N El Malhany1, M Gulisano, R Rizzo, P Curatolo. 1. Section of Child Neuropsychiatry, Department of Neurosciences, Tor Vergata University, Viale Oxford 81, 00133, Rome, Italy, elm.nadia@gmail.com.
Abstract
UNLABELLED: Attention deficit hyperactivity disorder (ADHD) is the most common comorbid condition in patients with Tourette syndrome (TS). The co-occurrence of ADHD and TS is in most cases associated with a higher social and psychopathological impairment. Comorbidity between Tourette and ADHD appears to have a complex and partially known pathogenesis in which genetic, environmental, and neurobiological factors can be implicated. Genetic studies have revealed an involvement of dopaminergic, catecholaminergic, and GABAergic genes that modulated the activity of neurotransmitters. Furthermore, there are a lot of networks implicated in the development of ADHD and TS, involving cortical and striatal areas and basal ganglia. Although a large number of studies tried to find a common pathogenesis, the complex pathways responsible are not clear. The genes implicated in both disorders are currently unidentified, but it is probable that epigenetic factors associated with neural modifications can represent a substrate for the development of the diseases. CONCLUSION: In this paper, recent advances in neurobiology of ADHD and TS are reviewed, providing a basis for understanding the complex common pathogenesis underlying the frequent co-occurrence of the two conditions and the therapeutic choices.
UNLABELLED: Attention deficit hyperactivity disorder (ADHD) is the most common comorbid condition in patients with Tourette syndrome (TS). The co-occurrence of ADHD and TS is in most cases associated with a higher social and psychopathological impairment. Comorbidity between Tourette and ADHD appears to have a complex and partially known pathogenesis in which genetic, environmental, and neurobiological factors can be implicated. Genetic studies have revealed an involvement of dopaminergic, catecholaminergic, and GABAergic genes that modulated the activity of neurotransmitters. Furthermore, there are a lot of networks implicated in the development of ADHD and TS, involving cortical and striatal areas and basal ganglia. Although a large number of studies tried to find a common pathogenesis, the complex pathways responsible are not clear. The genes implicated in both disorders are currently unidentified, but it is probable that epigenetic factors associated with neural modifications can represent a substrate for the development of the diseases. CONCLUSION: In this paper, recent advances in neurobiology of ADHD and TS are reviewed, providing a basis for understanding the complex common pathogenesis underlying the frequent co-occurrence of the two conditions and the therapeutic choices.
Authors: B J O'Roak; T M Morgan; D O Fishman; E Saus; P Alonso; M Gratacòs; X Estivill; O Teltsh; Y Kohn; K K Kidd; J Cho; R P Lifton; M W State Journal: Mol Psychiatry Date: 2010-03-30 Impact factor: 15.992
Authors: Gholson J Lyon; Stephanie M Samar; Christine Conelea; Marcel R Trujillo; Christina M Lipinski; Christopher C Bauer; Bryan C Brandt; Joshua J Kemp; Zoe E Lawrence; Jonathan Howard; F Xavier Castellanos; Douglas Woods; Barbara J Coffey Journal: J Child Adolesc Psychopharmacol Date: 2010-08 Impact factor: 2.576
Authors: Emily J Ricketts; Sara Beth Wolicki; Melissa L Danielson; Michelle Rozenman; Joseph F McGuire; John Piacentini; Jonathan W Mink; John T Walkup; Douglas W Woods; Rebecca H Bitsko Journal: Child Psychiatry Hum Dev Date: 2021-01-01
Authors: Sabin Khadka; Godfrey D Pearlson; Vince D Calhoun; Jingyu Liu; Joel Gelernter; Katie L Bessette; Michael C Stevens Journal: Front Psychiatry Date: 2016-07-25 Impact factor: 4.157