Med 1998; 338:20-24January 1, 1998DOI: 10.1056/NEJM199801013380104
As to the causal relationship:
The cause of epilepsy is largely unkown.
What causes epilepsy?
There are many causes of epilepsy, which vary with the age at which seizures begin and the nature of the seizures. However 50% of cases, the cause is unknown. ...
A brain injury, which results in scar tissue, predisposes individuals to developing epilepsy, although there can be a long period, often years, between the damage occurring and the seizures commencing. ...
What is a seizure?
A seizure occurs when the brains nerve cells misfire and generate sudden, uncontrolled burst of electrical activity in the brain. ...
It has been shown that the nature of the head injury influences the likelihood of developing seizures.
Nature of trauma
Intracranial hematomas, in which blood accumulates inside the skull, are one of the most important risk factors for PTE. Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue. Repeated intracranial surgery confers a high risk for late PTE, possibly because people who need more surgery are more likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling. In addition, the chances of developing PTE differ by the location of the brain lesion: brain contusion that occurs on in one or the other of the frontal lobes has been found to carry a 20% PTE risk, while a contusion in one of the parietal lobes carries a 19% risk and one in a temporal lobe carries a 16% chance. When contusions occur in both hemispheres, the risk is 26% for the frontal lobes, 66% for the parietal, and 31% for the temporal.
It is not clearly understood how traumatic brain injury causes seizures.
Epilepsy is a common outcome of traumatic brain injury (TBI), but the mechanisms of posttraumatic epileptogenesis are poorly understood. One clue is the occurrence of selective hippocampal cell death after fluid-percussion TBI in rats, consistent with the reported reduction of hippocampal volume bilaterally in humans after TBI and resembling hippocampal sclerosis, a hallmark of temporal-lobe epilepsy. Other features of temporal-lobe epilepsy, such as long-term seizure susceptibility, persistent hyperexcitability in the dentate gyrus (DG), and mossy fiber synaptic reorganization, however, have not been examined after TBI. To determine whether TBI induces these changes, we used a well studied model of TBI by weight drop on somatosensory cortex in adult rats. First, we confirmed an early and selective cell loss in the hilus of the DG and area CA3 of hippocampus, ipsilateral to the impact. Second, we found persistently enhanced susceptibility to pentylenetetrazole-induced convulsions 15 weeks after TBI. Third, by applying GABAA antagonists during field-potential and optical recordings in hippocampal slices 3 and 15 weeks after TBI, we unmasked a persistent, abnormal APV-sensitive hyperexcitability that was bilateral and localized to the granule cell and molecular layers of the DG. Finally, using Timm histochemistry, we detected progressive sprouting of mossy fibers into the inner molecular layers of the DG bilaterally 2–27 weeks after TBI. These findings are consistent with the development of posttraumatic epilepsy in an animal model of impact head injury, showing a striking similarity to the enduring behavioral, functional, and structural alterations associated with temporal-lobe epilepsy.
Physiological and Structural Evidence for Hippocampal Involvement in Persistent Seizure Susceptibility after Traumatic Brain Injury
Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study
Paul Vespa, M.D., et al
Brain injury induces c-fos protein(s) in nerve and glial-like cells in adult mammalian brain
M. DragunowCorresponding author contact information, 1, H.A. Robertson2
It would seem that seizure at the time of the injury, increase the chance of having late onset epilepsy.
TBI is a relatively rare cause of epilepsy in childhood, although immediate seizures are associated with an increased risk of developing post-traumatic epilepsy
Occurrence of epilepsy during the first 10 years after traumatic brain injury acquired in childhood up to the age of 18 years in the south western Swedish population-based series.
Emanuelson I, Uvebrant P.
Posttraumatic seizures may occur almost simultaneously with head injury or be delayed for several years.
• Once posttraumatic epilepsy has developed, it remits less often than previously reported.
• Patients with posttraumatic epilepsy appear to have a higher mortality rate than patients with traumatic brain injury without epilepsy.
• Posttraumatic epilepsy appears in many cases as temporal lobe epilepsy that possibly originates from the hippocampus.
... 40% to 50% of new cases of posttraumatic seizures occur within 6 months, 70% within 1 year, and 80% within 2 years after head injury ...
... Seizures occurring within 5 minutes of traumatic injury to the head are called "immediate" posttraumatic seizures (Majkowski 1991). Such seizures do not represent epilepsy, per se, and should be viewed as an acute response to the head injury.
Ravindra Kumar Garg MD, author. Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.
C P Panayiotopoulos MD PhD, editor. Dr. Panayiotopoulos of St. Thomas' Hospital received a publication grant and salary from UCB Pharma S.A.
J Neurol Neurosurg Psychiatry 2002;73:i8-i16 doi:10.1136/jnnp.73.suppl_1.i8
HEAD INJURY FOR NEUROLOGISTS
Given the swelling can expand over time, and there can be delayed hemorrhaging; this could account for some delayed onset seizures.
• A contusion consists of blood intermixed with brain tissue.
• Data have shown that traumatic intracerebral hemorrhages often expand over time.
• Delayed posttraumatic hemorrhages may sometimes result from coalesced blood within contusions.
Traumatic intracerebral hemorrhage
Ravindra Kumar Garg MD, author. Steven R Levine MD, editor.
My own thoughts would be, that if a brain injury occurs during childhood; given the degree of growth and change from childhood through to adulthood; and given the the predictive likelihood (that if epilepsy will develop) that it will do so before the ages of 18-21; I suspect that the growth and disruption to scar tissue and possible delay in disruption of existing contusions could account for the delay in onset of PTE.