Posttraumatic Epilepsy Prediction and Prophylaxis: Open Problems

D’Alessandro, Roberto; Ferrara, Raffaele; Cortelli, Pietro; Tinuper, Paolo; Pazzaglia, P; Lugaresi, E; Servadei, Franco

doi:10.1001/archneur.1983.04050120081022

Cited by 7 publications

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“…Risk factors for posttraumatic epilepsy (PTE) are still debated; however, the extensive use of computed tomography (CT) scanning in patients with traumatic brain injury (TBI) has confirmed the important role of documented focal brain lesions not only in military, but also in civilian TBI (1–17). This means that a precise neuroradiologic diagnosis is of paramount value in determining the individual PTE risk.…”

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Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

et al. 2005

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Summary:Purpose: Evaluation of morphologic risk factors for posttraumatic epilepsy (PTE) by using brain magnetic resonance imaging (MRI) in serial assessments ≤2 years after traumatic brain injury (TBI).Methods: Brain MRI hyperintense (gliosis) or hypointense (hemosiderin) areas or both were assessed in the images of 135 adult TBI inpatients who completed a 2-year clinical, EEG, and MRI study protocol. Overall clinical follow-up for the development of PTE was 5-10 years (median, 102 months). Morphologic risk factors for PTE were evaluated by using Kaplan-Meier curves and Cox regression analysis.Results: In 20 patients, PTE developed. Kaplan-Meier curves showed that gliomesenchymal sequelae of focal brain lesions (subdural hematomas/contusions) that required surgical treatment (sSDH-C) were a PTE risk factor (p < 0.001), as were sequelae of nonsurgical hemorrhagic contusions with gliosis wall incompletely surrounding hemosiderin dregs (IW) (p = 0.039) and mainly those with time-related changes from incomplete to complete gliosis wall around hemosiderin (I/CW) (p = 0.005); those with early hemosiderin completely surrounded by gliosis (CW) were not (p = 0.821). Cox regression analysis showed that for patients with sequelae of sSDH-C, the PTE risk was 4.38 (p = 0.023) times higher than for those who did not require surgical treatment or underwent surgery because of purely extradural hematoma; for those with IW and I/CW lesions, considered pooled, it was 6.61 times higher (p = 0.014) than for those with CW lesions.Conclusions: MRI follow-up examination in the early chronic stage can differentiate among low-, intermediate-, and high-risk sequelae of TBI. These findings yield new evidence for, but do not resolve, the debate on posttraumatic epileptogenesis. Key Words: Posttraumatic epilepsy-Brain MRI-HemosiderinGliosis.Risk factors for posttraumatic epilepsy (PTE) are still debated; however, the extensive use of computed tomography (CT) scanning in patients with traumatic brain injury (TBI) has confirmed the important role of documented focal brain lesions not only in military, but also in civilian TBI (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). This means that a precise neuroradiologic diagnosis is of paramount value in determining the individual PTE risk.Magnetic resonance imaging (MRI) has become the imaging method of choice for evaluation of TBI patients in the chronic stage because of its exquisite capability in showing posttraumatic brain abnormalities, provided that the appropriate pulse sequences are used. However, the relation between PTE and brain damage as revealed by MRI has not been established (18). A few years ago, our group participated in a joint prospective longitudinal study to evaluate risk factors for PTE in adults by using clini-

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confidence: 99%