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Background and purpose: In 2020, health professionals witnessed a dramatic increase in referrals of young people with rapid onset of severe tic-like behaviours. We assembled a working group to develop criteria for the clinical diagnosis of functional tic-like

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Cytokines are an important modulator of the immune system and have been found to be altered significantly in many neurological and psychiatric disorders, like obsessive compulsive disorder (OCD) and movement disorders. Also, in pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS), which are characterized by abrupt debut of symptoms of OCD and /or movement disorder symptoms, alterations in the immune system have been suggested. The aim of this paper was to review the current literature on the cytokine profile of pediatric patients with symptoms of OCD and/or movement disorder symptoms. A search of PubMed and Medline was performed with specific keywords to review studies measuring cytokines in pediatric patients with symptoms of OCD and/or movement disorders. Nineteen studies were found, twelve of which included a healthy control group, while four studies had control groups of children with other disorders, primarily neurological or psychiatric. One study compared cytokines measurements to reference intervals, and two studies had a longitudinal design. Many cytokines were found to have significant changes in patients with symptoms of OCD and/or movement disorders compared to both healthy controls and other control groups. Furthermore, differences were found when comparing cytokines in periods of exacerbation with periods of remission of symptoms in study participants. The cytokines that most studies with healthy control groups found to be significantly altered were TNF-α, IL-1β and IL-17. Although the exact role of these cytokines in OCD and movement disorder symptoms remains unclear, the available literature suggests a proinflammatory cytokine profile. This offers interesting perspectives on the pathogenesis of OCD and/or movement disorder symptoms in children, and further research into the implications of cytokines in neuropsychiatric disorders is warranted.

Tourette Syndrome (TS) is a complex neurodevelopmental disorder characterized by vocal and motor tics lasting more than a year. It is highly polygenic in nature with both rare and common previously associated variants. Epidemiological studies have shown TS to be correlated with other phenotypes, but large-scale phenome wide analyses in biobank level data have not been performed to date. In this study, we used the summary statistics from the latest meta-analysis of TS to calculate the polygenic risk score (PRS) of individuals in the UK Biobank data and applied a Phenome Wide Association Study (PheWAS) approach to determine the association of disease risk with a wide range of phenotypes. A total of 57 traits were found to be significantly associated with TS polygenic risk, including multiple psychosocial factors and mental health conditions such as anxiety disorder and depression. Additional associations were observed with complex non-psychiatric disorders such as Type 2 diabetes, heart palpitations, and respiratory conditions. Cross-disorder comparisons of phenotypic associations with genetic risk for other childhood-onset disorders (e.g.: attention deficit hyperactivity disorder [ADHD], autism spectrum disorder [ASD], and obsessive-compulsive disorder [OCD]) indicated an overlap in associations between TS and these disorders. ADHD and ASD had a similar direction of effect with TS while OCD had an opposite direction of effect for all traits except mental health factors. Sex-specific PheWAS analysis identified differences in the associations with TS genetic risk between males and females. Type 2 diabetes and heart palpitations were significantly associated with TS risk in males but not in females, whereas diseases of the respiratory system were associated with TS risk in females but not in males. This analysis provides further evidence of shared genetic and phenotypic architecture of different complex disorders.