Tourette’s syndrome begins in childhood and adolescence and is characterized by involuntary, repetitive, rapid motor and/or vocal tics in one or more muscles, which may be accompanied by inattention, hyperactivity, obsessive-compulsive movements or thoughts, and other behavioral symptoms. There are 3 clinical types: transient tics (often called Tourette’s syndrome), chronic motor or vocal tics, and Tourette’s syndrome (TS, Tourette’s-obscura syndrome), which is a disorder of combined vocal and multi-motor tics, with TS being the most typical, and transient tics being the most common. The etiology of this disorder has not been elucidated, and recent research reports suggest that it may be due to the interaction of genetic, neurobiochemical, psychological, and environmental factors during childhood development. Genetic factors Many familial and twin-born investigations have found that Tourette’s syndrome and TS are more common among family members of children with TS, with an incidence rate of 10% to 66%.The homozygosity rate of twin-born children with TS is higher, with monozygotic consistency ranging from 75% to 95%; and bi-zygotic consistency ranging from 8% to 23%. It is generally recognized that TS is inherited in an autosomal incomplete dominant or polygenic manner, and is an inherited disease with complex traits controlled by multiple microefficiency genes. There is a high prevalence of epistasis in males (nearly 100%) and a lower prevalence in females (70%). The site of gene action may be the midbrain dopaminergic system. Neurobiochemical Factors Several neural systems and different neurotransmitters may be involved in the pathogenesis of tic disorders, including the central dopaminergic, 5-hydroxytryptaminergic, noradrenergic, cholinergic, gamma-aminobutyric acid (GABA)ergic, and opioid systems. Disorders in one or some of these neural networks can lead to disturbances in neurotransmitter balance, resulting in neurological dysfunction. Organic factors Many studies suggest that TS is an organic disease. Imaging tests have revealed mild enlargement of the ventricles, marked deepening of the lateral fissure, intersphenoidal cavities, and mild cortical atrophy in some children. Positron emission tomography (PET) scans revealed excessive glucose metabolic rates in the basal ganglia, frontal cortex, and temporal lobes bilaterally in children with TS. Recent studies have suggested that abnormalities in the development of specific parts of the basal ganglia, frontal cortex, and limbic system may be the cause of TS, with lesions centered on the basal ganglia, and abnormalities in the structure and function of the cortico-sub-basal ganglia-thalamo-cortical neural circuit (CSTC). Psychosocial factors The cause of TS may be related to stressors, such as exposure to intense trauma or other major life events. Maternal stressful events during pregnancy, abnormalities in the mother-child relationship, rejection, and stressful life events are risk factors for later development of tic disorders. Postnatal stress can increase the onset or exacerbate symptoms in genetically susceptible individuals. Neuroimmune factors 20% to 25% of tic disorders are associated with post-infectious autoimmune damage, of which approximately 10% are associated with group A beta-hemolytic streptococcal infection. Children with tic disorders often have a history of viral or bacterial infections 4-6 weeks prior to onset of symptoms. The relationship between infectious factors and tic disorders is unclear, and it is possible that various pathogens cause tics by causing damage to the corresponding neural structures (e.g., basal ganglia and CSTC) through direct attack or crossimmune reaction. Other Perinatal anomalies Studies have found that there is a high prevalence of perinatal anomalies in children with tic disorders, so it is thought that perinatal factors may also be involved in the development of tic disorders. Preterm birth, twin births, severe reactions in the first trimester of pregnancy, maternal factors (poor mood, smoking, alcohol, coffee, etc.), and fetal or neonatal illnesses (intrauterine asphyxia, intrauterine infections, umbilical cord wrapping, neonatal asphyxia, low birth weight, neonatal ischemic-hypoxic encephalopathy, and intracranial hemorrhage, etc.) are factors that can lead to brain damage in the fetus or newborn, which is a risk factor for the development of Tourette’s syndrome. Diet A positive correlation has been found between the consumption of foods containing caffeine, refined sugar, and sweeteners and the worsening of Tourette’s syndrome. Consumption of colorings, additives and beverages may exacerbate the symptoms of Tourette’s syndrome. This may be due to the fact that after digestion and absorption of certain ingredients in food, they can interact with the dopaminergic and 5-hydroxytryptaminergic systems, resulting in an imbalance of neurotransmitter balance in the brain. It has been reported that frequent consumption of western fast food and puffed food is also associated with tic symptoms, which may be related to the high lead content in these foods. Dietary factors are generally considered to play a minor role in the etiology of tic disorders, but may have an effect on the severity of tics. Drugs It has been reported in the past that high doses of antipsychotics or central stimulants, certain antiepileptic drugs may cause tic disorders, as well as various types of poisoning (e.g., wasp poisoning, mercury poisoning, carbon monoxide poisoning, etc.). Other Increased blood lead, zinc or iron deficiencies may also be associated with tic disorders.