Post-traumatic epilepsy

Salazar, Andrés M.; Grafman, Jordan

doi:10.1016/b978-0-444-63521-1.00033-9

Cited by 29 publications

(4 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Agoston and colleagues showed that blast traumatic brain injury, in particular, causes persistent neuroinflammation, which leads to behavioral deficits ( 111 ). The neuroinflammation can also contribute to post-traumatic epilepsy and tauopathy ( 112 ). Investigating how tauopathy spreads is a topic warranting further investigation ( 113 ).…”

Section: Key Questions Going Forwardmentioning

confidence: 99%

Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery

et al. 2015

View full text Add to dashboard Cite

Despite the extensive media coverage associated with the diagnosis of chronic traumatic encephalopathy (CTE), our fundamental understanding of the disease pathophysiology remains in its infancy. Only recently have scientific laboratories and personnel begun to explore CTE pathophysiology through the use of preclinical models of neurotrauma. Some studies have shown the ability to recapitulate some aspects of CTE in rodent models, through the use of various neuropathological, biochemical, and/or behavioral assays. Many questions related to CTE development, however, remain unanswered. These include the role of impact severity, the time interval between impacts, the age at which impacts occur, and the total number of impacts sustained. Other important variables such as the location of impacts, character of impacts, and effect of environment/lifestyle and genetics also warrant further study. In this work, we attempt to address some of these questions by exploring work previously completed using single- and repetitive-injury paradigms. Despite some models producing some deficits similar to CTE symptoms, it is clear that further studies are required to understand the development of neuropathological and neurobehavioral features consistent with CTE-like features in rodents. Specifically, acute and chronic studies are needed that characterize the development of tau-based pathology.

show abstract

Section: Key Questions Going Forwardmentioning

confidence: 99%

Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Post-traumatic epilepsy (PTE) is one of the most common long-term consequences of traumatic brain injury (TBI). The incidence of PTE varies considerably in the literature depending on injury severity, between 4% of TBI cases (reported after hospitalized mild injuries) to up to 50% (higher rates for severe TBI, in pediatric populations, and in military personnel) [1,2,3,4,5]. PTE is generally defined as recurrent and unprovoked seizures that occur at least 1 week after TBI.…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets

et al. 2019

View full text Add to dashboard Cite

Epilepsy is a common chronic consequence of traumatic brain injury (TBI), contributing to increased morbidity and mortality for survivors. As post-traumatic epilepsy (PTE) is drug-resistant in at least one-third of patients, there is a clear need for novel therapeutic strategies to prevent epilepsy from developing after TBI, or to mitigate its severity. It has long been recognized that seizure activity is associated with a local immune response, characterized by the activation of microglia and astrocytes and the release of a plethora of pro-inflammatory cytokines and chemokines. More recently, increasing evidence also supports a causal role for neuroinflammation in seizure induction and propagation, acting both directly and indirectly on neurons to promote regional hyperexcitability. In this narrative review, we focus on key aspects of the neuroinflammatory response that have been implicated in epilepsy, with a particular focus on PTE. The contributions of glial cells, blood-derived leukocytes, and the blood–brain barrier will be explored, as well as pro- and anti-inflammatory mediators. While the neuroinflammatory response to TBI appears to be largely pro-epileptogenic, further research is needed to clearly demonstrate causal relationships. This research has the potential to unveil new drug targets for PTE, and identify immune-based biomarkers for improved epilepsy prediction.

show abstract

“…Seizures often occur after TBI, and TBI is a major risk factor for subsequent development of epilepsy [ 8 – 10 ]. There is a strong correlation between posttraumatic epilepsy (PTE) and the loss of brain volume after head injury [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Profound deficits in hippocampal synaptic plasticity after traumatic brain injury and seizure is ameliorated by prophylactic levetiracetam

et al. 2018

View full text Add to dashboard Cite

AimTo determine the precise effects of post-traumatic seizure activity on hippocampal processes, we induced seizures at various intervals after traumatic brain injury (TBI) and analyzed plasticity at CA1 Schaffer collateral synapses.Material and MethodsRats were initially separated into two groups; one exposed solely to fluid percussion injury (FPI) at 2 Psi and the other only receiving kainic acid (KA)-induced seizures without FPI. Electrophysiological (ePhys) studies including paired-pulse stimulation for short-term presynaptic plasticity and long-term potentiation (LTP) of CA1 Schaffer collateral synapses of the hippocampus for post-synaptic function survey were followed at post-event 1 hour, 3 and 7 days respectively. Additional rats were exposed to three seizures at weekly intervals starting 1 week or 2 weeks after TBI and compared with seizures without TBI, TBI without seizures, and uninjured animals. An additional group placed under the same control variables were treated with levetiracetam prior to seizure induction. The ePhys studies related to post-TBI induced seizures were also followed in these additional groups.ResultsSeizures affected the short- and long-term synaptic plasticity of the hippocampal CA3-CA1 pathway. FPI itself suppressed LTP and field excitatory post synaptic potentials (fEPSP) in the CA1 Schaffer collateral synapses; KA-induced seizures that followed FPI further suppressed synaptic plasticity. The impairments in both short-term presynaptic and long-term plasticity were worse in the rats in which early post-TBI seizures were induced than those in which later post-TBI seizures were induced. Finally, prophylactic infusion of levetiracetam for one week after FPI reduced the synaptic plasticity deficits in early post-TBI seizure animals.ConclusionOur data indicates that synaptic plasticity (i.e., both presynaptic and postsynaptic) suppression occurs in TBI followed by a seizure and that the interval between the TBI and seizure is an important factor in the severity of the resulting deficits. Furthermore, the infusion of prophylactic levetiracetam could partially reverse the suppression of synaptic plasticity.

show abstract

Post-traumatic epilepsy

Cited by 29 publications

References 67 publications

Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery

Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery

Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets

Profound deficits in hippocampal synaptic plasticity after traumatic brain injury and seizure is ameliorated by prophylactic levetiracetam

Contact Info

Product

Resources

About