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Modulation of autonomic activity in neurological conditions: Epilepsy and Tourette Syndrome.

Nagai Y - Front Neurosci (2015)

Bottom Line: Investigation is more limited in Tourette Syndrome.The role of the autonomic nervous system in the generation and prevention of epileptic seizures is largely overlooked.This approach also takes advantage of the current practical opportunity to utilize growing digital health technology.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Medicine, Clinical Imaging Sciences Centre, Brighton and Sussex Medical School, University of Sussex Brighton, UK.

ABSTRACT
This manuscript considers the central but neglected role of the autonomic nervous system in the expression and control of seizures in epilepsy (small) and tics in Tourette Syndrome (TS). In epilepsy, consideration of autonomic involvement is typically confined to differential diagnoses (e.g., syncope), or in relation to Sudden Unexpected Death in Epilepsy (SUDEP). Investigation is more limited in Tourette Syndrome. The role of the autonomic nervous system in the generation and prevention of epileptic seizures is largely overlooked. Emotional stimuli such as anxiety and stress are potent causes of seizures and tic activity in epilepsy and TS, respectively. This manuscript will describe a possible neural mechanism by which afferent autonomic projections linked to cognition and behavior influence central thalamo-cortical regulation, which appears to be an important means for controlling both seizure and tic activity. It also summarizes the link between the integrity of the default mode network and autonomic regulation in patients with epilepsy as well as the link between impaired motor control and autonomic regulation in patients with TS. Two neurological conditions; epilepsy and TS were chosen, as seizures and tics represent parameters that can be easily measured to investigate influences of autonomic functions. The EDA biofeedback approach is anticipated to gain a strong position within the next generation of treatment for epilepsy, as a non-invasive technique with minimal side effects. This approach also takes advantage of the current practical opportunity to utilize growing digital health technology.

No MeSH data available.


Related in: MedlinePlus

Brain activity modulated by the CNV amplitude. Neural activities associated with CNV generation. The observed regions during the CNV task include bilateral thalamus, ante- rior cingulate, SMA, pons, and cerebellum. A fixed-effect analysis was used (p < 0.05, cor- rected). (Nagai et al., 2004c, permission obtained).
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Figure 4: Brain activity modulated by the CNV amplitude. Neural activities associated with CNV generation. The observed regions during the CNV task include bilateral thalamus, ante- rior cingulate, SMA, pons, and cerebellum. A fixed-effect analysis was used (p < 0.05, cor- rected). (Nagai et al., 2004c, permission obtained).

Mentions: A neuroimaging study was conducted in healthy participants to identify brain regions involved in the generation of the CNV: on a trial-by-trial basis, CNV correlated with enhancement of activity within the thalamus, anterior cingulate and supplementary motor area (SMA), revealing the thalmo-cortical network ultimately responsible for generation of the CNV (Nagai et al., 2004c) (Figure 4). A parallel neuroimaging study also revealed brain regions engaged during EDA biofeedback. Activation within the ventro-medial prefrontal cortex (VMPFC) and adjacent medical orbitofrontal cortex (OFC) were linearly, yet inversely, correlated with the level of skin conductance during EDA biofeedback (Nagai et al., 2004d) (Figure 5). Thus increased EDA sympathetic arousal following biofeedback task performance resulted in a decrease in the activation of VMPFC and medial OFC, while biofeedback-induced decreases in EDA levels resulted in an enhanced activation of these regions. Interestingly, the VMPFC and medial OFC are both involved in viscerosensory and form an important hub within the default mode network, which deactivates during states of behavioral arousal. Arguably the functional manipulation of the reactivity of this brain region over a month of EDA biofeedback training may, for patients with epilepsy, enhance the degree to which thalamo-cortical excitability, and its gating by the ascending reticular activating system, is suppressed during behavioral arousal. The functional impairment of this network, reported in patients with epilepsy, may be normalized, ultimately leading to decreased vulnerability to internal and external seizure triggers. In the case of Tourette Syndrome and related tic disorders, the training to diminish levels of physiological arousal may help increase the threshold for tics through the interaction between motor pathways and autonomic central command. Alternatively, the relationship with premonitory urges and compulsive behavior may be an important mechanism: damage to the viscerosensory insula cortex is observed to inhibit addictive urges and compulsions to smoke (Gray and Critchley, 2007; Naqvi and Bechara, 2009). Arguably, biofeedback “relaxation” training can decrease viscerosensory arousal signals that underlie or reinforce the feelings of urge and compulsions. This effect may be mediated by the cortical representation of the arousal state within default mode and salience networks, which in turn influence motor excitability and ascending monoaminergic pathways. While this provides a neurobiological model, there needs to be further work in extending and translating current knowledge of autonomic interaction with tics.


Modulation of autonomic activity in neurological conditions: Epilepsy and Tourette Syndrome.

Nagai Y - Front Neurosci (2015)

Brain activity modulated by the CNV amplitude. Neural activities associated with CNV generation. The observed regions during the CNV task include bilateral thalamus, ante- rior cingulate, SMA, pons, and cerebellum. A fixed-effect analysis was used (p < 0.05, cor- rected). (Nagai et al., 2004c, permission obtained).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4584996&req=5

Figure 4: Brain activity modulated by the CNV amplitude. Neural activities associated with CNV generation. The observed regions during the CNV task include bilateral thalamus, ante- rior cingulate, SMA, pons, and cerebellum. A fixed-effect analysis was used (p < 0.05, cor- rected). (Nagai et al., 2004c, permission obtained).
Mentions: A neuroimaging study was conducted in healthy participants to identify brain regions involved in the generation of the CNV: on a trial-by-trial basis, CNV correlated with enhancement of activity within the thalamus, anterior cingulate and supplementary motor area (SMA), revealing the thalmo-cortical network ultimately responsible for generation of the CNV (Nagai et al., 2004c) (Figure 4). A parallel neuroimaging study also revealed brain regions engaged during EDA biofeedback. Activation within the ventro-medial prefrontal cortex (VMPFC) and adjacent medical orbitofrontal cortex (OFC) were linearly, yet inversely, correlated with the level of skin conductance during EDA biofeedback (Nagai et al., 2004d) (Figure 5). Thus increased EDA sympathetic arousal following biofeedback task performance resulted in a decrease in the activation of VMPFC and medial OFC, while biofeedback-induced decreases in EDA levels resulted in an enhanced activation of these regions. Interestingly, the VMPFC and medial OFC are both involved in viscerosensory and form an important hub within the default mode network, which deactivates during states of behavioral arousal. Arguably the functional manipulation of the reactivity of this brain region over a month of EDA biofeedback training may, for patients with epilepsy, enhance the degree to which thalamo-cortical excitability, and its gating by the ascending reticular activating system, is suppressed during behavioral arousal. The functional impairment of this network, reported in patients with epilepsy, may be normalized, ultimately leading to decreased vulnerability to internal and external seizure triggers. In the case of Tourette Syndrome and related tic disorders, the training to diminish levels of physiological arousal may help increase the threshold for tics through the interaction between motor pathways and autonomic central command. Alternatively, the relationship with premonitory urges and compulsive behavior may be an important mechanism: damage to the viscerosensory insula cortex is observed to inhibit addictive urges and compulsions to smoke (Gray and Critchley, 2007; Naqvi and Bechara, 2009). Arguably, biofeedback “relaxation” training can decrease viscerosensory arousal signals that underlie or reinforce the feelings of urge and compulsions. This effect may be mediated by the cortical representation of the arousal state within default mode and salience networks, which in turn influence motor excitability and ascending monoaminergic pathways. While this provides a neurobiological model, there needs to be further work in extending and translating current knowledge of autonomic interaction with tics.

Bottom Line: Investigation is more limited in Tourette Syndrome.The role of the autonomic nervous system in the generation and prevention of epileptic seizures is largely overlooked.This approach also takes advantage of the current practical opportunity to utilize growing digital health technology.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Medicine, Clinical Imaging Sciences Centre, Brighton and Sussex Medical School, University of Sussex Brighton, UK.

ABSTRACT
This manuscript considers the central but neglected role of the autonomic nervous system in the expression and control of seizures in epilepsy (small) and tics in Tourette Syndrome (TS). In epilepsy, consideration of autonomic involvement is typically confined to differential diagnoses (e.g., syncope), or in relation to Sudden Unexpected Death in Epilepsy (SUDEP). Investigation is more limited in Tourette Syndrome. The role of the autonomic nervous system in the generation and prevention of epileptic seizures is largely overlooked. Emotional stimuli such as anxiety and stress are potent causes of seizures and tic activity in epilepsy and TS, respectively. This manuscript will describe a possible neural mechanism by which afferent autonomic projections linked to cognition and behavior influence central thalamo-cortical regulation, which appears to be an important means for controlling both seizure and tic activity. It also summarizes the link between the integrity of the default mode network and autonomic regulation in patients with epilepsy as well as the link between impaired motor control and autonomic regulation in patients with TS. Two neurological conditions; epilepsy and TS were chosen, as seizures and tics represent parameters that can be easily measured to investigate influences of autonomic functions. The EDA biofeedback approach is anticipated to gain a strong position within the next generation of treatment for epilepsy, as a non-invasive technique with minimal side effects. This approach also takes advantage of the current practical opportunity to utilize growing digital health technology.

No MeSH data available.


Related in: MedlinePlus