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In 2011 a working group of the European Society for the Study of Tourette Syndrome (ESSTS) has developed the first European assessment guidelines for Tourette syndrome (TS). Now, we present an updated version 2.0 of these European clinical guidelines for Tourette syndrome and other tic disorders, part I: assessment. Therefore, the available literature has been thoroughly screened, supplemented with national guidelines across countries and discussions among ESSTS experts. Diagnostic changes between DSM-IV and DSM-5 classifications were taken into account and new information has been added regarding differential diagnoses, with an emphasis on functional movement disorders in both children and adults. Further, recommendations regarding rating scales to evaluate tics, comorbidities, and neuropsychological status are provided. Finally, results from a recently performed survey among ESSTS members on assessment in TS are described. We acknowledge that the Yale Global Tic Severity Scale (YGTSS) is still the gold standard for assessing tics. Recommendations are provided for scales for the assessment of tics and psychiatric comorbidities in patients with TS not only in routine clinical practice, but also in the context of clinical research. Furthermore, assessments supporting the differential diagnosis process are given as well as tests to analyse cognitive abilities, emotional functions and motor skills.

Part II of the European clinical guidelines for Tourette syndrome and other tic disorders (ECAP journal, 2011) provides updated information and recommendations for psychological interventions for individuals with tic disorders, created by a working group of the European Society for the Study of Tourette Syndrome (ESSTS). A systematic literature search was conducted to obtain original studies of psychological interventions for tic disorders, published since the initial European clinical guidelines were issued. Relevant studies were identified using computerized searches of the MEDLINE and PsycINFO databases for the years 2011–2019 and a manual search for the years 2019–2021. Based on clinical consensus, psychoeducation is recommended as an initial intervention regardless of symptom severity. According to a systematic literature search, most evidence was found for Habit Reversal Training (HRT), primarily the expanded package Comprehensive Behavioral Intervention for Tics (CBIT). Evidence was also found for Exposure and Response Prevention (ERP), but to a lesser degree of certainty than HRT/CBIT due to fewer studies. Currently, cognitive interventions and third-wave interventions are not recommended as stand-alone treatments for tic disorders. Several novel treatment delivery formats are currently being evaluated, of which videoconference delivery of HRT/CBIT has the most evidence to date. To summarize, when psychoeducation alone is insufficient, both HRT/CBIT and ERP are recommended as first-line interventions for tic disorders. As part of the development of the clinical guidelines, a survey is reported from ESSTS members and other tic disorder experts on preference, use and availability of psychological interventions for tic disorders.

Co-occurring psychiatric conditions are very common in tic disorders and Tourette syndrome. These additional symptoms are often detrimental to quality of life and may impact upon the implementation and efficacy of evidence-based behavioural therapies (BT) for tics. Combining a review of the available literature, relevant theory, and expert clinical practice, we present a guideline for implementing behavioural and psychosocial interventions when common comorbidities are present. These include attention-deficit hyperactivity disorder (ADHD), obsessive–compulsive disorder (OCD), anxiety, disruptive behaviour, autism spectrum disorder (ASD) and depression. Practical recommendations are provided for assessment, formulation and management of specific and multiple comorbidities in BT for both children and adults. Despite comorbidities being common in tic disorders, few studies have comprehensively addressed how they may influence the efficacy or implementation of existing therapies or how such treatments may need to be modified or sequenced. We outline recommendations for future research, including randomised control trials of BT for those with specific or multiple comorbidities, as well as adequately powered sub-group analyses within larger scale trials or naturalistic study designs. Transdiagnostic models of psychiatric disorders and treatment, including modular cross-diagnostic therapies, which recognise the dimensionality of psychiatric disorders are also highlighted as an important focus in treatment development in tic disorders.

The major symptoms of Tourette syndrome are motor and vocal tics, but Tourette syndrome is occasionally associated with cognitive alterations as well. Although Tourette syndrome does not affect the majority of cognitive functions, some of them improve. There is scarce evidence on the impairment of learning functions in patients with Tourette syndrome. The core symptoms of Tourette syndrome are related to dysfunction of the basal ganglia and the frontostriatal loops. Acquired equivalence learning is a kind of associative learning that is related to the basal ganglia and the hippocampi. The modified Rutgers Acquired Equivalence Test was used in the present study to observe the associative learning function of patients with Tourette syndrome. The cognitive learning task can be divided into two main phases: the acquisition and test phases. The latter is further divided into two parts: retrieval and generalization. The acquisition phase of the associative learning test, which mainly depends on the function of the basal ganglia, was affected in the entire patient group, which included patients with Tourette syndrome with attention deficit hyperactivity disorder, obsessive compulsive disorder, autism spectrum disorder, or no comorbidities. Patients with Tourette syndrome performed worse in building associations. However, the retrieval and generalization parts of the test phase, which primarily depend on the function of the hippocampus, were not worsened by Tourette syndrome.

Background Gilles de la Tourette Syndrome is a neurodevelopmental disorder that is caused by the interaction of environment with a complex genetic background. The genetic etiology of the disorder remains, so far, elusive, although multiple promising leads have been recently reported. The recent implication of the histamine decarboxylase (HDC) gene, the key enzyme in histamine production, raises the intriguing hypothesis of a possible role of histaminergic dysfunction leading to TS onset. Methods Following up on the finding of a nonsense mutation in a single family with TS, we investigated variation across the HDC gene for association with TS. As a result of a collaborative international effort, we studied a large sample of 520 nuclear families originating from seven European populations (Greek, Hungarian, Italian, Polish, German, Albanian, Spanish) as well as a sample collected in Canada. Results and Conclusions Interrogating 12 tagging SNPs (tSNP) across the HDC region, we find strong over-transmission of alleles at two SNPs (rs854150 and rs1894236) in the complete sample, as well as a statistically significant associated haplotypes. Analysis of individual populations also reveals signals of association in the Canadian, German and Italian samples. Our results provide strong support for the histaminergic hypothesis in TS etiology and point to a possible role of histamine pathways in neuronal development.

Among the monoaminergic modulatory neurotransmitters, norepinephrine is involved in task orienting, hence noradrenergic genetic variants have been studied in connection to attentional processes. The role of this catecholamine system is also highlighted by the selective norepinephrine transporter blocking atomoxetine, which has proved to be effective in the pharmacological treatment of Attention Deficit Hyperactivity Disorder (ADHD). In the present genetic association study three single nucleotide polymorphisms (rs28386840, rs2242446, rs3785143 SNPs) were analyzed from the 5' region of the norepinephrine transporter ( , ) gene, which have been linked to ADHD previously. Attention problems scores of the mother-rated Child Behavior Checklist (CBCL) were used in separate analyses of 88 preschoolers (59.1% male, 6 years of age) recruited from the general population and 120 child psychiatry patients with ADHD diagnosis (85.8% male, age: 9.8 ± 2.9). The SNPs showed associations with attention problems, but the direction was different in the two groups. Regarding the promoter variant rs28386840, which showed the most consistent association, the T-allele-carrier patients with ADHD had lower CBCL attention problems scores compared to patients with AA genotype ( = 0.023), whereas T-allele-carriers in the community sample had more attention problems ( = 0.042). Based on previous reports of lower NE levels in ADHD children and the inverted-U shape effect of NE on cognitive functions, we propose that rs28386840 (-3081) T-allele, which is associated with lower NET expression (and potentially higher synaptic NE level) would support attention processes among ADHD patients (similarly as atomoxetine increases NE levels), whereas it would hinder cortical functions in healthy children.

Although the genetic basis of Tourette Syndrome (TS) remains unclear, several candidate genes have been implicated. Using a set of 382 TS individuals of European ancestry we investigated four candidate genes for TS ( , and ) in an effort to identify possibly causal variants using a targeted re-sequencing approach by next generation sequencing technology. Identification of possible disease causing variants under different modes of inheritance was performed using the algorithms implemented in VAAST. We prioritized variants using Variant ranker and validated five rare variants via Sanger sequencing in and , all of which are predicted to be deleterious. Intriguingly, one of the identified variants is in linkage disequilibrium with a variant that is included among the top hits of a genome-wide association study for response to citalopram treatment, an antidepressant drug with off-label use also in obsessive compulsive disorder. Our findings provide additional evidence for the implication of these two genes in TS susceptibility and the possible role of these proteins in the pathobiology of TS should be revisited.

Tourette syndrome is a childhood-onset neurodevelopmental disorder characterized by motor and vocal tics. On the neural level, tics are thought to be related to the disturbances of the cortico-basal ganglia-thalamo-cortical loops, which also play an important role in procedural learning. Several studies have investigated the acquisition of procedural information and the access to established procedural information in TS. Based on these, the notion of procedural hyperfunctioning, i.e., enhanced procedural learning, has been proposed. However, one neglected area is the retention of acquired procedural information, especially following a long-term offline period. Here, we investigated the 5-hour and 1-year consolidation of two aspects of procedural memory, namely serial-order and probability-based information. Nineteen children with TS between the ages of 10 and 15 as well as 19 typically developing gender- and age-matched controls were tested on a visuomotor four-choice reaction time task that enables the simultaneous assessment of the two aspects. They were retested on the same task 5 hours and 1 year later without any practice in the offline periods. Both groups successfully acquired and retained the probability-based information both when tested 5 hours and then 1 year later, with comparable performance between the TS and control groups. Children with TS did not acquire the serial-order information during the learning phase; hence, retention could not be reliably tested. Our study showed evidence for short-term and long-term retention of one aspect of procedural memory, namely probability-based information in TS, whereas learning of serial-order information might be impaired in this disorder.

Gilles de la Tourette syndrome (GTS) is a disorder characterised by motor and vocal tics, which may represent habitual actions as a result of enhanced learning of associations between stimuli and responses (S‐R). In this study, we investigated how adults with GTS and healthy controls (HC) learn two types of regularities in a sequence: statistics (non‐adjacent probabilities) and rules (predefined order). Participants completed a visuomotor sequence learning task while EEG was recorded. To understand the neurophysiological underpinnings of these regularities in GTS, multivariate pattern analyses on the temporally decomposed EEG signal as well as sLORETA source localisation method were conducted. We found that people with GTS showed superior statistical learning but comparable rule‐based learning compared to HC participants. Adults with GTS had different neural representations for both statistics and rules than HC adults; specifically, adults with GTS maintained the regularity representations longer and had more overlap between them than HCs. Moreover, over different time scales, distinct fronto‐parietal structures contribute to statistical learning in the GTS and HC groups. We propose that hyper‐learning in GTS is a consequence of the altered sensitivity to encode complex statistics, which might lead to habitual actions. The formation of habits is a long‐discussed topic in GTS. Through the decoding of neurophysiological data, we show that increased habit formation in GTS is due to increased statistical but not rule‐based learning mechanisms in fronto‐parietal cortices.