Posttraumatic Epilepsy Epidemiology

Posttraumatic Epilepsy Epidemiology

In general, the incidence of Posttraumatic Epilepsy varies with the time period after injury and population age range under study, as well as the spectrum of severity of the inciting injuries, and has been reported to be anywhere from 4 to 53% 1).

Generally posttraumatic epilepsy accounts for less than 10% of epilepsy 2).

In a cohort study, the incidence of self-reported PTE after TBI was found to be 2.8% and was independently associated with unfavorable outcomes 3).

In a large cohort of post-concussion patients Wennberg et al. found no increased incidence of epilepsy. For at least the first 5-10 years post-injury, concussion/mTBI should not be considered a significant risk factor for epilepsy. In patients with epilepsy and a past history of concussion, the epilepsy should not be presumed to be post-traumatic 4).

The Vietnam Head Injury Study (VHIS) is a prospective, longitudinal follow-up of 1,221 Vietnam War veterans with mostly penetrating head injuries (PHIs). The high prevalence (45%-53%) of posttraumatic epilepsy (PTE) in this unique cohort makes it valuable for study.

A standardized multidisciplinary neurologic, cognitive, behavioral, and brain imaging evaluation was conducted on 199 VHIS veterans plus uninjured controls, some 30 to 35 years after injury, as part of phase 3 of this study.

The prevalence of seizures (87 patients, 43.7%) was similar to that found during phase 2 evaluations 20 years earlier, but 11 of 87 (12.6%) reported very late onset of PTE after phase 2 (more than 14 years after injury). Those patients were not different from patients with earlier-onset PTE in any of the measures studied. Within the phase 3 cohort, the most common seizure type last experienced was complex partial seizures (31.0%), with increasing frequency after injury. Of subjects with PTE, 88% were receiving anticonvulsants. Left parietal lobe lesions and retained ferric metal fragments were associated with PTE in a logistic regression model. Total brain volume loss predicted seizure frequency.

Patients with PHI carry a high risk of PTE decades after their injury, and so require long-term medical follow-up. Lesion location, lesion size, and lesion type were predictors of PTE 5).

A study was undertaken to determine the risk of developing posttraumatic epilepsy (PTE) within 3 years after discharge among a population-based sample of older adolescents and adults hospitalized with traumatic brain injury (TBI) in South Carolina. It also identifies characteristics related to development of PTE within this population.

A stratified random sample of persons aged 15 and older with TBI was selected from the South Carolina nonfederal hospital discharge dataset for four consecutive years. Medical records of recruits were reviewed, and they participated in up to three yearly follow-up telephone interviews.

The cumulative incidence of PTE in the first 3 years after discharge, after adjusting for loss to follow-up, was 4.4 per 100 persons over 3 years for hospitalized mild TBI, 7.6 for moderate, and 13.6 for severe. Those with severe TBI, posttraumatic seizures prior to discharge, and a history of depression were most at risk for PTE. This higher risk group also included persons with three or more chronic medical conditions at discharge.

These results raise the possibility that although some of the characteristics related to development of PTE are nonmodifiable, other factors, such as depression, might be altered with intervention 6).

Using Taiwan’s National Health Insurance Research Database of reimbursement claims, Yeh et al. conducted a retrospective cohort study of 19 336 TBI patients and 540 322 non-TBI participants aged ≥15 years as reference group. Data on newly developed epilepsy after TBI with 5-8 years’ follow-up during 2000 to 2008 were collected. HRs and 95% CIs for the risk of epilepsy associated with TBI were analysed with multivariate Cox proportional hazards regressions.

Results: Compared with the non-TBI cohort, the adjusted HRs of developing epilepsy among TBI patients with skull fracture, severe or mild brain injury were 10.6 (95% CI 7.14 to 15.8), 5.05 (95% CI 4.40 to 5.79) and 3.02 (95% CI 2.42 to 3.77), respectively. During follow-up, men exhibited higher risks of post-TBI epilepsy. Patients who had mixed types of cerebral haemorrhage were at the highest risk of epilepsy compared with the non-TBI cohort (HR 7.83, 95% CI 4.69 to 13.0). The risk of post-TBI epilepsy was highest within the first year after TBI (HR 38.2, 95% CI 21.7 to 67.0).

Conclusions: The risk of epilepsy after TBI varied by patient gender, age, latent interval and complexity of TBI. Integrated care for early identification and treatment of post-trauma epilepsy were crucial for TBI patients 7)

Christensen et al. aimed to assess the risk of epilepsy up to 10 years or longer after traumatic brain injury, taking into account sex, age, severity, and family history.

Methods: We identified 1 605 216 people born in Denmark (1977-2002) from the Civil Registration System. We obtained information on traumatic brain injury and epilepsy from the National Hospital Register and estimated relative risks (RR) with Poisson analyses.

Findings: Risk of epilepsy was increased after a mild brain injury (RR 2.22, 95% CI 2.07-2.38), severe brain injury (7.40, 6.16-8.89), and skull fracture (2.17, 1.73-2.71). The risk was increased more than 10 years after mild brain injury (1.51, 1.24-1.85), severe brain injury (4.29, 2.04-9.00), and skull fracture (2.06, 1.37-3.11). RR increased with age at mild and severe injury and was especially high among people older than 15 years of age with mild (3.51, 2.90-4.26) and severe (12.24, 8.52-17.57) injury. The risk was slightly higher in women (2.49, 2.25-2.76) than in men (2.01, 1.83-2.22). Patients with a family history of epilepsy had a notably high risk of epilepsy after mild (5.75, 4.56-7.27) and severe brain injury (10.09, 4.20-24.26) 8).

A total of 647 individuals (>/=16 y) with any of the following abnormal computed tomography (CT) scan findings: extent of midline shift and/or cisternal compression or presence of any focal pathology (eg, punctate, subarachnoid, or intraventricular hemorrhage; cortical or subcortical contusion; extra-axial lesions) during the first 7 days postinjury or best Glasgow Coma Scale (GCS) score of </=10 during the first 24 hours post-TBI. Subjects were enrolled from August 1993 through September 1997 and followed for up to 24 months, until death or their first late posttraumatic seizures.

Main outcome measures: Cumulative probability, relative risk, and survival analyses were used to stratify risks for development of late postttraumatic seizures on the basis of demographic factors, etiology of injury, initial GCS, early posttraumatic seizures, time post-TBI, types of intracerebral lesion by CT scan, and number and types of intracranial procedures.

Results: Sixty-six individuals had a late posttraumatic seizures; 337 had no late posttraumatic seizures during full 24-month follow-up; 167 had no late posttraumatic seizures during time followed (<24 mo); and 54 were placed on anticonvulsants without a late posttraumatic seizures, whereas 23 died before their first late posttraumatic seizures. The highest cumulative probability for late posttraumatic seizures included biparietal contusions (66%), dural penetration with bone and metal fragments (62.5%), multiple intracranial operations (36.5%), multiple subcortical contusions (33.4%), subdural hematoma with evacuation (27.8%), midline shift greater than 5mm (25.8%), or multiple or bilateral cortical contusions (25%). Initial GCS score was associated with the following cumulative probabilities for development of late posttraumatic seizures at 24 months: GCS score of 3 to 8, 16.8%; GCS score of 9 to 12, 24.3%; and GCS score of 13 to 15, 8.0%.

Conclusions: Stratification by CT scan findings and neurosurgical procedures performed were the most useful findings in defining individuals at highest risk for late posttraumatic seizures 9).

A cohort of 2747 patients with head injuries was followed for 28,176 person-years to determine the magnitude and duration of the risk of posttraumatic seizures. Injuries were classified as severe (brain contusion, intracerebral or intracranial hematoma, or 24 hours of eight unconsciousness of amnesia), moderate (skull fracture or 30 minutes to 24 hours of unconsciousness or amnesia), and mild (briefer unconsciousness or amnesia). The risk of posttraumatic seizures after severe injury was 7.1% within 1 year and 11.5% in 5 years, after moderate injury the risk was 0.7 and 1.6%, and after mild injury the risk was 0.1 and 0.6%. The incidence of seizures after mild head injuries was not significantly greater than in the general population 10)

The true incidence of PTE in children is still uncertain because most research has been based primarily on adults.

see Posttraumatic epilepsy in children.


Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia. 2003;44(s10):11-7. doi: 10.1046/j.1528-1157.44.s10.4.x. PMID: 14511389.

Christensen J. The Epidemiology of Posttraumatic Epilepsy. Semin Neurol. 2015 Jun;35(3):218-22. doi: 10.1055/s-0035-1552923. Epub 2015 Jun 10. PMID: 26060901.

Burke J, Gugger J, Ding K, Kim JA, Foreman B, Yue JK, Puccio AM, Yuh EL, Sun X, Rabinowitz M, Vassar MJ, Taylor SR, Winkler EA, Deng H, McCrea M, Stein MB, Robertson CS, Levin HS, Dikmen S, Temkin NR, Barber J, Giacino JT, Mukherjee P, Wang KKW, Okonkwo DO, Markowitz AJ, Jain S, Lowenstein D, Manley GT, Diaz-Arrastia R; TRACK-TBI Investigators, Badjatia N, Duhaime AC, Feeser VR, Gaudette E, Gopinath S, Keene CD, Korley FK, Madden C, Merchant R, Schnyer D, Zafonte R. Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury. JAMA Netw Open. 2021 Dec 1;4(12):e2140191. doi: 10.1001/jamanetworkopen.2021.40191. PMID: 34964854.

Wennberg R, Hiploylee C, Tai P, Tator CH. Is Concussion a Risk Factor for Epilepsy? Can J Neurol Sci. 2018 May;45(3):275-282. doi: 10.1017/cjn.2017.300. Epub 2018 Mar 20. PMID: 29557322.

Raymont V, Salazar AM, Lipsky R, Goldman D, Tasick G, Grafman J. Correlates of posttraumatic epilepsy 35 years following combat brain injury. Neurology. 2010 Jul 20;75(3):224-9. doi: 10.1212/WNL.0b013e3181e8e6d0. PMID: 20644150; PMCID: PMC2906177.

Ferguson PL, Smith GM, Wannamaker BB, Thurman DJ, Pickelsimer EE, Selassie AW. A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia. 2010 May;51(5):891-8. doi: 10.1111/j.1528-1167.2009.02384.x. Epub 2009 Oct 20. PMID: 19845734.

Yeh CC, Chen TL, Hu CJ, Chiu WT, Liao CC. Risk of epilepsy after traumatic brain injury: a retrospective population-based cohort study. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):441-5. doi: 10.1136/jnnp-2012-302547. Epub 2012 Oct 31. PMID: 23117492.

Christensen J, Pedersen MG, Pedersen CB, Sidenius P, Olsen J, Vestergaard M. Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet. 2009 Mar 28;373(9669):1105-10. doi: 10.1016/S0140-6736(09)60214-2. Epub 2009 Feb 21. PMID: 19233461.

Englander J, Bushnik T, Duong TT, Cifu DX, Zafonte R, Wright J, Hughes R, Bergman W. Analyzing risk factors for late posttraumatic seizures: a prospective, multicenter investigation. Arch Phys Med Rehabil. 2003 Mar;84(3):365-73. doi: 10.1053/apmr.2003.50022. PMID: 12638104.

Annegers JF, Grabow JD, Groover RV, Laws ER Jr, Elveback LR, Kurland LT. Seizures after head trauma: a population study. Neurology. 1980 Jul;30(7 Pt 1):683-9. doi: 10.1212/wnl.30.7.683. PMID: 7190235.

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cyst

Posttraumatic leptomeningeal cysts (PTLMC) (sometimes just traumatic leptomeningeal cysts), AKA growing skull fractures consists of a fracture line that widens with time.

The term cyst is actually a misnomer, as it is not a cyst, but an extension of the encephalomalacia 1).

Posttraumatic leptomeningeal cysts were first described in 18162).

Very rare, occurring in 0.05–0.6% of skull fracture3) 4). Usually requires both a widely separated fracture AND a dural tear.

Mean age at injury: < 1 year; over 90% occur before age 3 years 5) (formation may require the presence of a rapidly growing brain 6)), although rare adult cases have been described 7)8) 9) (a total of 5 cases in the literature as of 1998 10)).

The pathophysiology and some aspects of its management are still controversial.

It is thought they occur secondary to skull fractures causing dural tears allowing the leptomeninges and/or cerebral parenchyma to herniate into it

Pulsations from CSF erode the fracture margin, resulting in eventual expansion and non-union.

It occurs due to a wide skull defect with underlying dural defect and changes in pressure gradients within the skull cavity. Neglected cases may develop progressive neurological deficits and complications after second head trauma 11).

Enlarging scalp mass


Focal neurological deficit


Most often presents as scalp mass (usually subgaleal), although there are reports of presentation with head pain alone 12).

Kitumba and Mascarenhas presented a rare case of an adult with excruciating headache secondary to a post-traumatic fronto-orbital leptomeningeal cyst 13)

PTLMCs rarely occur > 6 mos out from the injury. Some children may develop a skull fracture that seems to grow during the initial few weeks that is not accompanied by a subgaleal mass, and that heals spontaneously within several months; the term “pseudogrowing fracture” has been suggested for these 14).

They can rupture and cause diffuse subgaleal CSF collection 15).

Radiographic findings: progressive widening of fracture and scalloping (or saucering) of edges.

round or oval lucency with smooth margins

CT scan is the modality of choice for the evaluation of leptomeningeal cyst. It consists of a lytic calvarial lesion with scalloped edges, in which encephalomalacia invaginates. The following features may also be present

extracranial brain herniation


unilateral ventricular dilatation

porencephalic cyst.

Guler I, Buyukterzi M, Oner O, Tolu I. Post-traumatic leptomeningeal cyst in a child: computed tomography and magnetic resonance imaging findings. J Emerg Med. 2015 May;48(5):e121-2. doi: 10.1016/j.jemermed.2014.12.042. Epub 2015 Feb 3. PMID: 25662419.

Not to be confused with arachnoid cysts (AKA leptomeningeal cysts, which are not posttraumatic).

Posttraumatic intradiploic leptomeningeal cyst.

Skull tumor 16).

eosinophilic granuloma

calvarial metastases

epidermoid cyst


congenital calvarial defect

Although usually asymptomatic, the cyst may cause a mass effect with neurologic deficit.

Distal cortical artery aneurysms: often associated with an overlying s skull fracture, sometimes a growing skull fracture

Neglected GSF can rupture and cause diffuse subgaleal CSF collection 17).

If early growth of a fracture line with no subgaleal mass is noted, repeat skull films in 1–2 months before operating (to rule out pseudogrowing fracture). In young patients with separated skull fractures (the width of the initial fracture is rarely mentioned), consider obtaining follow-up skull film 6–12 mos post-trauma. However, since most PTLMCs are brought to medical attention when the palpable mass is noticed, routine follow-up X-rays may not be cost-effective.

Treatment of true PTLMC is surgical, with dural closure mandatory. Since the dural defect is usually larger than the bony defect, it may be advantageous to perform a craniotomy around the fracture site, repair the dural defect, and replace the bone 18).

The dural substitutes used are either autografts (which may not be enough) or artificial grafts (which are foreign-body implantations and which also may be too expensive in a low-resource practice).

Adeleye presented the surgical description of the use of the cyst capsule as a cost-free autologous graft in the surgical repair of the dural defects of two cases of traumatic leptomeningeal cyst 19).

Pseudogrowing fractures should be followed with X- rays and operated only if expansion persists beyond several months or if a subgaleal mass is present.

Liu et al. performed a retrospective review of 27 patients with GSF, who were grouped according to 3 different GSF stages.

Over a period of 20 years, 27 patients with GSF (16 males and 11 females) were treated in the authors’ department. The mean follow-up period was 26.5 months. Six patients were in the pre-phase of GSF (Stage 1), 10 patients in the early phase (Stage 2), and 11 in the late phase (Stage 3). All patients underwent duraplasty. All 6 patients at Stage 1 and 5 patients at Stage 2 underwent craniotomy without cranioplasty. Five patients at Stage 2 and all of the patients at Stage 3 underwent cranioplasty with autologous bone and alloplastic materials, respectively. Among all patients, 5 underwent ventriculoperitoneal shunt placement. Symptoms in all patients at Stages 1 and 2 were alleviated or disappeared, and the cranial bones developed without deformity during follow-up. Among patients with Stage 3 GSF, no obvious improvement in neurological deficits was observed. Three patients underwent additional operations because of cranial deformation or infection.

The authors identify the stages of GSF according to a new hypothesis. They conclude that accurately diagnosing and treating GSF during Stages 1 and 2 leads to a better prognosis 20)

Kulkarni et al. presented a 14-year-old child who developed sudden-onset, diffuse, soft, fluctuant, circumferential swelling of the head after a road traffic accident. He had sustained a head injury at the age of 3-months leading to an asymptomatic soft swelling over the skull which was left untreated. The present CT scan of the brain showed a bony defect with ragged edges and cerebrospinal fluid (CSF) collection in subgaleal space circumferentially. He underwent exploration, duroplasty, and cranioplasty and had a good outcome.

Neglected GSF can rupture and cause diffuse subgaleal CSF collection. It should be managed with dural repair and cranioplasty 21).

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233 22).

A 4-year-old boy was brought to the emergency department after suffering from head trauma caused by a fall from a rooftop where he was treated conservatively at a local hospital. Later, he developed swelling in the occipital region and was brought to the department of neurosurgery where he was operated on. After the first surgery, recurrence of swelling was seen after a postoperative period of 2 months, and a computed tomography scan reported persistent epidural hygroma with extension into the subcutaneous space. The second surgery was performed, and a 12-month follow-up did not show any recurrence of swelling in the patient 23).

A full-term infant born after a nontraumatic, forceps-assisted spontaneous delivery, who developed an increasing cystic swelling over the left frontoparietal area that crossed over coronal and sagittal sutures. The lesion was initially misinterpreted as cephalhematoma. Clinical and radiological follow-up established the correct diagnosis of leptomeningeal cyst.

The collection was initially tapped. Surgical treatment was undertaken thereafter, consisting of decompression and resection of the cyst and dural repair. Two months after follow-up, the patient remains asymptomatic and the porencephalic cavity remains isolated from the extradural space, with no evidence of new fluid collections 24).

A 53-year-old female presented with a post-traumatic leptomeningeal cyst manifesting as bulging of the scalp, dizziness, and tinnitus. She had known of the bulging of her forehead for about 20 years. She had suffered an injury to the head in childhood. Brain CT revealed a bone cyst associated with a round bone defect in the left frontal bone, bulging of the very thin outer layer, and the defective inner layer. She was treated surgically with a diagnosis of a skull tumor, but only gray cystic membranous tissue was found. The dural defect was repaired with fascia and the bone defect with bone cement. Bulging of the skull in adults can be caused by a bone cyst originating from a skull fracture 25).

12 patients diagnosed and treated between 1980 and 2002. 11 patients were under the age of 3 years and one patient was 5 years old at the moment of HI. The most common cause of injury was a fall from height. In the initial plain x-rayfilms, 11 patients showed a diastatic skull fracture and one patient only had a linear fracture. At this time, CT scan showed cortical contussion underlying the fracture in every case. The mean time between injury and presentation of GSF was 11.6 weeks. Diagnosis was made by palpation of the cranial defect and confirmed with skull x-rayfilms. The most frecuent location of GSF was in the parietal region. Associated lesions like hydrocephalus, encephalomalacia, leptomenigeal cysts, brain tissue herniation and ipsilateral ventricular dilatation, were found in the preoperative CT or MRI. All patients underwent a dural repair with pericranium or fascia lata. The cranial defect was covered with local calvarial bone fragments in every case. Only one patient needed a cranioplasty with titanium mesh. Every child with a skull fracture must be followed until the fracture heals. Patients under the age of 3 years with a diastatic fracture and a dural tear, demostrated by TC or MRI, are more prone to develop GSF. In these cases, early repair must be adviced in order to prevent progressive brain damage 26).

A growing skull fracture associated with cerebrospinal fluid rhinorrhoea following trauma sustained in adult life. The natural history of its development, diagnosis, and the results of surgery are discussed. The literature is reviewed with regard to aetiology, incidence, imaging characteristics and management of this rare post-traumatic complication 27).

A lump in the right parietal region of this 53-year-old man prompted a computed tomography (CT) scan. The patient denied any symptoms and was in good health. The examination confirmed a firm, non-tender, non-pulsatile mass in the right parietal region of the skull. The CT scan demonstrated a 4 x 3 cm area of irregular bone destruction involving both the inner and outer table of the skull. At operation a distinctly raised paper-thin outer table was noted, and underneath was a soft, tan-colored mass, which measured approximately 2 x 2 cm and was connected to the underlying brain through a 1 cm dural defect. The extradural portion of the mass was amputated, the dura repaired with a pericranium patch, the skull defect was repaired with a split-thickness bone graft, and the final pathology was congruent with a gliotic brain 28).

Meloche BR, Sansregret A, Grégoire H, Gagnon J, Massicotte P. Un cas de kyste leptoméningé post-traumatique [A case of post-traumatic leptomeningeal cyst]. Union Med Can. 1967 Oct;96(10):1214-9. French. PMID: 5601803.

PEYSER E, WEISSBERG D. Post-traumatic arachnoidal cyst. Report of an unusual case. J Neurosurg. 1961 Jul;18:551-3. doi: 10.3171/jns.1961.18.4.0551. PMID: 13735101.

2) , 7) , 10) , 28)

Britz GW, Kim DK, Mayberg MR. Traumatic leptomeningeal cyst in an adult: a case report and review of the literature. Surg Neurol. 1998 Nov;50(5):465-9. doi: 10.1016/s0090-3019(97)00233-4. PMID: 9842874.

Ramamurthi B, Kalyanaraman S. Rationale for Surgery in Growing Fractures of the Skull. J Neurosurg. 1970; 32:427–430

Arseni CS. Growing Skull Fractures of Children. A Particular Form of Post-Traumatic Encephalopathy. Acta Neurochir. 1966; 15:159–172

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Gadoth N, Grunebaum M, Young LW. Leptomeningeal Cyst After Skull Fracture. Am J Dis Child. 1983; 137:1019–1020
8) , 12)

Halliday AL, Chapman PH, Heros RC. Leptomeningeal Cyst Resulting from Adulthood Trauma: Case Report. Neurosurgery. 1990; 26:150–153
9) , 18)

Iplikciglu AC, Kokes F, Bayar A, et al. Leptomeningeal Cyst. Neurosurgery. 1990; 27: 1027–1028

Drapkin AJ. Growing skull fracture: a posttraumatic neosuture. Childs Nerv Syst. 2006 Apr;22(4):394-7. doi: 10.1007/s00381-005-1158-9. Epub 2005 Apr 22. PMID: 15856258.
13) , 22)

Kitumba D, Mascarenhas L. Rare case of an adult with excruciating headache secondary to post-traumatic fronto-orbital leptomeningeal cyst. Neurochirurgie. 2020 Nov;66(5):410-411. doi: 10.1016/j.neuchi.2020.06.126. Epub 2020 Aug 7. PMID: 32777233.

Sekhar LN, Scarff TB. Pseudogrowth in Skull Fractures of Childhood. Neurosurgery. 1980; 6:285–289
15) , 17) , 21)

Kulkarni AV, Dikshit P, Devi BI, Sadashiva N, Shukla D, Bhat DI. Unusual Complication of a Neglected Growing Skull Fracture. Pediatr Neurosurg. 2021 Feb 24:1-5. doi: 10.1159/000513102. Epub ahead of print. PMID: 33626526.
16) , 25)

Kurosu A, Fujii T, Ono G. Post-traumatic leptomeningeal cyst mimicking a skull tumour in an adult. Br J Neurosurg. 2004 Feb;18(1):62-4. doi: 10.1080/02688690410001660463. PMID: 15040717.

Adeleye AO. Posttraumatic leptomeningeal cyst capsule as a cost-free autograft for its repair: case illustrated technical reports. Neurosurg Rev. 2020 Aug 8. doi: 10.1007/s10143-020-01364-6. Epub ahead of print. PMID: 32772295.

Liu XS, You C, Lu M, Liu JG. Growing skull fracture stages and treatment strategy. J Neurosurg Pediatr. 2012 Jun;9(6):670-5. doi: 10.3171/2012.2.PEDS11538. PMID: 22656261.

Harsh V, Gond PK, Kumar A. Post-Traumatic Diploic Leptomeningeal Cyst with Bilateral Posterior Cranial Fossa Epidural Hygroma: A Management Dilemma? World Neurosurg. 2020 Aug;140:258-261. doi: 10.1016/j.wneu.2020.05.129. Epub 2020 May 21. PMID: 32445897.

Miranda P, Vila M, Alvarez-Garijo JA, Perez-Nunez A. Birth trauma and development of growing fracture after coronal suture disruption. Childs Nerv Syst. 2007 Mar;23(3):355-8. Epub 2006 Oct 5. PubMed PMID: 17021730.

Mierez R, Guillén A, Brell M, Cardona E, Claramunt E, Costa JM. [Growing skull fracture in childhood. Presentation of 12 cases]. Neurocirugia (Astur). 2003 Jun;14(3):228-33; discussion 234. Spanish. PubMed PMID: 12872172.

Gupta V, Sinha S, Singh AK, Kumar S, Singh D. Growing skull fracture of ethmoid: a report of two cases. J Craniomaxillofac Surg. 2000 Aug;28(4):224-8. doi: 10.1054/jcms.2000.0141. PMID: 11110154.

Posttraumatic seizures management

Posttraumatic seizures management

Patient selection for seizure prophylaxis after traumatic brain injury (TBI) and duration of antiepileptic drug treatment for patients with early posttraumatic seizures (PTS) remain plagued with uncertainty. In early 2017, a collaborative group of neurosurgeons, neurologists, neurointensive care and rehabilitation medicine physicians was formed in the UK with the aim of assessing variability in current practice and gauging the degree of uncertainty to inform the design of future studies. The survey results demonstrated the variation in practice and uncertainty in both described aspects of management of patients who have suffered a TBI. The majority of respondents would want to participate in future research to help try and address this critical issue, and this shows the importance and relevance of these two clinical questions 1)


Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition:

Level I

• There was insufficient evidence to support a Level I recommendation for this topic.

Level II A

• Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS.

• Phenytoin is recommended to decrease the incidence of early PTS (within 7 days of injury), when the overall benefit is felt to outweigh the complications associated with such treatment. However, early PTS have not been associated with worse outcomes. At the present time there is insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity.

Changes from Prior Edition

The recommendations have not changed for this update from the 3rd Edition. Two new Class 2 studies and four new Class 3 studies were added as evidence, but these and the Class 3 studies included from the 3rd Edition did not provide sufficient evidence to inform new recommendations.




Wilson et al. assessed and compared the effectiveness of drugs on early and late PTS prevention.

A literature search revealed 120 articles. Data were included if the same factors were compared across studies with identical treatment arms. Random effects models were used for meta-analysis to combine data into an overriding odds ratio (OR) comparing PTS incidence. For early PTSs, PHT was compared with placebo and LEV with PHT. For late PTSs, each drug was compared with a placebo.

Sixteen studies were included. PHT was associated with decreased odds of early seizures relative to placebo (OR = 0.34, 95% confidence interval [CI] 0.19-0.62). There was no difference in early seizure incidence between LEV and PHT (OR = 0.83, 95% CI 0.33-2.1). Neither LEV (OR = 0.69, 95% CI 0.24-1.96) nor PHT (OR = 0.4, 95% CI 0.1-1.6) was associated with fewer late PTSs than placebo.

New literature is consistent with current guidelines supporting antiepileptic drug administration for prevention of early, but not late, PTSs. With regard to early PTS prevention, LEV and PHT are similarly efficacious, which is consistent with current guidelines. Side-effect profiles favor LEV administration over PHT 2).



Mee H, Kolias AG, Chari A, Ercole A, Lecky F, Turner C, Tudur-Smith C, Coles J, Anwar F, Belli A, Manford M, Ham T, McMahon C, Bulters D, Uff C, Duncan JS, Wilson MH, Marson AG, Hutchinson PJ. Pharmacological management of post-traumatic seizures in adults: current practice patterns in the UK and the Republic of Ireland. Acta Neurochir (Wien). 2019 Mar;161(3):457-464. doi: 10.1007/s00701-018-3683-9. Epub 2018 Oct 1. PubMed PMID: 30276544; PubMed Central PMCID: PMC6407744.

Wilson CD, Burks JD, Rodgers RB, Evans RM, Bakare AA, Safavi-Abbasi S. Early and Late Posttraumatic Epilepsy in the Setting of Traumatic Brain Injury: A Meta-analysis and Review of Antiepileptic Management. World Neurosurg. 2018 Feb;110:e901-e906. doi: 10.1016/j.wneu.2017.11.116. Epub 2017 Dec 2. Review. PubMed PMID: 29196247.
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