Epilepsy and trauma

Willmore, L. James; Lowenstein, Daniel H.

doi:10.1212/wnl.0b013e3181e8e94f

Cited by 5 publications

(6 citation statements)

References 15 publications

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“…These data are novel because studies examining outcomes after PTE have typically not shown a major association with overall outcome in adults. 29 Although there is a high level of evidence that prophylactically treating with antiepileptic drugs in severe TBI does not improve outcome, the very high risk of epilepsy in this patient population suggests that a continued search for antiepileptogenic therapies is warranted. 30,31 A novel feature of our study is that it included a large number of participants with relatively mild TBI, including many who were discharged from the ED without anomalous cranial CT findings.…”

Section: Discussionmentioning

confidence: 99%

Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury

et al. 2021

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IMPORTANCEPosttraumatic epilepsy (PTE) is a recognized sequela of traumatic brain injury (TBI), but the long-term outcomes associated with PTE independent of injury severity are not precisely known. OBJECTIVE To determine the incidence, risk factors, and association with functional outcomes and self-reported somatic, cognitive, and psychological concerns of self-reported PTE in a large, prospectively collected TBI cohort. DESIGN, SETTING, AND PARTICIPANTS This multicenter, prospective cohort study was conducted as part of the Transforming Research and Clinical Knowledge in Traumatic Brain Injury study and identified patients presenting with TBI to 1 of 18 participating level 1 US trauma centers from February 2014 to July 2018. Patients with TBI, extracranial orthopedic injuries (orthopedic controls), and individuals without reported injuries (eg, friends and family of participants; hereafter friend controls) were prospectively followed for 12 months. Data were analyzed from January 2020 to April 2021. EXPOSURE Demographic, imaging, and clinical information was collected according to TBI Common Data Elements. Incidence of self-reported PTE was assessed using the National Institute of Neurological Disorders and Stroke Epilepsy Screening Questionnaire (NINDS-ESQ). MAIN OUTCOMES AND MEASURES Primary outcomes included Glasgow Outcome Scale Extended, Rivermead Cognitive Metric (RCM; derived from the Rivermead Post Concussion Symptoms Questionnaire), and the Brief Symptom Inventory-18 (BSI). RESULTS Of 3296 participants identified as part of the study, 3044 met inclusion criteria, and 1885 participants (mean [SD] age, 41.3 [17.1] years; 1241 [65.8%] men and 644 [34.2%] women) had follow-up information at 12 months, including 1493 patients with TBI; 182 orthopedic controls, 210 uninjured friend controls; 41 patients with TBI (2.8%) and no controls had positive screening resultsfor PTE. Compared with a negative screening result for PTE, having a positive screening result for PTE was associated with presenting Glasgow Coma Scale score (8.1 [4.8] vs.13.5 [3.3]; P < .001) as well as with anomalous acute head imaging findings (risk ratio, 6.42 [95% CI,). After controlling for age, initial Glasgow Coma Scale score, and imaging findings, compared with patients with TBI and without PTE, patients with TBI and with positive PTE screening results had significantly lower Glasgow Outcome Scale Extended scores (mean [SD], 6.1 [1.7] vs 4.7 [1.5]; P < .001), higher BSI scores (mean [SD], 50.

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Section: Discussionmentioning

confidence: 99%

Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury

et al. 2021

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“…It is not uncommon for adults to develop PTE following TBI 47 . Studies of US veterans of WWI, WWII, and the Korean War found that 50% of military personnel that experienced head injuries developed PTE 31 .…”

Section: Discussionmentioning

confidence: 99%

Protection from Glutamate-Induced Excitotoxicity by Memantine

2011

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This study investigates whether the uncompetitive NMDA receptor antagonist, memantine, is able to protect dissociated cortical neurons from glutamate-induced excitotoxicity (GIE). Treatment with glutamate resulted in a significant loss of synchronization of neuronal activity as well as a significant increase in the duration of synchronized bursting events (SBEs). By administering memantine at the same time as glutamate, we were able to completely prevent these changes to the neuronal activity. Pretreatment with memantine was somewhat effective in preventing changes to the culture synchronization but was unable to fully protect the synchronization of electrical activity between neurons that showed high levels of synchronization prior to injury. Additionally, memantine pretreatment was unable to prevent the increase in the duration of SBEs caused by GIE. Thus, the timing of memantine treatment is important for conferring neuroprotection against glutamate-induced neurotoxicity. Finally, we found that GIE leads to a significant increase in the burst duration. Our data suggest that this may be due to an alteration in the inhibitory function of the neurons.

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“…In this study, we used the NODDI technique to evaluate the FLAIR hyperintense tissue surrounding the encephalomalacia, based on the theory of proliferation of glial cells, neurite density, and entanglement of synapses after brain trauma [ 24 , 25 ]. Studies have shown that the mechanisms of posttraumatic seizures are complex, with reactive astrocyte proliferation, increased neurite density, microglial proliferation, and release of neurotrophic factors; all of these could affect the sprouting of nerve fiber branches and increase neurite density.…”

Section: Discussionmentioning

confidence: 99%

Experimental Imaging Study of Encephalomalacia Fluid-Attenuated Inversion Recovery (FLAIR) Hyperintense Lesions in Posttraumatic Epilepsy

et al. 2021

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This study introduced new MRI techniques such as neurite orientation dispersion and density imaging (NODDI); NODDI applies a three-compartment tissue model to multishell DWI data that allows the examination of both the intra- and extracellular properties of white matter tissue. This, in turn, enables us to distinguish the two key aspects of axonal pathology—the packing density of axons in the white matter and the spatial organization of axons (orientation dispersion (OD)). NODDI is used to detect possible abnormalities of posttraumatic encephalomalacia fluid-attenuated inversion recovery (FLAIR) hyperintense lesions in neurite density and dispersion. Methods. 26 epilepsy patients associated with FLAIR hyperintensity around the trauma encephalomalacia region were in the epilepsy group. 18 posttraumatic patients with a FLAIR hyperintense encephalomalacia region were in the nonepilepsy group. Neurite density and dispersion affection in FLAIR hyperintense lesions around encephalomalacia were measured by NODDI using intracellular volume fraction (ICVF), and we compare these findings with conventional diffusion MRI parameters, namely, fractional anisotropy (FA) and apparent diffusion coefficient (ADC). Differences were compared between the epilepsy and nonepilepsy groups, as well as in the FLAIR hyperintense part and in the FLAIR hypointense part to try to find neurite density and dispersion differences in these parts. Results. ICVF of FLAIR hyperintense lesions in the epilepsy group was significantly higher than that in the nonepilepsy group ( P < 0.001 ). ICVF reveals more information of FLAIR(+) and FLAIR(-) parts of encephalomalacia than OD and FA and ADC. Conclusion. The FLAIR hyperintense part around encephalomalacia in the epilepsy group showed higher ICVF, indicating that this part may have more neurite density and dispersion and may be contributing to epilepsy. NODDI indicated high neurite density with the intensity of myelin in the FLAIR hyperintense lesion. Therefore, NODDI likely shows that neurite density may be a more sensitive marker of pathology than FA.

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Epilepsy and trauma

Cited by 5 publications

References 15 publications

Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury

Association of Posttraumatic Epilepsy With 1-Year Outcomes After Traumatic Brain Injury

Protection from Glutamate-Induced Excitotoxicity by Memantine

Experimental Imaging Study of Encephalomalacia Fluid-Attenuated Inversion Recovery (FLAIR) Hyperintense Lesions in Posttraumatic Epilepsy

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