Tic Disorders (Tourette Syndrome)

Tics are sudden, rapid, recurrent involuntary vocalisations or movements, occurring in bouts that wax and wane in intensity, frequency and type — e.g. grunting, blinking, shoulder shrugging, humming, yelling a word/phrase, throat clearing. See also ADHD & ODD (common comorbidity).

Classification

• Tourette syndrome (GTS) — motor and vocal tics for >1 year.
• Persistent (chronic) motor or vocal tic disorder — motor or vocal tics (not both) for >1 year.
• Provisional tic disorder — motor and/or vocal tics for <1 year.

Characteristics

• Prevalence ~1% of school-aged children; boys 4:1.
• Mean onset 6–7 years, peak severity ~10–12 years, typically improving by/after adolescence — ~80% substantially decrease by adulthood; ~20% do not decrease and may even increase.
• Average ~5 years from onset to diagnosis; associated with psychosocial distress and impaired functioning.
• Strong genetic component — first-degree relatives have a 10–100-fold increased risk of tics.
• ~90% have “Tourette-plus” — a comorbid condition — most commonly ADHD (60–75%), OCD (27%), obsessive-compulsive behaviours (32%), and self-injurious behaviour (25%). Less commonly: autism features, learning difficulties, anxiety, depression, phobia, irritability, aggression, sleep difficulties, oppositional/conduct problems. Only ~10% have “pure Tourette” (tics alone). ADHD symptoms often appear age 3–6, before tics manifest; OCD symptoms usually emerge later (late childhood/ adolescence).
• Can be simple (one muscle group/sound) or complex. Complex tics differ from OCD compulsions in being non-cognitive, not preplanned, and not anxiety-reducing — examples: copropraxia (obscene gestures), echopraxia (copying others), self-injury, echolalia (repeating others), palilalia (repeating oneself), coprolalia (involuntary swearing — occurs in ~10–15% of cases, not the majority).
• Tics are usually preceded by a premonitory urge (tightness, tension, itch) relieved by performing the tic — an urge-tic-relief cycle. Tics can be voluntarily suppressed briefly (hence “unvoluntary” rather than purely involuntary), at the cost of mounting tension and often a rebound afterward — this can be misread as the child “choosing” to tic more at home after suppressing all day at school, or as tics being purely psychological if stress worsens them.
• Rarely, tics can be triggered or worsened by group A streptococcal infection (PANDAS).
• Unknown overall aetiology; genetics play a major role (heritability ~0.77); pre-/perinatal factors (pregnancy difficulties, smoking, infection, immune/inflammatory factors, birth complications) also contribute. Excess dopamine in corticostriatal circuitry is implicated.

Assessment

Detailed history covering tics and associated conditions (ADHD, OCD/ OCB) in the patient and family members. Distinguish from other involuntary movement disorders (myoclonus, chorea, athetosis, dystonia, hemiballismus, tardive tourettism, acquired tourettism from adult-onset trauma/CO poisoning/basal ganglia infarct). A careful neurological exam reassures patient, family and clinician.

Management

There are effective treatments — not “no treatment” as previously recorded here.

• Education, explanation and support — for mild cases, this may be all that’s needed. Emphasise the tics are involuntary and outside the child’s control (not “bad parenting” or attention-seeking); link with the Tourette Syndrome Association of Australia.
• Behavioural treatment (mild–moderate tics) — refer to a psychologist (accessible via a mental health care plan): habit reversal therapy (HRT), exposure and response prevention (ERP), and comprehensive behavioural intervention for tics (CBIT) — which combines awareness training, competing-response training, and social support (praise/ reminders from a parent).
• Medication (moderate–severe tics/distress):
  • Centrally acting α-adrenergic agents (clonidine or guanfacine) — usually first-line, especially with comorbid hyperactivity/sleep problems; monitor BP (hypotension risk; avoid abrupt cessation — rebound hypertension).
  • Low-dose antipsychotics (risperidone, aripiprazole, amisulpride, haloperidol) — start low, titrate slowly. First-generation agents (haloperidol) used less now due to extrapyramidal risk; monitor weight/ metabolic effects with second-generation agents. Risperidone can help comorbid aggression; aripiprazole can augment SSRIs for comorbid OCD/ anxiety/depression.
  • Less commonly (complex/comorbid epilepsy cases): anticonvulsants (topiramate, carbamazepine, levetiracetam), benzodiazepines (clonazepam), cannabinoids.
  • Deep brain stimulation — adults only, severe refractory GTS, outcomes heterogeneous.
• Refer to a GTS-experienced specialist for severe tics, significant distress/dysfunction, or significant comorbidity.