Abstract
Recent animal experiments indicate a critical role for opening of the blood-brain barrier (BBB) in the pathogenesis of post-traumatic epilepsy (PTE). This study aimed to investigate the frequency, extent, and functional correlates of BBB disruption in epileptic patients following mild traumatic brain injury (TBI). Thirty-seven TBI patients were included in this study, 19 of whom suffered from PTE. All underwent electroencephalographic (EEG) recordings and brain magnetic resonance imaging (bMRI). bMRIs were evaluated for BBB disruption using novel quantitative techniques. Cortical dysfunction was localized using standardized low-resolution brain electromagnetic tomography (sLORETA). TBI patients displayed significant EEG slowing compared to controls with no significant differences between PTE and nonepileptic patients. BBB disruption was found in 82.4% of PTE compared to 25% of non-epileptic patients (P = .001) and could be observed even years following the trauma. The volume of cerebral cortex with BBB disruption was significantly larger in PTE patients (P = .001). Slow wave EEG activity was localized to the same region of BBB disruption in 70% of patients and correlated to the volume of BBB disrupted cortex. We finally present a patient suffering from early cortical dysfunction and BBB breakdown with a gradual and parallel resolution of both pathologies. Our findings demonstrate that BBB pathology is frequently found following mild TBI. Lasting BBB breakdown is found with increased frequency and extent in PTE patients. Based on recent animal studies and the colocalization found between the region of disrupted BBB and abnormal EEG activity, we suggest a role for a vascular lesion in the pathogenesis of PTE.
Highlights
Traumatic brain injury (TBI) is a common cause of mortality and morbidity with an occurrence of approximately 200 cases per 100,000 people a year
Based on recent animal studies and the colocalization found between the region of disrupted blood-brain barrier (BBB) and abnormal EEG activity, we suggest a role for a vascular lesion in the pathogenesis of posttraumatic epilepsy (PTE)
Lasting BBB Disruption in traumatic brain injury (TBI) Patients. 30 patients underwent brain magnetic resonance imaging (bMRI) scans (15 PTE and 15 non-epileptic) and the images were evaluated for parenchymal lesions and disruption volumes
Summary
Traumatic brain injury (TBI) is a common cause of mortality and morbidity with an occurrence of approximately 200 cases per 100,000 people a year. It is a known major risk factor for focal epilepsy [1]. Seizures may occur immediately following the trauma, though PTE usually develops several months and even years later. While immediate post-traumatic seizures may be successfully treated with antiepileptic drugs [7], the mechanisms underlying the development of PTE remain unknown with no means for preventing it [8]. It has been previously suggested that an increase in BBB permeability may be associated with the pathogenesis of neurological disorders [9,10,11]. It has been suggested that the most common serum protein, albumin, Control enhancement
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