Tic disorders (TD) are neuropsychiatric disorders that begin in childhood and have tics as the main clinical manifestation. The onset of TD is the result of the interaction of genetic, biological, psychological and environmental factors, and the exact etiology and pathogenesis are unclear, with central neurotransmitter imbalance, striatal dopamine overactivity or postsynaptic dopamine receptor hypersensitivity as the key links in its pathogenesis. the onset of TD has been on the rise in recent years, with a variety of clinical manifestations and complex co-morbidities, and the diagnosis and treatment need to be standardized. I. Clinical features 1. General features: the age of onset is 2 to 21 years old, with the most common being 5 to 10 years old. The disease is usually most severe at the age of 10-12; males are significantly more than females, and the ratio of males to females is 3-5:1. 2. Twitching: an involuntary, purposeless, rapid and stereotyped muscle contraction. The twitches are complex and diverse, and are classified in Table 1. motor twitches are involuntary, sudden, rapid contractions of the muscles of the head, face, neck, shoulders, trunk and limbs; vocal twitches are actually contractions of the mouth, nose, throat and respiratory muscles, and are vocalized by the airflow through the nose, mouth and throat. Motor tics or vocal tics can be further divided into two categories: simple and complex, and sometimes the two are not easily distinguished. Unlike other movement disorders, twitching occurs in the presence of normal motor function and is non-persistent. At the beginning of the disease, twitching symptoms usually start in the face and progress to the head, neck, and shoulder muscles, and then spread to the trunk and upper and lower extremities. The form of twitching may change from one form to another, with new forms of twitching constantly appearing. The frequency and intensity of twitching fluctuate significantly during the course of the disease, and new twitching symptoms may replace or superimpose on top of the old twitching symptoms. In children with a long course of the disease, the appearance of a twitch or vocalization is sometimes quickly followed by another movement in an attempt to mask it, further complicating the clinical picture. Twitching symptoms often come and go, and may resolve temporarily or spontaneously over time, or may be exacerbated or reduced by certain triggers. Factors that commonly aggravate tics include stress, anxiety, anger, shock, excitement, fatigue, infection, and being reminded of the tics. Forty to 55% of children with motor or vocal twitches are preceded by localized physical discomfort, called sensory twitches, which are considered aura symptoms (prodromal symptoms), especially in older children, including pressure, itching, pain, heat, cold or other unusual sensations. Motor or vocal twitches are likely to be associated with relief of local discomfort. Co-morbidity: About half of the children have one or more co-occurring psychological behavior disorders, including attention deficit hyperactivity disorder (ADHD), learning difficulties, obsessive-compulsive disorder, sleep disorders, mood disorders, self-injurious behavior, conduct disorders, and rage attacks. There are gender differences in the occurrence of TD co-morbidities, with ADHD, learning difficulties, conduct disorders, and rage attacks usually occurring more frequently in males, while obsessive-compulsive disorder and self-injurious behavior occur more frequently in females than in males. Co-morbidities further increase the complexity and severity of the disease, affecting the child’s learning, social adjustment, personality and psychological quality of healthy development, adding many difficulties to the treatment and management”. Diagnosis 1. Diagnostic methods: There is a lack of specific diagnostic indicators. At present, the diagnosis is mainly made by clinical descriptive diagnosis, based on the child’s tic symptoms and related accompanying psychiatric behavior. Therefore, a detailed history is the prerequisite for a correct diagnosis, and physical examination including psychiatric examination and necessary auxiliary examinations are also necessary to exclude other diseases. EEG, neuroimaging and laboratory tests are generally not characteristically abnormal. A few children may have nonspecific changes, such as background slowing or asymmetry in a few children on EEG; non-specific structural changes such as small volume of the caudate nucleus, slightly thin frontal and occipital cortices, mild enlargement of the ventricles, and deepening of the lateral fissure in a few children on cranial cT or MRI. The purpose of the examination is to rule out organic lesions in the basal ganglia, such as hepatomegaly (Wilson’s disease) and other organic extrapyramidal diseases. 2. Clinical typing: According to the clinical characteristics and duration of the disease, the disease can be divided into three types: transient TD, chronic TD and Tourette syndrome (TS). Transient TD is the most common type with the mildest disease, manifesting as one or more motor tics and/or vocal tics, and the duration of the disease is within 1 year. TS, also known as multiple tic disorder, is a relatively severe form of the disease, showing both motor and vocal tics, but not necessarily both at the same time, with a duration of more than 1 year. In the past, the term “Tourette’s syndrome” was not appropriate, because the incidence of obscenities was less than one-third, and obscenities were not a necessary condition for the diagnosis of Ts, and it had an obvious pejorative meaning. Transient TD can be converted to chronic TD, and chronic TD can be converted to Ts. Some patients cannot be classified in any of these categories and belong to other types of TD that have not yet been defined, such as TD with adult onset (late-onset TD). Refractory TD is a new concept that has gradually developed in pediatric neurology and psychiatry in recent years, which refers to children with TD who have been treated with conventional anti-TD drugs such as haloperidol and thiopride for more than 1 year in adequate amounts and have not recovered from the disease. A variety of organic diseases can also cause TD, i.e. secondary TD, which should be excluded clinically. There are many causes of secondary TD, including genetic factors (such as Down syndrome, fragile X syndrome, tuberous sclerosis, neuroborreliosis, etc.), infectious factors (such as streptococcal infection, encephalitis, neurosyphilis, Creutzfeldt-Jakob disease, etc.), toxic factors (such as carbon monoxide, mercury, bee poisoning, etc.), and drug factors (such as methylphenidate, pemoline, amphetamine, cocaine, carbamazepine, phenobarbital, phenytoin, lamotrigine, etc.). phenytoin, lamotrigine, etc.) and other factors (e.g. stroke, head trauma, developmental disorders, neurodegenerative diseases, etc.).