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Sir: Dopamine agonists, such as carbidopa-levodopa, have utility in alleviating symptoms of movement disorders, e.g., parkinsonism, and can reduce distressing movement disturbances arising from a variety of other conditions, e.g., restless legs syndrome, and tremor arising from head injury. We report a case illustrating that utilization of a dopamine agonist can precipitate tics in a patient with a clinically unrecognized history of tic disorder that had been in remission for years.  Case report. Mr. A, an 18-year-old man, was admitted to the hospital in late 2004 after sustaining multiple injuries from a motor vehicle accident. In addition to fractures, he had a left temporal contusion with intraventricular hemorrhage requiring ventriculostomy. After surgical intervention, he required intensive physical and occupational therapy and was admitted to the physiatry service to address his generalized deconditioning. A mild bilateral tremor was noted in both upper extremities, and although there was no associated cogwheel rigidity or bradykinesia, carbidopa-levodopa, 25 mg/100 mg t.i.d., was initiated.  After 2 days of treatment, psychiatric consultation was requested for “agitation.” Specifically, Mr. A was noted to blurt out obscenities in a recurrent and compulsive manner; this was uncharacteristic of him earlier in his hospital course or even prior to the head injury. In addition, he was noted to exhibit rapidly occurring head tossing, facial twitching, frowning, and grimacing repeatedly throughout the day. There were no changes in his cognitive functioning as compared with his condition in previous days, and he had no notable inattentiveness or fluctuations in consciousness. There were no associated mood disturbances, perceptual disturbances, or delusions. There were no electrolyte disturbances noted, no hypoxia, and no evidence of infection. Computed tomography scan of the head failed to reveal any progression of the original central nervous system injury. The psychiatric consultants recommended discontinuation of carbidopa-levodopa. Within 3 days of discontinuation, the aforementioned tics abated completely.  Collateral information provided by Mr. A's mother revealed that he had a remote history of childhood tics, at approximately 9 to 10 years of age, that appeared to have remitted entirely by the time he entered adolescence. He displayed transient mild vocal tics (e.g., throat clearing and barking, but never coprolalia) and mild motor tics (e.g., facial twitching), generally for weeks at a time and occasionally exacerbated by periods of distress. The tics never interfered with his personal or social life and reportedly were never severe enough to warrant formal dopamine antagonist therapy.  Tourette's disorder consists of a combination of vocal and multiple motor tics that generally develop early in childhood, often before 7 years of age, and persist for at least 1 year.1 There is wide variability in the presentation and severity of Tourette's disorder, i.e., number, type, and duration of symptoms.2 In milder variants of the disorder, symptoms often decrease as an individual proceeds through adolescence. Mild tic disorders may go unrecognized and fail to receive medical attention. The patient described herein lacked the symptom cluster consistent with classic Tourette's disorder and never required formal dopamine antagonist therapy. His symptoms appeared to be consistent with the variant classified as transient tic disorder.1  Dopaminergic excess has been postulated to underlie the pathophysiology of Tourette's disorder.2,3 This postulation has been based upon the observation that dopamine antagonists mitigate tics, while dopamine agonists, e.g., levodopa, and stimulants, e.g., methylphenidate, may exacerbate them.3,4 However, data are emerging that suggest that dopamine agonists may have a role in reducing tic severity.5 Such conflicting lines of evidence suggest that much has yet to be learned about the pathophysiology of Tourette's disorder and its variants.  What is striking in the case presented here is that administration of levodopa appeared to result in a recrudescence of a previously dormant tic disorder. The temporal relationship between the initiation of carbidopa-levodopa and the onset of motor and vocal tics in this patient, along with the rapid cessation of symptoms shortly after drug discontinuation, suggests that the medication was responsible for the tic recrudescence observed in our patient. It is possible that the central nervous system injury sustained may have rendered him vulnerable to untoward effects of dopamine augmentation. Use of dopamine agonists in medical and/or surgical patients can potentially complicate their clinical course, particularly if a current or remote history of tic disorder is overlooked or ignored.

Carbidopa-Levodopa-Induced Recrudescence of Premorbid Tic Disorder in Remission