Which treatment strategy in patients with epilepsy with focal seizures uncontrolled by the first anti-seizure medication?

Zaccara, Gaetano; Lattanzi, Simona; Brigo, Francesco

doi:10.1016/j.yebeh.2021.108031

Cited by 6 publications

(5 citation statements)

References 64 publications

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Section: Treatment Options After Failure Of the First Antiseizure Med...mentioning

confidence: 99%

“…Because of the lack of differences in efficacy and tolerability between these two strategies, other aspects should be taken into consideration when choosing the appropriate therapy ( figure 9-1 34 ). An alternative monotherapy appears preferable and advisable for patients with poor adherence.…”

Section: Treatment Options After Failure Of the First Antiseizure Med...mentioning

confidence: 99%

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Approach to the Medical Treatment of Epilepsy

Brigo¹,

Marson²

2022

CONTINUUM: Lifelong Learning in Neurology

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Section: Treatment Options After Failure Of the First Antiseizure Med...mentioning

confidence: 99%

Section: Treatment Options After Failure Of the First Antiseizure Med...mentioning

confidence: 99%

Approach to the Medical Treatment of Epilepsy

Brigo¹,

Marson²

2022

CONTINUUM: Lifelong Learning in Neurology

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“…Most patients with PTE have focal with secondarily generalized seizures [19][20][21], but other seizure types are related to hippocampal sclerosis and primary generalized seizures [22,23]. A variety of antiepileptic drugs (AEDs)-including phenytoin [24], levetiracetam [25], lamotrigine, gabapentin, and valproic acid-have been developed to reduce the onset of post-injury seizures, with relative success [26]. While AEDs can be effective in controlling acute or symptomatic seizures (<1 week post-TBI), they do not prevent post-traumatic epileptogenesis, and ~30% of individuals with PTE will develop drug resistance [27,28].…”

Section: Introductionmentioning

confidence: 99%

Atypical Neurogenesis, Astrogliosis, and Excessive Hilar Interneuron Loss Are Associated with the Development of Post-Traumatic Epilepsy

Basso

Shandra

Volanth

et al. 2023

Cells

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Background: Traumatic brain injury (TBI) remains a significant risk factor for post-traumatic epilepsy (PTE). The pathophysiological mechanisms underlying the injury-induced epileptogenesis are under investigation. The dentate gyrus—a structure that is highly susceptible to injury—has been implicated in the evolution of seizure development. Methods: Utilizing the murine unilateral focal control cortical impact (CCI) injury, we evaluated seizure onset using 24/7 EEG video analysis at 2–4 months post-injury. Cellular changes in the dentate gyrus and hilus of the hippocampus were quantified by unbiased stereology and Imaris image analysis to evaluate Prox1-positive cell migration, astrocyte branching, and morphology, as well as neuronal loss at four months post-injury. Isolation of region-specific astrocytes and RNA-Seq were performed to determine differential gene expression in animals that developed post-traumatic epilepsy (PTE+) vs. those animals that did not (PTE−), which may be associated with epileptogenesis. Results: CCI injury resulted in 37% PTE incidence, which increased with injury severity and hippocampal damage. Histological assessments uncovered a significant loss of hilar interneurons that coincided with aberrant migration of Prox1-positive granule cells and reduced astroglial branching in PTE+ compared to PTE- mice. We uniquely identified Cst3 as a PTE+-specific gene signature in astrocytes across all brain regions, which showed increased astroglial expression in the PTE+ hilus. Conclusions: These findings suggest that epileptogenesis may emerge following TBI due to distinct aberrant cellular remodeling events and key molecular changes in the dentate gyrus of the hippocampus.

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“…Most patients with PTE have focal with secondary generalized seizures [19][20][21], but other seizure types are related to hippocampal sclerosis and primary generalized seizures [22,23]. A variety of antiepileptic drugs (AED), including phenytoin [24], levetiracetam [25], lamotrigine, gabapentin, and valproic acid, have been developed to reduce the onset of seizures post-injury with relative success [26]. While AEDs can be effective in controlling acute or symptomatic seizures (<1 week post-TBI), they do not prevent post-traumatic epileptogenesis and ~30% of individuals with PTE will develop drug resistance [27,28].…”

Section: Introductionmentioning

confidence: 99%

Atypical Neurogenesis, Astrogliosis, and Excessive Hilar Interneuron Loss Are Associated With the Development of Post-Traumatic Epilepsy

Basso¹,

Shandra²,

Volanth³

et al. 2023

Preprint

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Background: Traumatic brain injury (TBI) remains a significant risk factor for post-traumatic epilepsy (PTE). The pathophysiological mechanisms underlying the injury-induced epileptogenesis are under under investigation. The dentate gyrus, a structure highly susceptible to injury, and has been implicated in the evolution of seizure development. Methods: Utilizing the murine unilateral focal control cortical impact (CCI) injury, we evaluated seizure onset using 24/7 EEG video analysis at 2-4 months post-injury. Cellular changes in the dentate gyrus and hilus of the hippocampus were quantified by non-biased stereology and Imaris image analysis to evaluate Prox1-positive cell migration, astrocyte branching and morphology, as well as neuronal loss at four months post-injury. Isolation of region-specific astrocytes and RNA-seq was performed to determine differential gene expression in PTE+ vs. PTE- that may comport with the epileptogenic process. Results: CCI injury resulted in 37% PTE+-incidence, which increased with injury severity and hippocampal damage. Histological assessments uncovered a significant loss of hilar interneurons that coincided with aberrant migration of Prox1-positive granule cells and reduced astroglial branching in PTE+ compared to PTE- mice. We uniquely identified Cst3 as a PTE+-specific gene signature in astrocytes across all brain regions. Conclusions: These findings suggest that epileptogenesis may emerge following TBI due to distinct aberrant cellular remodeling events and key molecular changes in the dentate gyrus of the hippocampus.

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Which treatment strategy in patients with epilepsy with focal seizures uncontrolled by the first anti-seizure medication?

Cited by 6 publications

References 64 publications

Approach to the Medical Treatment of Epilepsy

Approach to the Medical Treatment of Epilepsy

Atypical Neurogenesis, Astrogliosis, and Excessive Hilar Interneuron Loss Are Associated with the Development of Post-Traumatic Epilepsy

Atypical Neurogenesis, Astrogliosis, and Excessive Hilar Interneuron Loss Are Associated With the Development of Post-Traumatic Epilepsy

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