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Tics: neurological disorders determined by a deficit in sensorimotor gating processes

Authors :
Schilke, E
Tremolizzo, L
Appollonio, I
Ferrarese, C
Schilke, Edoardo Dalmato
Tremolizzo, Lucio
Appollonio, Ildebrando
Ferrarese, Carlo
Schilke, E
Tremolizzo, L
Appollonio, I
Ferrarese, C
Schilke, Edoardo Dalmato
Tremolizzo, Lucio
Appollonio, Ildebrando
Ferrarese, Carlo
Publication Year :
2022

Abstract

Tic related disorders affect 4–20% of the population, mostly idiopathic, can be grouped in a wide spectrum of severity, where the most severe end is Tourette Syndrome (TS). Tics are arrhythmic hyperkinesias to whom execution the subject is forced by a “premonitory urge” that can be classified as sensory tic, just-right experience or urge without obsession. If an intact volitional inhibition allows patients to temporarily suppress tics, a lack or deficit in automatic inhibition is involved in the genesis of the disorder. Studies have assessed the presence of intrinsic microscopic and macroscopic anomalies in striatal circuits and relative cortical areas in association with a hyperdopaminergic state in the basal forebrain. Prepulse inhibition (PPI) of the startle reflex is a measure of inhibitory functions by which a weak sensory stimulus inhibits the elicitation of a startle response determined by a sudden intense stimulus. It is considered an operation measure of sensorimotor gating, a neural process by which unnecessary stimuli are eliminated from awareness. Evidence points out that the limbic domain of the CSTC loops, dopamine and GABA receptors within the striatum play an important role in PPI modulation. It is conceivable that a sensorimotor gating deficit may be involved in the genesis of premonitory urge and symptoms. Therefore, correcting the sensorimotor gating deficit may be considered a target for tic-related disorders therapies; in such case PPI (as well as other indirect estimators of sensorimotor gating) could represent therapeutic impact predictors.

Details

Database :
OAIster
Notes :
STAMPA, English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1343244750
Document Type :
Electronic Resource