Objective: To report a unique case of cocaine induced choreiform dyskinetic movements with literature review of this condition.

Background: Various abnormal movements have been known to occur with cocaine abuse. These typically involve stereotypical behaviors, dystonia, opsoclonus-myoclonus, exacerbation of tic disorders, and exacerbation of dystonic reactions to neuroleptics. Choreiform movements have been reported, although infrequently [1]. Typically, it is for 2-6 days duration [6]. Several cases have been reported with symptoms lasting over 15 years [9]. Akathisia and choreiform movements have been described more colloquially amongst illicit drug users as “crack dancing” [4]. Many of these symptoms are likely underreported. Most cases with choreiform movements following cocaine exposure have been associated with prior exposure to neuroleptics, amphetamines, or pre-existent brain disease [2] [10][11]. The case presented demonstrates a transient movement disorder of unusually short duration, without these preexisting conditions.

Methods: We report a case of sudden and brief choreiform dyskinesias in a patient, following first time cocaine ingestion.

Results: A 35 year-old right handed male presented with uncontrollable movements after a first-time cocaine use. Examination showed uncontrollable oral buccal lingual dyskinesia with choreoathetoid movements in all limbs. There were intermittent tic blinks in the both eyes. He had mild truncal dyskinesia with torso tilted to the left. This appeared at rest and improved with repositioning. There were no parkinsonian findings. The patient was able to ambulate without assistance, demonstrating normal stride pattern. His speech was fluent, with normal concentration and attention. His abnormal movements persisted into the evening and had completely resolved spontaneously by the next morning, less than 24 hours later.

Conclusions: Although the exact mechanism for cocaine induced choreoathetoid movements is unclear, this case suggests that an acute alteration in dopamine concentrations occurs at the level of the basil ganglia. The patient demonstrated features consistent with both an increase and decrease in dopamine levels. Whether these acute abnormal movements occur from dopamine concentration elevation, depression, or some combination of both, remains speculative. Regardless, it is important to recognize these transient physical findings in the acute setting and should raise high suspicion for cocaine exposure.

References: 1. Weiner WJ, Rabinstein A, Levin B, Weiner C, Shulman LM. Cocaine-induced persistent dyskinesias. Neurology 2001;56:964-965. 2. Pascual-Leone A, Dhuna A. Cocaine-associated multifocal tics. Neurology 1990;40:999-1000. 3. Valkow ND, Hitzemann R, Wang G-J, et al. Long-term frontal brain metabolic changes in cocaine abusers. Synapse 1992;11:184-190. 4. Daras M, Koppel BS, Atos-Radzion E. Cocaine-induced choreoathetoid movements (“crack dancing”). Neurology 1994;151:641-648. 5. Kumor K, Sherer M, Jaffe J. Haloperidol-induced dystonia in cocaine addicts. Lancet 1986;2:1341-1342. 6. Kamath S, Bajaj n. Crack Dancing in the United Kingdom: Apropos a Video Case Presentation. Movement Disorders 2007;8:1190-1191. 7. Bonnet U, Banger M, Wolstein J, et al. Choreoathetoid movements associated with rapid adjustment to methadone. Pharmacopsychiatry 1998:31;143-145. 8. D. Lussier. Choreiform movements after a single dose of methadone. J Pain Symptom Manage 2003;26:688-691. 9. Bartzokis G, Beckson M, Wirshing A, et al. Choreoathetoid Movements in Cocaine Dependence. Biological Psychiatry 1999;45:1630-1635. 10. Bennett BA, Hyde CE, Pecora JR, Clodfelter JE. Differing neurotoxic potencies of methamphetamine, mazindol, and cocaine in mesencephalic cultures. Neurochem 60:1444-1452.

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