A Case Report of Methylphenidate-Induced Dyskinesia.

Abstract

Sir: Movement disorders have long been associated with a wide variety of medications and illicit drugs. Dopaminergic agents are well-known precipitants of various dyskinesias, including chorea, choreoathetosis, dystonia, and ballism. For example, levodopa-induced dyskinesias are a relatively common side effect of the treatment of Parkinson's disease, with up to 45% of patients affected after 5 years of such treatment.1 Stimulants, such as methylphenidate, have also been associated with dyskinesias. Most case reports, however, implicate large dosages2 or chronic use of stimulant medications.3 Another recognized effect of methylphenidate is the development of motor tics in children.4 In contrast, the case presented here involves the acute development of choreoathetosis in an elderly patient after only 2 small doses of methylphenidate, with rapid resolution of the movement disorder following discontinuation of the offending agent. Case report. Mr. A is an 87-year-old man with a history of Parkinson's disease, hypothyroidism, and depression. He was admitted to the medical service for progressive weakness and inability to manage his activities of daily living. Mr. A had been diagnosed with Parkinson's disease over 10 years ago. Treatment consisted of 3 tablets of carbidopa/levodopa sustained release, 50 mg/200 mg 3 times per day. Historically, Mr. A's compliance had been suboptimal, but over the prior 6 months, in-home nursing had optimized compliance. The patient was euthyroid on treatment with levothyroxine, 125 mg/day. His depression had been treated successfully with sertraline, 50 mg/day, for approximately 3 years. Psychiatric consultation was requested to evaluate Mr. A for depression as an etiology for his observed “failure to thrive.” Psychiatric assessment revealed a thin, elderly appearing man lying comfortably in bed. A mild pill-rolling tremor and cogwheel rigidity were noted on physical examination. Mr. A denied a subjective feeling of depression and, despite obvious bradykinesia and masked facies, did not appear clinically depressed. However, he was quite cognitively impaired, scoring only 17/30 on the Folstein Mini-Mental State Examination.5 (Mr. A lost 6 points for time and place disorientation. Immediate recall was intact. Delayed recall was impaired, with loss of 2 points. Attention was impaired on serial 7s, resulting in the loss of 3 points. The last 2 points were lost due to inability to follow a simple 3-step command.) The admission laboratory tests included electrolytes, liver function, thyroid-stimulating hormone, and a complete blood count. The only abnormality found was a mild normocytic anemia, with a hemoglobin level of 11.4 g/dL. The consultation service assessed Mr. A's primary problem not as a depressive disorder, but rather as a dementing process coupled with advanced Parkinson's disease. A complete laboratory workup for reversible causes of dementia was negative, and a computed tomographic scan of the head revealed cerebral volume loss and areas of periventricular hypodensity. Mr. A was placed on treatment with methylphenidate, 2.5 mg twice per day, by the medical service to improve appetite and “mood.” After only 2 doses of methylphenidate, the patient was found to have significant choreoathetosis and a change in mental status consistent with a delirium. Methylphenidate was subsequently discontinued and quetiapine, 25 mg twice per day, was initiated. Carbidopa/levodopa administration was maintained, although the dosing schedule was adjusted to ensure 8 hours between each dose. Mr. A responded well to the discontinuation of the methylphenidate and the administration of small doses of quetiapine. He experienced a significant resolution of the dyskinesia and a clearing of the delirium. The patient was subsequently discharged to a rehabilitation facility. Methylphenidate, when given in therapeutic doses, has recently been shown to increase extracellular dopamine in the human brain.6 This capacity of methylphenidate to increase dopamine within the striatum is the proposed mechanism by which methylphenidate and other stimulants may induce movement disorders. Mr. A's case is complicated by the presence of Parkinson's disease and concurrent therapy with carbidopa/levodopa, an agent known to be associated with iatrogenic dyskinesia. However, the temporal relationship between the start of methylphenidate therapy and the onset of the movement disorder suggests that the stimulant is the etiologic agent behind the observed choreoathetosis. The damage to the basal ganglia inherent in Parkinson's disease may provide a predilection to the development of movement disorders with dopaminergic medications. The development of Mr. A's choreoathetosis early in the course of low-dose methylphenidate treatment may indicate the importance of a “primed” brain in the development of dyskinesia associated with various dopaminergic stimulant medications.