Monthly Case

Twelve months ago, a 32-year-old male patient suffered a first generalized tonic clonic seizure from sleep. Since then, two further episodes with impaired consciousness and swallowing lasting less than 1 min. have occurred – these are typical clinical signs of an automotor (= complex partial) epileptic seizure. Postictally, the patient was immediately able to speak. EEG – from awakening and sleep – showed right temporal slowing, no increased neuronal excitability. Brain MRI was normal. This patient suffers from cryptogenic partial epilepsy, seizure onset presumably is confined to the right temporal lobe.

We counselled the patient on some basics of epilepsy and recommended – the patient was untreated so far – the regular intake of an antiepileptic drug. The patient was overweight with 105 kg and he asked for a rather uncomplicated treatment regimen. We advised him to take zonisamide (=Zonegran®) that commonly does not result in weight gain but rather has the potential to decrease weight. In addition, the long elimination half-life allows to take the drug once daily.

We told the patient that he has to be free of epileptic seizures for 12 months before he is allowed to drive a car on his own.

At the end of the consultation, the patient asked the question which he had in his mind the preceding weeks: Do epileptic seizures cause irreversible loss of neuronal cells? And does that mean that he has to fear for his cognitive capabilities if further seizures occur? We were able to put his mind at ease and explained to him that current knowledge does not give any hint that “normal” epileptic seizures, lasting less than 2 min., delete neuronal cells. Methodologically, this is difficult to assess. But there are long-term studies covering the brain of people with epilepsy for more than 3 years, and despite frequent epileptic seizures – compared to subjects without epilepsy – no deleterious effects were seen.

Neuropsychological long-term studies covering decades have shown that all people assessed had a slow decline regarding memory, the same was seen in people with epilepsy. The difference was that in average people with epilepsy at onset of the disease had slightly lower memory capabilities – commonly without any consequences in everyday life. These data indicate that slight memory problems in epilepsy – if present at all – are caused by the underlying brain disorder and not by epilepsy or recurrent epileptic seizures. Older antiepileptic drugs may have caused impaired cognition and thus have contributed to this problem. Currently available newer antiepileptic drugs generally do not have this risk.

In summary, epileptic seizures do not cause loss of neuronal cells and do not cause development of memory problems.

Cases of the months before