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NEUROLOGIA DZIECIĘCA

Pismo Polskiego Towarzystwa Neurologów Dziecięcych

PL ISSN 1230-3690
e-ISSN 2451-1897
DOI 10.20966
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Urazy czaszkowo-mózgowe u dzieci a padaczka


Traumatic brain injury in children and epilepsy




Klinika Neurologii Dzieci i Młodzieży, Instytut Matki i Dziecka w Warszawie

Neurol Dziec 2011; 20, 39: 11-21
Pełen tekst artykułu PDF Urazy czaszkowo-mózgowe u dzieci a padaczka



STRESZCZENIE
Według WHO urazy czaszkowo-mózgowe (UCM) stanowią jedną z częstszych przyczyn padaczki. Wśród chorych na padaczkę są przyczyną tego schorzenia u około 4–10% populacji. Padaczka pourazowa może ujawnić się w różnym czasie po urazie i mieć różny przebieg. Badania epidemiologiczne wskazują na związek pomiędzy ciężkością urazu i długością obserwacji a ryzykiem wystąpienia padaczki. Patomechanizm prowadzący do rozwoju padaczki po urazie nie jest dobrze poznany. U podłoża epileptogenezy leży wiele procesów, które mogą współistnieć u jednego chorego. Wyniki badań wskazują, że leczenie drgawek pourazowych wczesnych nie zapobiega rozwojowi padaczki. Zatem profilaktyczne stosowanie leków przeciwpadaczkowych u osób z UCM nie jest zalecane. Leki te powinny być wprowadzone po rozpoznaniu padaczki. Obecność okresu latencji pomiędzy UCM a ujawnieniem się padaczki wskazuje na celowość zastosowania u tych chorych leczenia modyfikującego proces epileptogenezy. Obecnie jednak terapia ta nie jest dostępna ze względu na brak wiarygodnych biomarkerów epileptogenezy.

Słowa kluczowe: padaczka pourazowa, drgawki, dzieci, uraz czaszkowo-mózgowy, epileptogeneza, biomarkery


ABSTRACT
According to WHO, traumatic brain injury (TBI) has been recognized as one of the most common causes of epilepsy. Trauma accounts for approximately 4-10% of chronic epilepsy in the community. Posttraumatic epilepsy (PTE) can appear several years after TBI with variable latency of onset and course. Epidemiologic studies have showed a relationship between the severity of injury, follow-up period and the likelihood of developing epilepsy. The exact mechanism that connects the brain tissue trauma to recurrent seizures remains unknown. Epileptogenesis is due to a number of mechanisms, which often coexist within a single patient. According to current evidence the treatment of early post-traumatic seizures does not influence the incidence of post-traumatic epilepsy. Therefore, the routine preventive anticonvulsants are not recommended for patients with TBI. Antiepileptic drugs should be introduced after the diagnosis of PTE is established. The existence of latency period between trauma and onset of chronic seizures indicates the advisability to include these patients in antiepileptogenesis therapies. However, antiepileptogenic therapy is still not available due to the lack of reliable and valid biomarkers of epileptogenic process.

Key words: posttraumatic epilepsy, seizures, children, traumatic brain injury, epileptogenesis, biomarkers.


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