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Network Analysis of Foramen Ovale Electrode Recordings in Drug-resistant Temporal Lobe Epilepsy Patients
Published on: December 18, 2016
Impaired vigilance networks in temporal lobe epilepsy: Mechanisms and clinical implications
Dario J Englot1,2,3,4,5, Victoria L Morgan1,2,3,5, Catie Chang3,4,5
1Department of Neurological Surgery, Vanderbilt University Medical Center, Nashville, Tennessee.
Abstract:
Mesial temporal lobe epilepsy (mTLE) is a neurological disorder in which patients suffer from frequent consciousness-impairing seizures, broad neurocognitive deficits, and diminished quality of life. Although seizures in mTLE originate focally in the hippocampus or amygdala, mTLE patients demonstrate cognitive deficits that extend beyond temporal lobe function-such as decline in executive function, cognitive processing speed, and attention-as well as diffuse decreases in neocortical metabolism and functional connectivity. Given prior observations that mTLE patients exhibit impairments in vigilance, and that seizures may disrupt the activity and long-range connectivity of subcortical brain structures involved in vigilance regulation, we propose that subcortical activating networks underlying vigilance play a critical role in mediating the widespread neural and cognitive effects of focal mTLE. Here, we review evidence for impaired vigilance in mTLE, examine clinical implications and potential network underpinnings, and suggest neuroimaging strategies for determining the relationship between vigilance, brain connectivity, and neurocognition in patients and healthy controls.
Insights
Mesial temporal lobe epilepsy (mTLE) causes widespread cognitive issues by disrupting subcortical vigilance networks. Understanding these networks may explain cognitive deficits and inform treatment for epilepsy patients.
Area of Science:
- Neuroscience
- Epilepsy Research
Background:
- Mesial temporal lobe epilepsy (mTLE) is characterized by focal seizures originating in the hippocampus or amygdala.
- mTLE patients experience significant neurocognitive deficits extending beyond temporal lobe functions, impacting executive function, processing speed, and attention.
- Widespread decreases in neocortical metabolism and functional connectivity are observed in mTLE.
Purpose of the Study:
- To investigate the role of subcortical activating networks in regulating vigilance in mTLE.
- To explore the relationship between impaired vigilance, brain connectivity, and neurocognitive deficits in mTLE.
- To review clinical implications and suggest neuroimaging strategies for mTLE research.
Main Methods:
- Review of existing literature on vigilance impairments in mTLE.
- Examination of clinical evidence and potential network mechanisms.
- Discussion of neuroimaging approaches to study vigilance, connectivity, and cognition.
Main Results:
- Evidence suggests impaired vigilance in patients with mTLE.
- Seizures may disrupt subcortical structures crucial for vigilance regulation and long-range connectivity.
- Subcortical networks underlying vigilance are proposed as critical mediators of widespread neural and cognitive effects in mTLE.
Conclusions:
- Vigilance deficits are a significant feature of mTLE, contributing to broader cognitive impairments.
- Disruption of subcortical vigilance networks offers a potential explanation for diffuse neurological and cognitive effects in mTLE.
- Further neuroimaging research is needed to elucidate the precise relationship between vigilance, brain connectivity, and neurocognition in mTLE.
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