It is just 3 or 4 weeks after my diagnosis of Tourette syndrome (TS). I have been slowly and conscientiously titrating upward the dose of medication prescribed by my neurologist, waiting skeptically, but not without hope, for some amelioration of my tics. A typical scientist/patient, I have downloaded all available information about this drug from the Internet and have been recalculating the increasing dose in mg/kg body weight every few days. Today I have ducked out of my lab and am doing a very hard training run along the Muddy River in Boston, gearing up for my 21st year of spring and summer races, when I am caught unprepared by a flash of insight. I am speeding along the path with a smoothness and crispness of rhythm that I have seldom felt—maybe just one of those rare great days?—when it occurs to me that I am taking a good deep breath every four strides, in-and-out without fail, every four strides. And only at that moment do I realize that I have always suffered from “skipping” breaths, even on the hardest runs, and have always taken it for granted. Indeed, I have always assumed that all other runners' breathing is as ragged as my own. But now—how remarkable!—I am not missing a single precious breath. This, I realize, is because my phonic tic is gone. So my teammates and competitors must have never missed those breaths, not a single one, because they don't have TS!

Over the past century researchers have attributed the symptoms that today are labeled as Tourette syndrome to various etiologies. Although most investigators have accepted Gilles de la Tourette's initial description of a symptom complex of tics and involuntary vocalizations, most have rejected his claim that “tic disease” resulted from hereditary degeneration. Subsequent investigators have offered an array of contradictory etiological explanations including viewing these symptoms as a subset of choreas, a result of insufficient inhibition, a failure to control infantile habits, a sequel to encephalitis and other infections, or the result of unconscious psychosexual childhood conflict. With the advent of effective pharmacologic treatments in the 1960s, psychiatrists, often urged on by the parents of afflicted children, began to insist that the disorder resulted from organic factors, most likely connected to transmission of the neurotransmitter dopamine and signaling in the basal ganglia. Since the 1970s, research has focused on a variety of possible organic substrates, but disputes over which symptoms to include in the syndrome's phenotype continue to constrain efforts to locate its etiology.

Tic disorders may manifest in a wide variety of clinical presentations, ranging from single tics of relatively short duration to a series of complex tics that may last for years. An understanding of the etiology of various tic disorders is essential to establish a differential diagnosis of Tourette syndrome (TS). Because TS is incurable, improvement in quality of life is the primary goal of pharmacologic therapy. Although neuroleptics have been the most effective medications to date in managing the symptoms of TS, they may have significant adverse effects that limit their use. Several alternative pharmacologic options are either available or under investigation.

Tourette syndrome (TS) has been conceptualized as a psychological problem, a neurological problem, and more recently a neurobehavioral problem. Each conceptual model has had an impact on how persons with TS view themselves and how practitioners view individuals with TS, as well as an impact on what both clinicians and patients expect from diagnosis and treatment. This article reviews the common comorbid psychiatric disorders and their relationship to TS, and discusses how the evolving conceptions of TS have impacted psychologically on persons with tics and TS, as well as on the providers who treat them.

Sydenham's chorea is currently recognized as the only neurologic sequela of rheumatic fever. Recent evidence suggests that there may be a spectrum of neurobehavioral disturbances, particularly including tics and obsessive-compulsive disorder, that develops following streptococcal infection by the process of molecular mimicry, whereby antibodies directed against bacterial antigens cross-react with brain targets. This proposed postinfectious, immune-mediated condition has been termed “pediatric autoimmune neuropsychiatric disorders after streptococcal infection” (PANDAS). This article reviews research evidence in favor and also against the PANDAS concept and discusses the implications of the hypothesis.

Stemming from the finding that nicotine potentiates haloperidol-induced catalepsy in rats, nicotine in the form of nicotine gum and as transdermal nicotine patch (TNP) has been used in open-label studies to obtund motor and vocal tics of children (age≥8 years, weighi≥25 kg), adolescents, and adults. Reduction of tics was seen during chewing of nicotine gum; the improvement lasted no longer than 1 hour after chewing. With a TNP in subjects who were not responding well to a variety of dopamine blockers, with some also receiving clonidine or a variety of selective serotonin reuptake inhibitors, motor and vocal tics were obtunded 45% over baseline in 85% of 35 subjects within 30 minutes to 3 hours after TNP application. Moreover, the relief of symptoms with a single 7-mg TNP, remaining on the skin for 24 hours, persisted for a variable period of time ranging from 1 to 120 days with an average of 10±2 days. Application of a second TNP for 24 hours when symptoms began to return resulted in a similar reduction in tic severity and frequency, which persisted an average of l3±3 days. Nicotine alone, without D2 blockers, was successful in reducing premonitory urges to tic. After follow-up of 3 to 5 years, 19 of 35 patients continued to use the TNP in gradually decreasing frequency and with gradual reduction in dose of D2 blockers. However, 16 patients (45%), as they grew into middle adolescence, discontinued use of the TNP, stating that they objected to the nausea induced by the patch. There was no evidence of habituation to nicotine. Side effects were not life threatenting; the most disturbing side effect was nausea, appearing 1 to 4 hours after the application of the patch and lasting 1 to 3 hours. There was no change in blood pressure; pulse rate increased from 5 to 10% within 3 hours but returned to baseline after 24 hours. Unsolved problems using TNP are mentioned and a putative mechanism for nicotine effectiveness in Tourette syndrome is briefly discussed.

There is a well-established overlap in phenomenology between anorexia nervosa and obsessive-compulsive disorder, and between obsessive-compulsive symptoms and Tourette syndrome (TS). Five cases of eating disorders in patients with obsessive-compulsive symptoms and TS are presented. The identification of four similar cases in the literature putatively marks a subset of eating disorders with a link to TS and to obsessive-compulsive symptomatology. This association may reflect a common underlying neurobiologic imbalance.