The basal ganglia and thalamus are implicated in<unk> . The exact mechanism affecting the inherited vulnerability to<unk> 's is not well established. Tics are believed to result from dysfunction in cortical and subcortical brain regions: the thalamus, basal ganglia and frontal cortex. Neuroanatomic models suggest failures in circuits connecting the brain's cortex and subcortex; imaging techniques implicate the frontal cortex and basal ganglia. In the 2010s, neuroimaging and postmortem brain studies, as well as animal and genetic studies, made progress towards better understanding the neurobiological mechanisms leading to<unk> 's. These studies support the basal ganglia model, in which neurons in the striatum are activated and inhibit outputs from the basal ganglia. Cortico-striato-thalamo-cortical (CSTC) circuits, or neural pathways, provide inputs to the basal ganglia from the cortex. These circuits connect the basal ganglia with other areas of the brain to transfer information that regulates planning and control of movements, behavior, decision-making, and learning. Behavior is regulated by cross-connections that "allow the integration of information" from these circuits. Involuntary movements may result from impairments in these CSTC circuits, including the sensorimotor, limbic, language and decision making pathways. Abnormalities in these circuits may be responsible for tics and premonitory urges. The caudate nuclei may be smaller in subjects with tics compared to those without tics, supporting the hypothesis of pathology in CSTC circuits in<unk> 's. The ability to suppress tics depends on brain circuits that "regulate response inhibition and cognitive control of motor behavior". Children with<unk>  are found to have a larger prefrontal cortex, which may be the result of an adaptation to help regulate tics. It is likely that tics decrease with age as the capacity of the frontal cortex increases. Cortico-basal ganglia (CBG) circuits may also be impaired, contributing to "sensory, limbic and executive" features. The release of dopamine in the basal ganglia is higher in people with<unk> 's, implicating biochemical changes from "overactive and dysregulated dopaminergic transmissions". Histamine and the H3 receptor may play a role in the alterations of neural circuitry. A reduced level of histamine in the H3 receptor may result in an increase in other neurotransmitters, causing tics. Postmortem studies have also implicated "dysregulation of neuroinflammatory processes".
Tourette syndrome
Lesch–Nyhan syndrome
Conduct disorder
Tardive dyskinesia  Tardive dyskinesia  1
Autism spectrum
High-functioning autism
Oppositional defiant disorder
Klismaphilia