News - Special focus: Assessing the increased risk of PTE

Special focus: Assessing the increased risk of PTE

Post traumatic epilepsy (PTE) can be defined as one or more unprovoked  seizures occurring more than a week after a brain injury. Here Mike  Barnes, professor of neurorehabilitation at Hunters Moor, explains more  about the condition.

The risk of post traumatic  epilepsy increases with the  severity of the brain injury. In  one study, for example, a five year  cumulative probability of PTE was  0.7% in those with mild brain injury,  1.2% with moderate brain injury  and 10% with severe brain injury  (defined as loss of consciousness  or post traumatic amnesia of  greater than 24 hours).

There are  a few indicators of higher risk of  PTE – depressed skull fractures,  brain contusion, intracranial  haemorrhage, a low Glasgow Coma  Scale and older age.
The risk is also  higher in penetrating brain injuries  such as from gunshot wounds.
In  one study after Vietnam over half  of those with penetrating head  injury developed at least one post  traumatic seizure.

In one study 86% of people  who had one unprovoked post  traumatic seizure experienced a  second seizure within two years. Frequency of seizures in the first  year seems to determine the pattern  in subsequent years. Seizure  remission rates are around 25 –  40% but on the other hand around  13% of those with PTE become  refractory to anti-convulsant  medication. Most seizures after a  brain injury occur within the first  five years (and most of those within  the first year) but the literature has  described very long latent periods,  up to twenty years or so.

Social Consequences  Obviously there are significant  social consequences to the  development of post traumatic  epilepsy. The seizures will cause  the loss of a driving licence and  make the chances of employment  significantly worse. Seizures can,  albeit rarely, can cause death during  the fit but premature death is more  likely as a result of the Sudden  Unexpected Death and Epilepsy  (SUDEP) Syndrome.

So what can be done? As there  is such a high chance of a second  seizure after a first unprovoked  seizure then most clinicians would  start anti-convulsant medication  after the first seizure. Fortunately  most people (over 80%) can get  their epilepsy under full control  with a single anti-convulsant  drug. This does leave a minority  who require two or more anticonvulsants  (with their attendant  side effects) or who regrettably  develop intractable epilepsy. There is no clear guidance  on which anti-convulsant drug  should be used. All anti-convulsant  drugs have some side effects,  such as fatigue and weakness  which may already be a problem  in the brain injury population. As  there is no convincing evidence  that prophylatic anti-convulsant  medication reduces the risk of Post  Traumatic Epilepsy (as opposed  to medication in the first few days  which does control seizures within  the first week) it is probably unwise  to start anti-convulsant medication  until the first unprovoked seizure  has occurred. It is important to try  to keep to one anti-convulsant if at  all possible as this will minimise  side-effects.
 The minimum dose  compatible with best control of  the seizures should be used.

Thus  monitoring of the medication  and, if appropriate, drug levels is  necessary and the individual needs  careful neurological follow up. There is no clear consensus  which drug should be used  and indeed there have been  surprisingly few studies specifically  looking at the management of PTE.  Phenytion and Carbamazepine are  known to reduce the incidence  of PTE.  Phenytoin is, of course,  well known to be rather difficult  to control and requires regular  blood testing. There have been  very few trials on the newer  anti-convulsants. I would  personally favour Carbamazepine.

It is sometimes worth considering  the secondary benefits of such  agents such as the possibility of  mood stabilisation or a neuralgic  analgesic effect. However there are a few drugs that are probably best avoided after brain injury because of the risk of agitation or behavioural disturbances and aggression. Levetiracetam (Keppra), as one example, is known to cause behavioural disturbance in a small number (perhaps around 2%) and may be best avoided – see case study below.

It may be possible to obtain provisional damages in a legal settlement if it is found that there is a reasonably high risk of post traumatic epilepsy.
Perhaps interim damages should be considered if the risk of post traumatic epilepsy is thought to be four or five times the risk of the general population.
In an the award for provisional damages the claimant can go back to the court should epilepsy develop, to cover increased costs such as more care, loss of work, etc.
Specialist lawyers should always be involved in the early stages of such claims.

Summary

Post Traumatic Epilepsy is a very well recognised problem after brain injury and unfortunately can occur many years after the initial trauma.
In most cases it can be fully controllable but a significant minority become refractory to treatment. PTE has serious social and economic complications. There is no clear treatment of choice but drugs with higher risk of central nervous systems effects, particularly those that can cause agitation and behavioural disturbance, should preferably be avoided.

CASE STUDY: POST TRAUMATIC EPILEPSY

Mr AB is a 36 year old man who was knocked down by a car whilst walking home one night and suffered severe brain injury with a Glasgow Coma Score of 3 at the scene of the accident and post traumatic amnesia of many weeks.

He had previously been fit and healthy except for insulin dependent diabetes mellitus.

In the weeks after the accident it became clear that he had a marked right sided hemiparesis with global aphasia, He was doubly incontinent and initially required PEG feeding.

He also suffered post traumatic epilepsy with recurrent generalised seizures.

He was put on Keppra.

He was then transferred to the Hunters Moor Olive Carter behavioural unit a couple of months after his accident.

At first his behaviour was very difficult to control and he was unpredictably aggressive to staff.

However, whilst his behaviour improved modestly in the first few weeks there was no significant change until his Keppra was withdrawn and replaced by Carbamazepine.

After that change his behaviour improved.

A couple of weeks after the withdrawal of the Keppra he was transferred to the Janet Barnes unit for more intensive physical rehabilitation.

At the time of writing he is making steady progress.

His epilepsy is now well controlled and, whilst he still has moments of shouting, he is easily managed.

He has begun to walk independently and is no longer incontinent.

His PEG tube has been removed and he is eating, with assistance, a normal diet.

He will no doubt need rehabilitation for many more months but he is now steadily improving.

There was a step change in his behaviour after the withdrawal of Keppra and substitution with Carbamazepine.

Keppra is known to cause behavioural disturbance and is a drug that might be best avoided after brain injury, particularly if behavioural issues are a problem.

Some details of this case have been changed to protect this client’s identity.