**6.2 Adults with tics and comorbidities**

Tics and vocalizations developing in later life in association with neuroacanthocytosis80, Sydenham's chorea and L-dopa–treated postencephalitic parkinsonian syndrome81. There are a few reports of isolated and spontaneous adult-onset tics disorders.

Chouinard and colleagues reported on 7 cases of idiopathic tic disorder that presented after the patients were 21 years of age75. Adult-onset tic disorder in the absence of any other primary neurological disorder has onset of tic symptoms from 23 to 52 years76.

Adult-onset cases need to be evaluated using a wide screening, like the National Hospital Interview Schedule for the assessment of GTS and related behavior82; this is a standardized, semistructured instrument that includes systematic assessment of personal and family history of GTS, ADHD, and obsessive compulsive behavior (OCB). The interview is conducted with the patient and a family member (usually a parent) who knows the patient well enough to give relevant details about childhood.

Several cases of secondary tourettism have been described in the literature. The causes have included postencephalic syndrome and carbon monoxide intoxication, and other causes have been degenerative or vascular75. Tourettism has also occurred secondary to trauma83, infection84, alcohol withdrawal85, or intake of certain drugs such as stimulants, anticholinergics, or antipsychotics86 87. In almost all patients there was a potential trigger event, such as drug exposure, viral or bacterial infection, physical trauma, cerebrovascular disease, or psychiatric illness prior to the onset of tic symptomatology. These may have acted as a trigger to unmask the symptoms in a constitutionally predisposed individual. In this regard, it is interesting to note that in 50% of cases there is either a personal or family history of GTS-related behavior. However, it is also possible that these represented secondary tics. It is now recognized that GTS has a genetic cause, with some studies suggesting an autosomal dominant transmission and others a mixed model88.

Goetz and coworkers in a study of 58 adult GTS patients diagnosed during childhood observed that childhood tic severity had no predictive value and that coprolalia did not increase the risk for severe tics in adult life89. Features predictive of mild tics in adulthood were mild tics during the patients' worst preadulthood function and mild tics during adolescence. The phenomenology of tics encountered in later life may also be somewhat different from those in early-onset GTS. For example, it has been reported reduced response to treatment (31%), a high degree of social morbidity (89%) and a low frequency of spontaneous complete remission in adult-onset cases. It seems that adult-onset tic disorder, whether idiopathic, secondary or a recurrence of childhood tics, may be different from younger-onset GTS.

A majority of patients exhibit OCB in childhood and have a positive family history of tics or OCB. It may also be noted that childhood rheumatic chorea may resolve only to return in late adult life89. Linazasoro and colleagues described a patient who had presented with only OCD since childhood but developed GTS symptoms at the age of 72 years and suggested that the expression of the gene may be different in the same patient during the course of his life90.
