Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study

Christensen, Jakob; Pedersen, Marianne G.; Pedersen, Carsten Bøcker; Sidenius, Per; Olsen, Jørn; Vestergaard, Mogens

doi:10.1016/s0140-6736(09)60214-2

Cited by 324 publications

(291 citation statements)

References 26 publications

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“…Children who survive TBI may develop chronic cognitive and behavioral disturbances (Christensen et al 2009;Fay et al 1994;Levin et al 2002). Despite a long history of clinical research into pediatric TBI (Bruce et al 1979;Raphaely et al 1980), the pathological mechanisms of TBI in childhood are still coming to light (Jankowitz and Adelson 2006).…”

Section: Introductionmentioning

confidence: 99%

Experimental Mild Traumatic Brain Injury Induces Functional Alteration of the Developing Hippocampus

Morrison

2010

Journal of Neurophysiology

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Section: Introductionmentioning

confidence: 99%

Experimental Mild Traumatic Brain Injury Induces Functional Alteration of the Developing Hippocampus

Morrison

2010

Journal of Neurophysiology

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“…15 In broader populations of adults with mild TBI, the likelihood of major depressive disorder and epilepsy increased, although effects were also confounded by prior history. 16,17 A literature review found that the prevalence of chronic pain was greater in patients with mild TBI than in those with moderate or severe TBI. 18 The diagnosis and treatment of TBI is hindered by the lack of a definitive biomarker, especially for mild TBI or concussion.…”

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confidence: 99%

GFAP-BDP as an Acute Diagnostic Marker in Traumatic Brain Injury: Results from the Prospective Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study

Okonkwo

Yue

Puccio

et al. 2013

Journal of Neurotrauma

177

120

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Reliable diagnosis of traumatic brain injury (TBI) is a major public health need. Glial fibrillary acidic protein (GFAP) is expressed in the central nervous system, and breakdown products (GFAP-BDP) are released following parenchymal brain injury. Here, we evaluate the diagnostic accuracy of elevated levels of plasma GFAP-BDP in TBI. Participants were identified as part of the prospective Transforming Research And Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) Study. Acute plasma samples (< 24 h post-injury) were collected from patients presenting with brain injury who had CT imaging. The ability of GFAP-BDP level to discriminate patients with demonstrable traumatic lesions on CT, and with failure to return to pre-injury baseline at 6 months, was evaluated by the area under the receiver operating characteristic curve (AUC). Of the 215 patients included for analysis, 83% had mild, 4% had moderate, and 13% had severe TBI; 54% had acute traumatic lesions on CT. The ability of GFAP-BDP level to discriminate patients with traumatic lesions on CT as evaluated by AUC was 0.88 (95% confidence interval [CI], 0.84-0.93). The optimal cutoff of 0.68 ng/mL for plasma GFAP-BDP level was associated with a 21.61 odds ratio for traumatic findings on head CT. Discriminatory ability of unfavorable 6 month outcome was lower, AUC 0.65 (95% CI, 0.55-0.74), with a 2.07 odds ratio. GFAP-BDP levels reliably distinguish the presence and severity of CT scan findings in TBI patients. Although these findings confirm and extend prior studies, a larger prospective trial is still needed to validate the use of GFAP-BDP as a routine diagnostic biomarker for patient care and clinical research. The term ''mild'' continues to be a misnomer for this patient population, and underscores the need for evolving classification strategies for TBI targeted therapy. (ClinicalTrials.gov number NCT01565551; NIH Grant 1RC2 NS069409)

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“…The risk of epilepsy is increased after a mild brain injury (relative risks 2.22, 95% 2.07–2.38) and a severe brain injury (7.40, 6.16–8.89). The risk is increased by more than 10 years after mild brain injury (1.51, 1.24–1.85) and severe brain injury (4.29, 2.04–9.00) 18. Emanuelson I identified PTE 10 years after TBI in a population‐based, retrospective, follow‐up study, and 12 of 109 participants developed active epilepsy during the follow‐up period.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility‐weighted and diffusion kurtosis imaging to evaluate encephalomalacia with epilepsy after traumatic brain injury

Wang

Wei

et al. 2018

Ann Clin Transl Neurol

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ObjectiveEncephalomalacia after traumatic brain injury (TBI) is one of the factors leading to epilepsy. In this study, magnetic resonance imaging (MRI) was used to explore the brain image features of epilepsy after traumatic encephalomalacia, and to provide objective evidence for predicting the possible occurrence of epilepsy after traumatic encephalomalacia.MethodsTwo‐hundred‐fifty‐two patients with traumatic encephalomalacia were prospectively enrolled in the study. All patients underwent MRI after discharge from the hospital. At the 1‐year follow‐up, participants were divided into epilepsy and nonepilepsy groups. All participants underwent MRI including conventional imaging, susceptibility‐weighted imaging (SWI), and diffusion kurtosis imaging (DKI). The lesion volume, iron deposition, mean diffusion (MD), and mean kurtosis (MK) around the lesions were calculated for each group and compared using t‐tests. P values < 0.05 were considered statistically significant.ResultsSixty patients with epilepsy and 91 without epilepsy were reported. There were no significant differences in Glasgow Coma Scale (GCS), lesion volume, encephalomalacia, or MD values between the two groups. Iron deposition was significantly higher in the epilepsy group (P < 0.05). The MK values were significantly different (P < 0.05).InterpretationAdvanced MRI is an important means of evaluating risk of developing epilepsy at 1 year due to encephalomalacia in patients with TBI. SWI and DKI could be used to assess the microstructural changes around the encephalomalacia, and therefore be used to evaluate risk of developing epilepsy at 1 year.

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Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study

Cited by 324 publications

References 26 publications

Experimental Mild Traumatic Brain Injury Induces Functional Alteration of the Developing Hippocampus

Experimental Mild Traumatic Brain Injury Induces Functional Alteration of the Developing Hippocampus

GFAP-BDP as an Acute Diagnostic Marker in Traumatic Brain Injury: Results from the Prospective Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study

Susceptibility‐weighted and diffusion kurtosis imaging to evaluate encephalomalacia with epilepsy after traumatic brain injury

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