The early and aggressive management of extradural hematomas (EDH) is a classical teaching
during neurosurgery residency.[1]
[2]
[3] Posttraumatic seizures (PTS) after EDH share a significant percentage of causality,
but apparently remain a less studied entity. The major literature analyzing EDH with
PTS dates back to the late 20th century and there are only a couple of recent studies.[4]
[5]
[6]
[7] Additionally, an often-debated issue is the role of prophylactic antiepileptic drugs
(AEDs) in patients suspected of having high chances of developing PTS.[8]
[9] Uniform use of AEDs in all cases can lead to drug-related side effects and complications
and in some cases unnecessary AED dependence.[9]
[10]
An online search PubMed database was performed by using literature and using the search
strategy “(((“extradural haematoma”[All Fields] OR “hematoma, epidural, cranial”[MeSH
Terms] OR (“hematoma”[All Fields] AND “epidural”[All Fields] AND “cranial”[All Fields])
OR “cranial epidural hematoma”[All Fields] OR (“extradural”[All Fields] AND “hematoma”[All
Fields]) OR “extradural hematoma”[All Fields]) AND (“epilepsy”[MeSH Terms] OR “epilepsy”[All
Fields])) AND (“seizures”[MeSH Terms] OR “seizures”[All Fields])) AND (“anticonvulsants”[All
Fields] OR “anticonvulsants”[MeSH Terms] OR “anticonvulsants”[All Fields])” on PTS
after EDH returned only a handful of articles ([Fig. 1]).[4]
[5]
[7] Three studies were excluded as there was no clear categorization of intracranial
hematomas,[11] diagnosis of extradural hematoma not clearly mentioned,[12] and no clear description of seizure groups.[13]
Fig. 1 Prisma chart of the studies extracted using keyword-based PubMed search.
One of the early reports was by Bryan Jennett from the Institute of Neurological Sciences,
Glasgow in 1975.[5] The peculiarity of this report was that the case series was of the pre-CT era and
surgical interventions were based only on clinical findings. Among patients of seizures
due to posttraumatic intracranial hematomas (excluding chronic subdural hematomas),
EDH was reported as a cause of early seizures (within 1 week of head injury) in 10%
(15/146) and late seizures in 22% (13/59) patients. Jennet also found out that only
2% of early PTS patients had an evolving EDH. The next significant report came in
1991 by Jamjoom et al from Bristol.[4] They categorized EDH patients with epilepsy in two subgroups, based on CT findings
into those with exclusive EDH and those with other intradural traumatic insults.[4] Although they found the overall incidence of late epilepsy to be 6%, in the pure
EDH group, it was only 2% as against 17% of those with additional intradural damage.
Another data analysis from a multicentre North American TBI database of 795 patients
from 1989 to 2000 was reported by Ritter et al in 2016.[7] Among the various findings, EDH was found to be the cause of early and late PTS
in 14.5% and 16.9%, respectively. The most recent report on the incidence of PTS due
to EDH came from the series of 484 TBI patients by Pormontree et al from Thailand
in 2019.[6] The authors analyzed early PTS in TBI patients from April 2017 to March 2018. Twenty-seven
patients (5.6%) had early PTS due to various intracranial insults. Among these, EDH
was found to have an adjusted odds ratio of 3.98 on multivariate analysis (p value = 0.001).
PTS is a known complication of head injury.[6]
[7]
[10]
[14]
[15]
[16]
[17] Whether they occur in the early (within a week) or in late posttraumatic period,
this sequela of brain injury can significantly deteriorate the quality of life and
is considered an independent factor.[6]
[7]
[14]
[15]
[16]
[17] All the contemporary studies on posttraumatic epilepsy (PTE) are in patients with
intradural injuries.[10]
[16]
[18] Hence, considering the significant share of PTE attributed to EDH in the tune of
15 to 20%, there is an emergent need to undertake a well-formulated study to understand
the exact correlation in the current advanced imaging era and then accordingly tailor
the prophylactic antiepileptic treatment.
