A review of seizures and epilepsy following traumatic brain injury

Fordington, Surina; Manford, Mark

doi:10.1007/s00415-020-09926-w

Cited by 101 publications

(95 citation statements)

References 59 publications

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“…Major risk factors are haemorrhagic strokes (10.6–15.4%) [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ] and the time interval of seizure onset following a stroke [ 16 , 34 , 35 ]. In addition, epilepsy is common in traumatic brain injury, which may arise after many years [ 36 ]. Its incidence ranges from 1.9% to over 30%, depending on the severity of trauma and the duration of follow-up [ 36 , 37 , 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

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Risk of Developing Epilepsy after Autoimmune Encephalitis

et al. 2021

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Background: Acute symptomatic seizures (ASS) are a common manifestation of autoimmune encephalitis (AE), but the risk of developing epilepsy as a sequela of AE remains unknown, and factors predisposing the development of epilepsy have not been fully identified. Objective: To assess the risk of developing epilepsy in AE and study related risk factors. Materials and methods: This was a retrospective single centre study including patients diagnosed with AE according to criteria described by Graus et al., with a minimum follow-up of 12 months after AE resolution. The sample was divided according to whether patients developed epilepsy or not. Results: A total of 19 patients were included; 3 (15.8%) had AE with intracellular antibodies, 9 (47.4%) with extracellular antibodies, and 7 (36.8%) were seronegative. During follow-up, 3 patients (15.8%) died, 4 (21.1%) presented relapses of AE, and 11 (57.89%) developed epilepsy. There was a significant association between the development of epilepsy and the presence of hippocampal atrophy in control brain magnetic resonance imaging (MRI) (p = 0.037), interictal epileptiform discharges (IED) on control electroencephalogram (EEG) (p = 0.045), and immunotherapy delay (p = 0.016). Conclusions: Hippocampal atrophy in neuroimaging, IED on EEG during follow-up, and immunotherapy delay could be predictors of the development of epilepsy in patients with AE.

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Section: Discussionmentioning

confidence: 99%

“…In addition, epilepsy is common in traumatic brain injury, which may arise after many years [ 36 ]. Its incidence ranges from 1.9% to over 30%, depending on the severity of trauma and the duration of follow-up [ 36 , 37 , 38 , 39 ]. Intracerebral haemorrhage (mainly subarachnoid and subdural) carries an increased risk [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Risk of Developing Epilepsy after Autoimmune Encephalitis

et al. 2021

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“…A common denominator of astrocytic pathophysiology associated with epileptogenesis is the process of reactive astrogliosis (Burda and Sofroniew, 2014;Pekny and Pekna, 2016). This is a graded response to a wide array of insults, which is a hallmark of many neurological disorders (Burda and Sofroniew, 2014;Ferlazzo et al, 2016;Glushakov et al, 2016;Pekny and Pekna, 2016;Fordington and Manford, 2020;Galovic et al, 2021).…”

Section: Astrocytic Ca 2+ Signaling and Epileptogenesismentioning

confidence: 99%

“…Specifically they proliferate, undergo hypertrophy and increase their expression of intermediary filament proteins like glial fibrillary acid protein (GFAP) and vimentin (Yang et al, 1994;Pekny and Nilsson, 2005;Sofroniew, 2009;Cregg et al, 2014;Escartin et al, 2021). In extremis, these changes may lead to the formation of a glial scar (Miller, 2005;Barres, 2008;Sofroniew, 2009;Burda and Sofroniew, 2014;Ferlazzo et al, 2016;Glushakov et al, 2016;Pekny and Pekna, 2016;Fordington and Manford, 2020;Galovic et al, 2021). Reactive astrogliosis can be observed in several acquired forms of epilepsy but has mostly been investigated in the context of mTLE (Wieser and ILAE Commission on Neurosurgery of Epilepsy., 2004;Blümcke et al, 2013;Cendes et al, 2014).…”

Section: Astrocytic Ca 2+ Signaling and Epileptogenesismentioning

confidence: 99%

Astrocytic Ca2+ Signaling in Epilepsy

Enger

2021

Front. Cell. Neurosci.

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Epilepsy is one of the most common neurological disorders – estimated to affect at least 65 million worldwide. Most of the epilepsy research has so far focused on how to dampen neuronal discharges and to explain how changes in intrinsic neuronal activity or network function cause seizures. As a result, pharmacological therapy has largely been limited to symptomatic treatment targeted at neurons. Given the expanding spectrum of functions ascribed to the non-neuronal constituents of the brain, in both physiological brain function and in brain disorders, it is natural to closely consider the roles of astrocytes in epilepsy. It is now widely accepted that astrocytes are key controllers of the composition of the extracellular fluids, and may directly interact with neurons by releasing gliotransmitters. A central tenet is that astrocytic intracellular Ca2+ signals promote release of such signaling substances, either through synaptic or non-synaptic mechanisms. Accruing evidence suggests that astrocytic Ca2+ signals play important roles in both seizures and epilepsy, and this review aims to highlight the current knowledge of the roles of this central astrocytic signaling mechanism in ictogenesis and epileptogenesis.

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“…Traumatic brain injury is the third most common cause of all epilepsies and results from either direct (primary) or indirect (secondary) damage to brain parenchyma ( Kaur and Sharma, 2018 ; Fordington and Manford, 2020 ). Trauma or brain injury results in both focal and diffuse injury to the central nervous system (CNS) that can trigger epileptogenesis ( Shlosberg et al, 2010 ; Webster et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy

Sharma

Tiarks

Haight

et al. 2021

Front. Mol. Neurosci.

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Traumatic brain injury (TBI) is a leading cause of death in young adults and a risk factor for acquired epilepsy. Severe TBI, after a period of time, causes numerous neuropsychiatric and neurodegenerative problems with varying comorbidities; and brain homeostasis may never be restored. As a consequence of disrupted equilibrium, neuropathological changes such as circuit remodeling, reorganization of neural networks, changes in structural and functional plasticity, predisposition to synchronized activity, and post-translational modification of synaptic proteins may begin to dominate the brain. These pathological changes, over the course of time, contribute to conditions like Alzheimer disease, dementia, anxiety disorders, and post-traumatic epilepsy (PTE). PTE is one of the most common, devastating complications of TBI; and of those affected by a severe TBI, more than 50% develop PTE. The etiopathology and mechanisms of PTE are either unknown or poorly understood, which makes treatment challenging. Although anti-epileptic drugs (AEDs) are used as preventive strategies to manage TBI, control acute seizures and prevent development of PTE, their efficacy in PTE remains controversial. In this review, we discuss novel mechanisms and risk factors underlying PTE. We also discuss dysfunctions of neurovascular unit, cell-specific neuroinflammatory mediators and immune response factors that are vital for epileptogenesis after TBI. Finally, we describe current and novel treatments and management strategies for preventing PTE.

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A review of seizures and epilepsy following traumatic brain injury

Cited by 101 publications

References 59 publications

Risk of Developing Epilepsy after Autoimmune Encephalitis

Risk of Developing Epilepsy after Autoimmune Encephalitis

Astrocytic Ca2+ Signaling in Epilepsy

Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy

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