Impaired consciousness in epilepsy

Departments of Neurology, Neurobiology, and Neurosurgery, Yale University School of Medicine, New Haven, CT 06520, USA.
The Lancet Neurology (Impact Factor: 21.82). 09/2012; 11(9):814-26. DOI: 10.1016/S1474-4422(12)70188-6
Source: PubMed

ABSTRACT Consciousness is essential to normal human life. In epileptic seizures consciousness is often transiently lost, which makes it impossible for the individual to experience or respond. These effects have huge consequences for safety, productivity, emotional health, and quality of life. To prevent impaired consciousness in epilepsy, it is necessary to understand the mechanisms that lead to brain dysfunction during seizures. Normally the consciousness system-a specialised set of cortical-subcortical structures-maintains alertness, attention, and awareness. Advances in neuroimaging, electrophysiology, and prospective behavioural testing have shed light on how epileptic seizures disrupt the consciousness system. Diverse seizure types, including absence, generalised tonic-clonic, and complex partial seizures, converge on the same set of anatomical structures through different mechanisms to disrupt consciousness. Understanding of these mechanisms could lead to improved treatment strategies to prevent impairment of consciousness and improve the quality of life of people with epilepsy.

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    • "Here, we further demonstrated the altered functional connectivity between these RSNs, suggesting that the abnormality in the two anticorrelated systems might reflect the disturbed management of introspective and extrospective information, thereby facilitating the loss of consciousness during absence seizures. This finding is consistent with previous suggestions of network inhibition or network disruption as a plausible mechanism for impaired consciousness during epilepsy seizure [3]. In addition, many studies have shown that the methods used in functional connectivity analyses would influence the anti-correlation in fMRI data [43] [44] [45]. "
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    ABSTRACT: Altered functional connectivity has been associated with the influence of epileptic activity. Abnormalities in connectivity, particularly in dorsal attention (DAN), salience (SN) and default mode (DMN) networks, might contribute to the loss of consciousness during seizures and cognitive deficits in patients with children absence epilepsy (CAE). The objective of the present study was to identify whether the functional network connectivity (FNC) is changed between patients with CAE and healthy controls. Using independent component analysis, twelve resting state networks (RSNs) were identified in resting state functional magnetic resonance imaging data sets in eighteen CAE patients and twenty-one healthy controls. Analyses of the group differences in FNC strength were conducted, controlling for age and gender effects. The findings showed that some functional networks were clustered into two subgroups, correlated within subgroups and antagonized with each other. Compared with the controls, patients with CAE demonstrated abnormal FNC strength among three networks: DMN, DAN and SN. In addition, the antagonism of two subgroups was altered. These results might reflect the underlying neuronal functional impairment or altered integration among these RSNs in CAE, suggesting that the abnormal functional connectivity is likely to imply the pathological mechanism associated with the accumulative influence of epileptic activity. These findings contribute to the understanding of the behavior abnormality in CAE, such as disturbed executive and attentional functions and the loss of consciousness during absence seizures. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of the neurological sciences 05/2015; 354(1-2). DOI:10.1016/j.jns.2015.04.054 · 2.26 Impact Factor
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    • "Our finding further suggests that the claustrum appears to be a component of the neural correlates of consciousness mediating increased synchronization between various cortical regions. Another hypothesis regarding the alteration of consciousness that accompanies seizures, the " network inhibition hypothesis " , suggests that propagation of ictal discharges from the mesial temporal structures to the brainstem and diencephalon results in inhibition of the subcortical arousal system, which results in widespread depression of cortical activity [6]. Because of a widespread connectivity with neocortical areas, it is possible that the claustrum participates in the widespread cortical depression. "
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    ABSTRACT: The neural mechanisms that underlie consciousness are not fully understood. We describe a region in the human brain where electrical stimulation reproducibly disrupted consciousness. A 54-year-old woman with intractable epilepsy underwent depth electrode implantation and electrical stimulation mapping. The electrode whose stimulation disrupted consciousness was between the left claustrum and anterior-dorsal insula. Stimulation of electrodes within 5mm did not affect consciousness. We studied the interdependencies among depth recording signals as a function of time by nonlinear regression analysis (h(2) coefficient) during stimulations that altered consciousness and stimulations of the same electrode at lower current intensities that were asymptomatic. Stimulation of the claustral electrode reproducibly resulted in a complete arrest of volitional behavior, unresponsiveness, and amnesia without negative motor symptoms or mere aphasia. The disruption of consciousness did not outlast the stimulation and occurred without any epileptiform discharges. We found a significant increase in correlation for interactions affecting medial parietal and posterior frontal channels during stimulations that disrupted consciousness compared with those that did not. Our findings suggest that the left claustrum/anterior insula is an important part of a network that subserves consciousness and that disruption of consciousness is related to increased EEG signal synchrony within frontal-parietal networks.
    Epilepsy & Behavior 06/2014; 37C:32-35. DOI:10.1016/j.yebeh.2014.05.027 · 2.06 Impact Factor
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    • "Moreover, these brain regions presented different temporal patterns responding to GSWD during the evolution course of seizures. The accumulating imaging evidence may support the proposal that multiple cognitive processes are specifically involved in AS [7] [8]. However, the precise alterations of brain processes associated with GSWD and the relationship among them have yet to be thoroughly assessed. "
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    ABSTRACT: Intrinsic connectivity network (ICN) technique provides a feasible way for evaluating cognitive impairments in epilepsy. This EEG-fMRI study aims to comprehensively assess the alterations of ICNs affected by generalized spike-and-wave discharge (GSWD) during absence seizure (AS). Twelve fMRI sessions with GSWD, and individually paired non-GSWD sessions were acquired from 16 patients with AS. Ten ICNs corresponding to seizure origination and cognitive processes were extracted using independent component analysis. Intra- and inter-network connectivity alterations of the ICNs were observed through comparisons between GSWD and non-GSWD sessions. Sequential correlation analysis between GSWD and the ICN time courses addressed the immediate effects of GSWD on ICNs during AS. GSWD-related increase of intra-network connectivity was found only in the thalamus, and extensive decreases were found in the ICNs corresponding to higher-order cognitive processes including the default-mode network, dorsal attention network, central executive network and salience network. The perceptive networks and motor network were less affected by GSWD. Sequential correlation analysis further demonstrated different responses of the ICNs to GSWD. In addition to GSWD-related functional excitation in the thalamus and functional suspension in the default-mode network, this study revealed extensive inhibitions in the other ICNs corresponding to higher-order cognitive processes, and spared perceptive and motor processes in AS. GSWD elevated synchronization of brain network activity and sequentially affected the ICNs.
    Journal of the neurological sciences 10/2013; 336(1-2). DOI:10.1016/j.jns.2013.10.024 · 2.26 Impact Factor
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