Streptococcus and Tics: Another Brick in the Wall?

Tourette syndrome (TS) is a neurodevelopmental condition characterized by multiple tics. Tics are the most common hyperkinetic manifestations in youth, often causing physical discomfort, emotional distress, social difficulties, and interference with education and desired activities. It has been established that tic severity does not remain constant, but fluctuates over time in a typical waxing and waning pattern. Moreover, patients with TS frequently present with challenging neuropsychiatric comorbidities, most notably obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD).1 Despite its epidemiologic relevance and its potential effect on patients’ health-related quality of life, there are still several crucial known unknowns about TS. Specifically, the clinical management of TS continues to be difficult, as the genetics, neurophysiology, and neuropathology of this disorder are largely unknown.2 As in most neuropsychiatric conditions, it is thought that both genetic and environmental factors are likely to play a role as etiologic mechanisms: the commonly agreed view is that “the genes load the gun and the environment pulls the trigger.” Among the environmental factors, prenatal and perinatal difficulties, as well as hormonal and immunologic contributions, have emerged as promising candidates. Over the past 2 decades, group A Streptococcus (GAS) has been investigated as a possible environmental agent associated with tic disorders. Isolated clinical observations, interpreted in the light of the established motor presentation of Sydenham chorea, have suggested the inclusion of tic disorders as a collateral feature within a group of conditions called pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS).3 PANDAS are currently incorporated in the broader concept of pediatric acute neuropsychiatric syndromes.4 The link between Streptococcus and tics is the subject of intense debate, as a few longitudinal clinical studies including mixed populations of PANDAS and chronic tic disorders found that tic exacerbations were unrelated to GAS infection in the majority of cases.5,6 Interestingly, the results of a case–control study of a large primary care database also led to arguing against this association.7

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