PURPOSE: Evaluation of morphologic risk factors for posttraumatic epilepsy (PTE) by using brain magnetic resonance imaging (MRI) in serial assessments <or=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.
PURPOSE: Evaluation of morphologic risk factors for posttraumatic epilepsy (PTE) by using brain magnetic resonance imaging (MRI) in serial assessments <or=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.
Authors: Tessandra H Stewart; Clifford L Eastman; Peter A Groblewski; Jason S Fender; Derek R Verley; David G Cook; Raimondo D'Ambrosio Journal: J Neurophysiol Date: 2010-09-22 Impact factor: 2.714
Authors: Marianna La Rocca; Rachael Garner; Nicola Amoroso; Evan S Lutkenhoff; Martin M Monti; Paul Vespa; Arthur W Toga; Dominique Duncan Journal: Front Neurosci Date: 2020-11-30 Impact factor: 4.677