some individuals with ocd; "tic-related ocd" is hypothesized to be a subgroup of ocd, distinguished from non-tic related ocd by the type and nature of obsessions and compulsions. compared to the more typical compulsions of ocd without tics that relate to contamination, tic-related ocd presents with more "counting, aggressive thoughts, symmetry and touching" compulsions. compulsions associated with ocd without tics are usually related to obsessions and anxiety, while those in tic-related ocd are more likely to be a response to a premonitory urge. there are increased rates of anxiety and depression in those adults with ts who also have ocd. among individuals with ts studied in clinics, between 2.9% and 20% had autism spectrum disorders, but one study indicates that a high association of autism and ts may be partly due to difficulties distinguishing between tics and tic-like behaviors or ocd symptoms seen in people with autism. not all people with tourette's have adhd or ocd or other comorbid conditions, and estimates of the rate of pure ts or ts-only vary from 15% to 57%; in clinical populations, a high percentage of those under care do have adhd. children and adolescents with pure ts are not significantly different from their peers without ts on ratings of aggressive behaviors or conduct disorders, or on measures of social adaptation. similarly, adults with pure ts do not appear to have the social difficulties present in those with ts plus adhd. among those with an older age of onset, more substance abuse and mood disorders are found, and there may be self-injurious tics. adults who have severe, often treatment-resistant tics are more likely to also have mood disorders and ocd. coprolalia is more likely in people with severe tics plus multiple comorbid conditions. neuropsychological function there are no major impairments in neuropsychological function among people with tourette's, but conditions that occur along with tics can cause variation in neurocognitive function. a better understanding of comorbid conditions is needed to untangle any neuropsychological differences between ts-only individuals and those with comorbid conditions. only slight impairments are found in intellectual ability, attentional ability, and nonverbal memory—but adhd, other comorbid disorders, or tic severity could account for these differences. in contrast with earlier findings, visual motor integration and visuoconstructive skills are not found to be impaired, while comorbid conditions may have a small effect on motor skills. comorbid conditions and severity of tics may account for variable results in verbal fluency, which can be slightly impaired. there might be slight impairment in social cognition, but not in the ability to plan or make decisions. children with ts-only do not show cognitive deficits. they are faster than average for their age on timed tests of motor coordination, and constant tic suppression may lead to an advantage in switching between tasks because of increased inhibitory control. learning disabilities may be present, but whether they are due to tics or comorbid conditions is controversial; older studies that reported higher rates of learning disability did not control well for the presence of comorbid conditions. there are often difficulties with handwriting, and disabilities in written expression and math are reported in those with ts plus other conditions. causes main article: causes and origins of tourette syndrome the exact cause of tourette's is unknown, but it is well established that both genetic and environmental factors are involved. genetic epidemiology studies have shown that tourette'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 ts 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 tourette's—can affect the severity of ts 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 ts. 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 syndrome (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 ts. some forms of ocd may be genetically linked to tourette's, although the genetic factors in ocd with and without tics may differ. the genetic relationship of adhd to tourette syndrome, however, has not been fully established. a genetic link between autism and tourette's has not been established as of 2017. mechanism the basal ganglia and thalamus are implicated in tourette syndrome. the exact mechanism affecting the inherited vulnerability to tourette'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 tourette'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 tourette's. the ability to suppress tics depends on brain circuits that "regulate response inhibition and cognitive control of motor behavior". children with ts 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 tourette'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". diagnosis according to the diagnostic and statistical manual of mental disorders (dsm-5), tourette's may be diagnosed when a person exhibits both multiple motor tics and one or more vocal tics over a period of one year. the motor and vocal tics need not be concurrent. the onset must have occurred before the age of 18 and cannot be attributed to the effects of another condition or substance (such as cocaine). hence, other medical conditions that include tics or tic-like movements—for example, autism or other causes of tics—must be ruled out. patients referred for a tic disorder are assessed based on their family history of tics, vulnerability to adhd, obsessive–compulsive symptoms, and a number of other chronic medical, psychiatric and neurological conditions. in individuals with a typical onset and a family history of tics or ocd, a basic physical and neurological examination may be sufficient. there are no specific medical or screening tests that can be used to diagnose tourette's; the diagnosis is usually made based on observation of the individual's symptoms and family history, and after ruling out secondary causes of tic disorders (tourettism). delayed diagnosis often occurs because professionals mistakenly believe that ts is rare, always involves coprolalia, or must be severely impairing. the dsm has recognized since 2000 that many individuals with tourette's do not have significant impairment; diagnosis does not require the presence of coprolalia or a comorbid condition, such as adhd or ocd. tourette's may be misdiagnosed because of the wide expression of severity, ranging from mild (in the majority of cases) or moderate, to severe (the rare but more widely recognized and publicized cases). about 20% of people with tourette syndrome do not realize that they have tics. tics that appear early in the course of ts are often confused with allergies, asthma, vision problems, and other conditions. pediatricians, allergists and ophthalmologists are among the first to see or identify a child as having tics, although the majority of tics are first identified by the child's parents. coughing, blinking, and tics that mimic unrelated conditions such as asthma are commonly misdiagnosed. in the uk, there is an average delay of three years between symptom onset and diagnosis. differential diagnosis main screening and assessment tools yale global tic severity scale (ygtss), recommended in international guidelines to assess "frequency, intensity, complexity, distribution, interference and impairment" of or due to ticstourette syndrome clinical global impression (ts–cgi) and shapiro ts severity scale (stss), for a briefer assessment of tics than ygtsstourette's disorder scale (tods), to assess tics and comorbiditiespremonitory urge for tics scale (puts), for individuals over age tenmotor tic, obsessions and compulsions, vocal tic evaluation survey (moves), to evaluate complex tics and other behaviorsautism—tics, ad/hd, and other comorbities (a–tac), to screen for other conditions tics that may appear to mimic those of tourette's—but are associated with disorders other than tourette's—are known as tourettism and are ruled out in the differential diagnosis for tourette syndrome. the abnormal movements associated with choreas, dystonias, myoclonus, and dyskinesias are distinct from the tics of tourette's in that they are more rhythmic, not suppressible, and not preceded by an unwanted urge. developmental and autism spectrum disorders may manifest tics, other stereotyped movements, and stereotypic movement disorder. the stereotyped movements associated with autism typically have an earlier age of onset; are more symmetrical, rhythmical and bilateral; and involve the extremities (for example, flapping the hands). if another condition might better explain the tics, tests may be done; for example, if there is diagnostic confusion between tics and seizure activity, an eeg may be ordered. an mri can rule out brain abnormalities, but such brain imaging studies are not usually warranted. measuring thyroid-stimulating hormone blood levels can rule out hypothyroidism, which can be a cause of tics. if there is a family history of liver disease, serum copper and ceruloplasmin levels can rule out wilson's disease. the typical age of onset of ts is before adolescence. in teenagers and adults with an abrupt onset of tics and other behavioral symptoms, a urine drug screen for stimulants might be requested. increasing episodes of tic-like behavior among teenagers (predominantly adolescent girls) were reported in several countries during the covid-19 pandemic. researchers linked their occurrence to followers of certain tiktok or youtube artists. described in 2006 as psychogenic, abrupt-onset movements resembling tics are referred to as a functional movement disorder or functional tic-like movements. functional tic-like movements can be difficult to