TRAPing Seizures in the Striatum

Forcelli, Patrick A.

doi:10.1177/15357597211029517

Cited by 3 publications

(2 citation statements)

References 15 publications

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“… 52 , 53 , 54 , 55 It has been suggested that overt clinical seizures may thus depend on both an epileptogenic focus and a compromised inhibitory control mechanism. 44 This hypothesis of inhibitory control to suppress or even prevent seizures has seen renewed interest, 56 as it may help explain why patients with epilepsy do not continuously seize, 57 why only some seizures generalize, 58 , 59 and why seizures stop. 47 However, where this inhibitory control network might be localized in the human brain has remained a debate and whether it plays a role in epileptogenesis is unknown.…”

Section: Discussionmentioning

confidence: 99%

Mapping Lesion-Related Epilepsy to a Human Brain Network

et al. 2023

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ImportanceIt remains unclear why lesions in some locations cause epilepsy while others do not. Identifying the brain regions or networks associated with epilepsy by mapping these lesions could inform prognosis and guide interventions.ObjectiveTo assess whether lesion locations associated with epilepsy map to specific brain regions and networks.Design, Setting, and ParticipantsThis case-control study used lesion location and lesion network mapping to identify the brain regions and networks associated with epilepsy in a discovery data set of patients with poststroke epilepsy and control patients with stroke. Patients with stroke lesions and epilepsy (n = 76) or no epilepsy (n = 625) were included. Generalizability to other lesion types was assessed using 4 independent cohorts as validation data sets. The total numbers of patients across all datasets (both discovery and validation datasets) were 347 with epilepsy and 1126 without. Therapeutic relevance was assessed using deep brain stimulation sites that improve seizure control. Data were analyzed from September 2018 through December 2022. All shared patient data were analyzed and included; no patients were excluded.Main Outcomes and MeasuresEpilepsy or no epilepsy.ResultsLesion locations from 76 patients with poststroke epilepsy (39 [51%] male; mean [SD] age, 61.0 [14.6] years; mean [SD] follow-up, 6.7 [2.0] years) and 625 control patients with stroke (366 [59%] male; mean [SD] age, 62.0 [14.1] years; follow-up range, 3-12 months) were included in the discovery data set. Lesions associated with epilepsy occurred in multiple heterogenous locations spanning different lobes and vascular territories. However, these same lesion locations were part of a specific brain network defined by functional connectivity to the basal ganglia and cerebellum. Findings were validated in 4 independent cohorts including 772 patients with brain lesions (271 [35%] with epilepsy; 515 [67%] male; median [IQR] age, 60 [50-70] years; follow-up range, 3-35 years). Lesion connectivity to this brain network was associated with increased risk of epilepsy after stroke (odds ratio [OR], 2.82; 95% CI, 2.02-4.10; P &lt; .001) and across different lesion types (OR, 2.85; 95% CI, 2.23-3.69; P &lt; .001). Deep brain stimulation site connectivity to this same network was associated with improved seizure control (r, 0.63; P &lt; .001) in 30 patients with drug-resistant epilepsy (21 [70%] male; median [IQR] age, 39 [32-46] years; median [IQR] follow-up, 24 [16-30] months).Conclusions and RelevanceThe findings in this study indicate that lesion-related epilepsy mapped to a human brain network, which could help identify patients at risk of epilepsy after a brain lesion and guide brain stimulation therapies.

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Section: Discussionmentioning

confidence: 99%

Mapping Lesion-Related Epilepsy to a Human Brain Network

et al. 2023

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“…9 Many previous studies have demonstrated electrographic activation of the basal ganglia structures during seizures. [10][11][12][13][14][15][16] Drug experiments such as GABAergic inhibition of the SNR 14 or pharmacological activation of the striatum 17 exhibited anticonvulsant effects, demonstrating that the basal ganglia modulate seizures. Yet, direct cellular evidence of basal ganglia circuit activation was lacking.…”

Section: Frontal Lobe Onset Seizuresmentioning

confidence: 99%

Connectivity and Excitability Shape Seizure Circuits

Brodovskaya

2022

Epilepsy Curr

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Mapping neuronal circuits that generate focal to bilateral tonic–clonic seizures is essential for understanding general principles of seizure propagation and modifying the risk of death and injury due to bilateral motor seizures. We used novel techniques developed over the past decade to study these circuits. We propose the general hypothesis that at the mesoscale, seizures follow anatomical projections of the seizure focus, preferentially activating more excitable neurons.

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Receptor expression and signaling properties in the brain, and structural ligand motifs that contribute to delta opioid receptor agonist-induced seizures

Blaine

Rijn

2023

Neuropharmacology

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TRAPing Seizures in the Striatum

Cited by 3 publications

References 15 publications

Mapping Lesion-Related Epilepsy to a Human Brain Network

Mapping Lesion-Related Epilepsy to a Human Brain Network

Connectivity and Excitability Shape Seizure Circuits

Receptor expression and signaling properties in the brain, and structural ligand motifs that contribute to delta opioid receptor agonist-induced seizures

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