One very serious and tragic consequence of a TBI is post-traumatic epilepsy (PTE). Epilepsy is a disorder involving excessive excitation or insufficient inhibition of neuronal networks in the brain with resultant “storms” caused by massive, uncontrolled “firing” of neurons. Recent research shows a clear genetic predisposition in certain individuals, who would be at much higher risk of developing PTE from brain trauma. At this time two different mechanisms have been identified as likely culprits in delayed onset of PTE following TBI.

One is intracranial bleeding which bathes portions of the brain tissue in blood and deposits an iron compound from hemoglobin called hemosiderian which is toxic to the brain and may precipitate seizures after a latency period. The other mechanism is regrowth of neuronal networks in the place where “focal” brain damage killed off “inhibitory” brain cells (those which suppress uncontrolled firing). The new cells and connections are helpful in restoring lost movement, cognition or speech, but harmful in that they are hyperexcitable and likely to contribute to generation of seizures.

Fortunately PTE occurs very rarely in association with mild TBI. The known risk factors for onset of PTE following a brain injury are: depressed skull fracture; bleeding in the brain; positive CT scan; craniotomy to remove a blood clot; abnormal reflexes on admission to the hospital; and a seizure within the first week of injury. When confronted with a hospital patient in the highest risk group for PTE, physicians will typically prescribe an anti-seizure medication such as phenytoin on a prophylatic basis to prevent seizures from ever starting. Disputes arise over how quickly to wean the patient off such medication, and whether to use the medication in TBI patients at moderate or low risk of PTE. Some physicians prefer rapid weaning; others are relaxed about leaving the patient on medication for 6-12 months.

Although the medical literature is in conflict, it appears that when patients in the highest risk group are given an anticonvulsant medication like phenytoin in the hospital on a prophylactic basis, many are spared from having a seizure. For patients who do not seize in the hospital the risk of developing PTE continues at an elevated level for 2 years, then gradually drops. At the end of the 5th year, their risk is no greater than anyone else, including people who never had a head injury. The diagnosis of epilepsy is made clinically on the basis of history and observation.

EEG studies are of limited helpfulness. EEG measures only the electric output of neurons at the surface of the cortex, and not neurons deeps in the brain where any seizure focus would likely be found. Given the infrequency of seizures, most EEGs are administered in between seizures, and such EEGs have only a 50/50 chance of catching epileptiform wave activity. Thus a negative EEG can NEVER rule out epilepsy. To increase the likelihood of catching abnormal wave patterns, a physician can order 4 repeat EEGs; have the EEG performed after the patient has been sleep deprived and fallen asleep; have the EEG done while flashing lights in the patient’s eyes; or pay for telemetry which is continuous 24 our per day EEG monitoring with a portable device over a period of 3 days.

Children are considerably more vulnerable to PTE from cranio-cerebral trauma, in part because their skulls are relatively soft, their brains do not fill their skulls and their brains are still developing. PTE in children is much more likely to involve grand or petit mal seizures than PTE in adults. By far the most common form of PTE in adults is temporal lobe epilepsy (TLE) manifested by complex, partial seizure disorder. This disorder does not involve falling to the floor, flopping one’s limbs and rolling one’s eyes.

It is far more subtle, and therefore diagnosis is frequently delayed for years or missed altogether. Complex, partial seizure disorder is associated with visual hallucinations (ranging from religious scenes to tunnel vision), olfactory hallucinations (smelling coffee or burnt rubber or tasting metal) and blanking (becoming mentally absent for short periods, often just 30-60 seconds). About 5-7% of TLE patients have intermittent explosive disorder (IED), which involves sudden, unpredictable violent rages. Studies of these patients show they sustained traumatic damage to a brain structure called the amygdala in their left temporal lobe at the time of the brain injury.

People living with epilepsy can reduce the frequency of seizures by following certain health rules. They should not skip meals, drink alcohol, use street drugs, drink a lot of coffee or cola, or start a new medication without consulting their epileptologist. They should get adequate rest and sleep, drink plenty of fluids, learn stress management/relaxation techniques and stay in close communication with their doctor.

People with epilepsy, and their families, should also educate themselves as much as possible about the disorder. Organizations that teach the warning signs of an impending seizure, what to do for a person in seizure, when to seek emergency medical care, etc., are posted in the Links section of the Resources Page of this website. People with epilepsy who wish to purchase a medical alert bracelet should contact

If you have suffered a serious head injury call (877)-833-1168 or contact us at to find a Brain Injury Lawyer to fight for the compensation you deserve.