The exact cause of<unk> 's is unknown, but it is well established that both genetic and environmental factors are involved. Genetic epidemiology studies have shown that<unk> 's is highly heritable, and 10 to 100 times more likely to be found among close family members than in the general population. The exact mode of inheritance is not known; no single gene has been identified, and hundreds of genes are likely involved. Genome-wide association studies were published in 2013 and 2015 in which no finding reached a threshold for significance; a 2019 meta-analysis found only a single genome-wide significant locus on chromosome 13, but that result was not found in broader samples. Twin studies show that 50 to 77% of identical twins share a<unk>  diagnosis, while only 10 to 23% of fraternal twins do. But not everyone who inherits the genetic vulnerability will show symptoms. A few rare highly penetrant genetic mutations have been found that explain only a small number of cases in single families (the SLITRK1, HDC, and CNTNAP2 genes). Psychosocial or other non-genetic factors—while not causing<unk> 's—can affect the severity of<unk>  in vulnerable individuals and influence the expression of the inherited genes. Pre-natal and peri-natal events increase the risk that a tic disorder or comorbid OCD will be expressed in those with the genetic vulnerability. These include paternal age; forceps delivery; stress or severe nausea during pregnancy; and use of tobacco, caffeine, alcohol, and cannabis during pregnancy. Babies who are born premature with low birthweight, or who have low Apgar scores, are also at increased risk; in premature twins, the lower birthweight twin is more likely to develop<unk> . Autoimmune processes may affect the onset of tics or exacerbate them. Both OCD and tic disorders are hypothesized to arise in a subset of children as a result of a post-streptococcal autoimmune process. Its potential effect is described by the controversial hypothesis called PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), which proposes five criteria for diagnosis in children. PANDAS and the newer pediatric acute-onset neuropsychiatric<unk>  (PANS) hypotheses are the focus of clinical and laboratory research, but remain unproven. There is also a broader hypothesis that links immune-system abnormalities and immune dysregulation with<unk> . Some forms of OCD may be genetically linked to<unk> 's, although the genetic factors in OCD with and without tics may differ. The genetic relationship of ADHD to<unk> , however, has not been fully established. A genetic link between autism and<unk> 's has not been established as of 2017.
Tourette syndrome
Lesch–Nyhan syndrome
Conduct disorder
Tardive dyskinesia  Tardive dyskinesia  1
Autism spectrum
High-functioning autism
Oppositional defiant disorder
Klismaphilia