Education, and a "watch and wait" strategy, are the only treatment needed for many, and the majority of individuals with tics do not seek treatment; treatment of tic disorders is similar to treatment of Tourette syndrome.

The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.

There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.

Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.

Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.

Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.

Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.

, studies on the impact of dietary interventions on the symptoms of Tourette's are scarce and methodologically poor, and a single dietary pattern has not been established. Anecdotal reports suggest that certain dietary interventions may relieve symptoms, such as gluten-free and low-sugar diets.

Tic disorders is defined in the "Diagnostic and Statistical Manual of Mental Disorders" (DSM) based on type (motor or phonic) and duration of tics (sudden, rapid, nonrhythmic movements). Tic disorders are defined similarly by the World Health Organization (ICD-10 codes).

Tourette syndrome is found among all social, racial and ethnic groups and has been reported in all parts of the world; it is three to four times more frequent among males than among females. The tics of Tourette syndrome begin in childhood and tend to remit or subside with maturity; thus, a diagnosis may no longer be warranted for many adults, and observed prevalence rates are higher among children than adults. As children pass through adolescence, about one-quarter become tic-free, almost one-half see their tics diminish to a minimal or mild level, and less than one-quarter have persistent tics. Only 5 to 14% of adults experience worse tics in adulthood than in childhood.

Up to 1% of the overall population experiences tic disorders, including chronic tics and transient tics of childhood. Chronic tics affect 5% of children, and transient tics affect up to 20%. Prevalence rates in special education populations are higher.

The reported prevalence of TS varies "according to the source, age, and sex of the sample; the ascertainment procedures; and diagnostic system", with a range reported between .4% and 3.8% for children ages 5 to 18. Robertson (2011) says that 1% of school-age children have Tourette's. According to Lombroso and Scahill (2008), the emerging consensus is that .1 to 1% of children have Tourette's, with several studies supporting a tighter range of .6 to .8%. Bloch and Leckman (2009) and Swain (2007) report a range of prevalence in children of .4 to .6%, Knight et al. (2012) estimate .77% in children, and Du et al. (2010) report that 1 to 3% of "Western" school-age children have Tourette's.

Singer (2011) states the prevalence of TS in the overall population at any time is .1% for impairing cases and .6% for all cases, while Bloch and colleagues (2011) state the overall prevalence as between .3 and 1%. Robertson (2011) also suggests that the rate of Tourette's in the general population is 1%. Using year 2000 census data, a prevalence range of .1 to 1% yields an estimate of 53,000–530,000 school-age children with Tourette's in the US, and a prevalence estimate of .1% means that in 2001 about 553,000 people in the UK age 5 or older would have Tourette's.

Tourette syndrome was once thought to be rare: in 1972, the US National Institutes of Health (NIH) believed there were fewer than 100 cases in the United States, and a 1973 registry reported only 485 cases worldwide. However, multiple studies published since 2000 have consistently demonstrated that the prevalence is much higher than previously thought. Discrepancies across current and prior prevalence estimates come from several factors: ascertainment bias in earlier samples drawn from clinically referred cases, assessment methods that may fail to detect milder cases, and differences in diagnostic criteria and thresholds. There were few broad-based community studies published before 2000 and until the 1980s, most epidemiological studies of Tourette syndrome were based on individuals referred to tertiary care or specialty clinics. Individuals with mild symptoms may not seek treatment and physicians may not confer an official diagnosis of TS on children out of concern for stigmatization; children with milder symptoms are unlikely to be referred to specialty clinics, so prevalence studies have an inherent bias towards more severe cases. Studies of Tourette syndrome are vulnerable to error because tics vary in intensity and expression, are often intermittent, and are not always recognized by clinicians, patients, family members, friends or teachers; approximately 20% of persons with Tourette syndrome do not recognize that they have tics. Newer studies—recognizing that tics may often be undiagnosed and hard to detect—use direct classroom observation and multiple informants (parent, teacher, and trained observers), and therefore record more cases than older studies relying on referrals. As the diagnostic threshold and assessment methodology have moved towards recognition of milder cases, the result is an increase in estimated prevalence.

Tourette's is associated with several comorbid conditions, or co-occurring diagnoses, which are often the major source of impairment for an affected child. Most individuals with tics do not seek medical attention, so epidemiological studies of TS "reflect a strong ascertainment bias", but among those who do warrant medical attention, the majority have other conditions, and up to 50% have ADHD or OCD.

There is no consistently effective medication for SMD, and there is little evidence for any effective treatment. In non-autistic or "typically developing children", habit reversal training may be useful. No treatment is an option when movements are not interfering with daily life.

Prognosis depends on the severity of the disorder. Recognizing symptoms early can help reduce the risk of self-injury, which can be lessened with meditations. Stereotypic movement disorder due to head trauma may be permanent.

Once the patient and family have been educated about the nature, management and treatment of the disorder and a decision has been made to treat, the European ADHD Guidelines group recommends medication rather than behavioral training as the first treatment approach; and the UK's National Institute for Health and Clinical Excellence recommends medication as first line treatment for those with hyperkinesis/severe ADHD, and the provision of group parent-training in all cases of ADHD.

Some patients have been treated by injecting botulinum toxin (botox) near the vocal cords. This does not prevent the vocalizations, but the partial paralysis that results helps to control the volume of any outbursts. Surprisingly, botox injections result in more generalized relief of tics than the vocal relief expected.

The severity and frequency of outbursts can also be decreased by surgically disabling nuclei in the thalamus, the globus pallidus and the cingulate cortex.

The naturally occurring sugar inositol has been suggested as a treatment for OCD.

Nutrition deficiencies may also contribute to OCD and other mental disorders. Vitamin and mineral supplements may aid in such disorders and provide nutrients necessary for proper mental functioning.

μ-Opioids, such as hydrocodone and tramadol, may improve OCD symptoms. Administration of opiate treatment may be contraindicated in individuals concurrently taking CYP2D6 inhibitors such as fluoxetine and paroxetine.

Much current research is devoted to the therapeutic potential of the agents that affect the release of the neurotransmitter glutamate or the binding to its receptors. These include riluzole, memantine, gabapentin, N-acetylcysteine, topiramate and lamotrigine.

Hyperkinetic disorder is a psychiatric neurodevelopmental condition emerging in early childhood that features an enduring pattern of severe, developmentally inappropriate symptoms, namely inattention, hyperactivity, and impulsivity across different settings (e.g., home and school) that significantly impair academic, social and work performance. The disorder, which appears in the World Health Organization's ICD-10, is roughly similiar to the "combined presentation" of attention deficit hyperactivity disorder in the American Psychiatric Association's DSM-V.

Hyperkinetic people display disorganized, poorly controlled and excessive activity; they lack perseverance in tasks involving thought and attention, and tend to move from one activity to the next without completing any. They are frequently accident-prone, reckless and impulsive, and may thoughtlessly (rather than defiantly) break rules. Cognitive impairment and delayed language and motor development are more common in this group than in the general population; and they may experience low self-esteem and engage in dissocial behavior as a consequence of the disorder.

While hyperkinetic children are commonly incautious and unreserved with adults, they might be isolated and unpopular with other children.

The medications most frequently used are the selective serotonin reuptake inhibitors (SSRIs). Clomipramine, a medication belonging to the class of tricyclic antidepressants, appears to work as well as SSRIs but has a higher rate of side effects.

SSRIs are a second line treatment of adult obsessive compulsive disorder (OCD) with mild functional impairment and as first line treatment for those with moderate or severe impairment. In children, SSRIs can be considered as a second line therapy in those with moderate-to-severe impairment, with close monitoring for psychiatric adverse effects. SSRIs are efficacious in the treatment of OCD; people treated with SSRIs are about twice as likely to respond to treatment as those treated with placebo. Efficacy has been demonstrated both in short-term (6–24 weeks) treatment trials and in discontinuation trials with durations of 28–52 weeks.

In 2006, the National Institute of Clinical and Health Excellence (NICE) guidelines recommended antipsychotics for OCD that does not improve with SSRI treatment. For OCD the evidence for the atypical antipsychotic drugs risperidone and quetiapine is tentative with insufficient evidence for olanzapine. A 2014 review article found two studies that indicated that aripiprazole was "effective in the short-term" and found that "[t]here was a small effect-size for risperidone or anti-psychotics in general in the short-term"; however, the study authors found "no evidence for the effectiveness of quetiapine or olanzapine in comparison to placebo." While quetiapine may be useful when used in addition to an SSRI in treatment-resistant OCD, these drugs are often poorly tolerated, and have metabolic side effects that limit their use. None of the atypical antipsychotics appear to be useful when used alone. Another review reported that no evidence supports the use of first generation antipsychotics in OCD.

A guideline by the APA suggested that dextroamphetamine may be considered by itself after more well supported treatments have been tried.

While the cause of conduct disorder is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of conduct disorder including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g., neurodevelopmental basis) and adolescent (e.g., social/peer relationships) onset.

Treatment for OCPD includes psychotherapy, cognitive behavioral therapy, behavior therapy or self-help. Medication may be prescribed. In behavior therapy, a person with OCPD discusses with a psychotherapist ways of changing compulsions into healthier, productive behaviors. Cognitive analytic therapy is an effective form of behavior therapy.

Treatment is complicated if the person does not accept that they have OCPD, or believes that their thoughts or behaviors are in some sense correct and therefore should not be changed. Medication alone is generally not indicated for this personality disorder. Selective serotonin reuptake inhibitors (SSRIs) may be useful in addition to psychotherapy by helping the person with OCPD be less bogged down by minor details, and to lessen how rigid they are.

People with OCPD are three times more likely to receive individual psychotherapy than people with major depressive disorder. There are higher rates of primary care utilization. There are no known properly controlled studies of treatment options for OCPD. More research is needed to explore better treatment options.

There are several different classes of pharmacological treatment agents that have some support for treating excoriation disorder: (1) SSRIs; (2) opioid antagonists; and (3) glutamatergic agents. In addition to these classes of drugs, some other pharmacological products have been tested in small trials as well.

SSRIs have shown to be effective in the treatment of OCD and this has provided an argument in favor of treating excoriation disorder with the same therapy. Unfortunately, the clinical studies have not provided clear support for this, because there have not been large double-blind placebo-controlled trials of SSRI therapy for excoriation disorder.

Review of treatment of excoriation disorder have shown that the following medications may be effective in reducing picking behavior: doxepin, clomipramine, naltrexone, pimozide, and olanzapine. Small studies of fluoxetine, an SSRI, in treating excoriation disorder showed that the drug reduced certain aspects of skin picking, as compared to placebo, but full remission was not observed. One small study of patients with excoriation disorder treated with citalopram, another SSRI, showed that those that took the drug significantly reduced their scores on the Yale-Brown Obsessive Compulsive Scale compared to placebo, but that there was no significant decrease on the visual-analog scale of picking behavior.

While there have been no human studies of opioid antagonists for the treatment of excoriation disorder, there have been studies showing that these products can reduce self-chewing in dogs with acral lick, which some have proposed is a good animal model for the body-focused repetitive behavior. Furthermore, there have been case reports that support the use of these opioid antagonists to treat excoriation disorder. Opioid antagonists work by affecting dopamine circuitry, thereby decreasing the pleasurable effects of picking.

Another class of possible pharmacological treatments are glutamatergic agents such as n-acetyl cysteine (NAC). These products have shown some ability to reduce other problematic behaviors such as cocaine addiction and trichotillomania. Some case studies and some small studies of NAC have shown a decrease in picking by treatment with NAC, as compared to placebo.

Excoriation disorder, and trichotillomania have been treated with inositol.

Topiramate, an anti-epileptic drug, has been used to treat excoriation disorder; in a small study of individuals with Prader–Willi syndrome, it was found to reduce skin picking.

The most effective treatment for an individual with conduct disorder is one that seeks to integrate individual, school, and family settings. Additionally, treatment should also seek to address familial conflict such as marital discord or maternal depression.

Knowledge about effective treatments for excoriation disorder is sparse despite the prevalence of the condition. There are two major classes of therapy for excoriation disorder: pharmacological and behavioral.

Individuals with excoriation disorder often do not seek treatment for their condition largely due to feelings of embarrassment, alienation, lack of awareness, or belief that the condition cannot be treated. One study found that only 45% of individuals with excoriation disorder ever sought treatment and only 19% ever received dermalogical treatment. Another study found that only 30% of individuals with this disorder sought treatment.

Individual approaches to treatment are recommended, usually involving a combination of mood stabilizers and atypical antipsychotics. Psychotherapy may be beneficial and should be started early.

Attention-Deficit Hyperactivity Disorder (ADHD)[33][34]

Obsessive-Compulsive Disorder (OCD)[33][34]

Anxiety [33][34]

Lower Quality of Life [33][34]

Depression [33][34]

Aggression [34]

Emotional Dysregulation [34]

Physical consequences such as pain and discomfort of the repetitive movements [33]

Low Self-Esteem [33]

Autism Spectrum Disorder [33]

Multiple complex developmental disorder (MCDD) is a research category, proposed to involve several neurological and psychological symptoms where at least some symptoms are first noticed during early childhood and persist throughout life. It was originally suggested to be a subtype of autistic spectrum disorders (PDD) with co-morbid schizophrenia or another psychotic disorder; however, there is some controversy that not everyone with MCDD meets criteria for both PDD and psychosis. The term "multiplex developmental disorder" was coined by Donald J. Cohen in 1986.

Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. However, with diseases of chronic psychosis such as schizophrenia, this strategy must be balanced with the fact that increased dosages of neuroleptics are more beneficial in preventing recurrence of psychosis. If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal of the drug for months, years or even permanently. Some studies suggest that physicians should consider using atypical antipsychotics as a substitute to typical antipsychotics for patients requiring medication. These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia.

Recent studies have tested the use of melatonin, high dosage vitamins, and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current prevalence rate for those taking antipsychotic drugs.

Treatment for children suspected of PANDAS is generally the same as the standard treatments for TS and OCD. These include cognitive behavioral therapy and medications to treat OCD such as selective serotonin reuptake inhibitors (SSRIs); and "conventional therapy for tics".

A controlled study (Garvey, Perlmutter, "et al", 1999) of prophylactic antibiotic treatment of 37 children found that penicillin V did not prevent GABHS infections or exacerbation of other symptoms; however, compliance was an issue in this study. A later study (Snider, Lougee, "et al", 2005) found that penicillin and azithromycin decreased infections and symptom exacerbation. The sample size, controls, and methodology of that study were criticized. Murphy, Kurlan and Leckman (2010) say, "The use of prophylactic antibiotics to treat PANDAS has become widespread in the community, although the evidence supporting their use is equivocal. The safety and efficacy of antibiotic therapy for patients meeting the PANDAS criteria needs to be determined in carefully designed trials"; de Oliveira and Pelajo (2009) say that because most studies to date have "methodologic issues, including small sample size, retrospective reports of the baseline year, and lack of an adequate placebo arm ... it is recommended to treat these patients only with conventional therapy".

Evidence is insufficient to determine if tonsillectomy is effective.

It is possible for this disorder to progress over time. A patient suffering from the disorder can improve the condition with treatments. There are several types of therapies that may improve the condition, but depending on a patient’s experience of the disorder or the cause of the disorder, treatments will vary.

- Psychotherapy including behaviour therapy, Gestalt therapy, Adlerian therapy, psychoanalytic therapy and existential therapy.

- Pharmacotherapy through medications including antidepressants.

STPD is rarely seen as the primary reason for treatment in a clinical setting, but it often occurs as a comorbid finding with other mental disorders. When patients with STPD are prescribed pharmaceuticals, they are most often prescribed the same drugs used to treat patients suffering from schizophrenia including traditional neuroleptics such as haloperidol and thiothixene. In order to decide which type of medication should be used, Paul Markovitz distinguishes two basic groups of schizotypal patients:

- Schizotypal patients who appear to be almost schizophrenic in their beliefs and behaviors (aberrant perceptions and cognitions) are usually treated with low doses of antipsychotic medications, e.g. thiothixene. However, it must be mentioned that long-term efficacy of neuroleptics is doubtful.

- For schizotypal patients who are more obsessive-compulsive in their beliefs and behaviors, SSRIs like Sertraline appear to be more effective.

Lamotrigine, an anti-convulsant, appears to be helpful in dealing with social isolation.

According to Theodore Millon, the schizotypal is one of the easiest personality disorders to identify but one of the most difficult to treat with psychotherapy. Persons with STPD usually consider themselves to be simply eccentric, productive, or nonconformist. As a rule, they underestimate maladaptiveness of their social isolation and perceptual distortions. It is not so easy to gain rapport with people who suffer from STPD due to the fact that increasing familiarity and intimacy usually increase their level of anxiety and discomfort. In most cases they do not respond to informality and humor.

Group therapy is recommended for persons with STPD only if the group is well structured and supportive. Otherwise, it could lead to loose and tangential ideation. Support is especially important for schizotypal patients with predominant paranoid symptoms, because they will have a lot of difficulties even in highly structured groups.

Valbenazine has been approved by the FDA for tardive dyskinesia. Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders. However, it is only approved to treat chorea associated with Huntington's disease. The related VMAT2 inhibitor, reserpine, has also been tried in one small randomised double-blind placebo-controlled trial as a treatment for TD with success, as has α-methyldopa. Ondansetron has shown some benefit in experimental studies on tardive dyskinesia and a variety of anti-Parkinsonian medications are used such as donepezil, baclofen, and pramipexole. Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage. Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia. Benzodiazepines are an effective treatment for TD, however their use is limited by the development of tolerance which requires ever increasing doses of the benzodiazepines to be used to attenuate TD symptoms. The most popular benzodiazepine for the treatment of TD is clonazepam. Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials.

In males, the branched-chain amino acid formula Tarvil, containing the amino acids valine, isoleucine, and leucine in a 3:3:4 ratio was reported as beneficial for motor symptoms in a small, non-blinded study.