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 Tourettes—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 Tourettes, although the genetic factors in OCD with and without tics may differ.
Cortical desmoid (also called tug lesion or periosteal desmoid) is an irregularity of the distal femoral cortex caused by repetitive stress at the attachment of the adductor magnus aponeurosis. It is most commonly seen in adolescents and is usually asymptomatic. It is a benign and self-limiting lesion. References
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