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Nat Rev Dis Primers. 2017 Feb 2;3:16097. doi: 10.1038/nrdp.2016.97.

Gilles de la Tourette syndrome.

Author information

1
Department of Neuropsychiatry, UCL Division of Psychiatry, 6th Floor, Maple House, 149 Tottenham Court Road, London W1T 7NF, UK.
2
Department of Psychiatry, Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa.
3
Infant, Child and Adolescent Psychiatry, School of Psychiatry, University of New South Wales, Sydney, New South Wales, Australia.
4
Academic Unit of Child Psychiatry, South Western Sydney Local Health District and Ingham Institute, Liverpool Hospital, Mental Health Centre, Locked Bag 7103, Liverpool, 1871, New South Wales, Australia.
5
Department of Neurology and Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
6
Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.
7
Departments of Neurology and Psychiatry, Center for Human Genetics Research, Massachusetts General Hospital, Boston, Massachusetts, USA.
8
Division of Cognitive and Behavioral Neurology, Brigham &Women's Hospital, Boston, Massachusetts, USA.
9
Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA.
10
Department of Biological Sciences, Purdue University, West Lafayette, Indiana, USA.
11
Department of Molecular Biology and Genetics, Democritus University of Thrace, Alexandroupoli, Greece.
12
Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Dresden, Germany.
13
Department of Psychology, Marquette University, Milwaukee, Wisconsin, USA.
14
Unit of Functional Neurosurgery, UCL Institute of Neurology, London, UK.
15
Department of Clinical Neuroscience, Umeå University, Umeå, Sweden.
16
Department of Psychiatry and Genetics Institute, University of Florida, Gainesville, Florida, USA.
17
Department of Psychiatry, Pediatrics, and Psychology, Child Study Center, Yale University, New Haven, Connecticut, USA.

Abstract

Gilles de la Tourette syndrome (GTS) is a childhood-onset neurodevelopmental disorder that is characterized by several motor and phonic tics. Tics usually develop before 10 years of age, exhibit a waxing and waning course and typically improve with increasing age. A prevalence of approximately 1% is estimated in children and adolescents. The condition can result in considerable social stigma and poor quality of life, especially when tics are severe (for example, with coprolalia (swearing tics) and self-injurious behaviours) or when GTS is accompanied by attention-deficit/hyperactivity disorder, obsessive-compulsive disorder or another neuropsychiatric disorder. The aetiology is complex and multifactorial. GTS is considered to be polygenic, involving multiple common risk variants combined with rare, inherited or de novo mutations. These as well as non-genetic factors (such as perinatal events and immunological factors) are likely to contribute to the heterogeneity of the clinical phenotype, the structural and functional brain anomalies and the neural circuitry involvement. Management usually includes psychoeducation and reassurance, behavioural methods, pharmacotherapy and, rarely, functional neurosurgery. Future research that integrates clinical and neurobiological data, including neuroimaging and genetics, is expected to reveal the pathogenesis of GTS at the neural circuit level, which may lead to targeted interventions.

PMID:
28150698
DOI:
10.1038/nrdp.2016.97
[Indexed for MEDLINE]

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