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at time of writing, PharmD Student College of Pharmacy and Health Sciences Mercer University Atlanta, Georgia now, Pharmacy Practice Resident Atlanta Medical Center Atlanta
Director of Pharmacyc Dekalb Regional Crisis Center Decatur, Georgia
Associate Professor Clinical and Administrative Sciences College of Pharmacy and Health Sciences Mercer University 3001 Mercer University Drive Atlanta, Georgia 30341-4155 fax 678/547-6384 Kissack_jc{at}mercer.edu
Published Online, June 27, 2006. www.theannals.com, DOI 10.1345/aph.1G596
Case Report. A 26-year-old Hispanic male was admitted to a psychiatric crisis center. He displayed pressured speech, auditory hallucinations, paranoia, and erratic movements of the shoulders, head, and nose. The patient reported a previous diagnosis of bipolar II disorder and obsessive-compulsive disorder but was otherwise healthy with no substance abuse history. He stated that he had not taken any medications for 1 week. Prior to that time, he had taken valproic acid 500 mg/day, olanzapine 2.5 mg/day, and escitalopram (dose unknown). On admission, he was started on extended-release valproic acid 500 mg at bedtime, as well as quetiapine 50 mg twice daily and 25 mg every 4 hours as needed for agitation. Olanzapine was not reinitiated because of its adverse effect profile. On day 3 of treatment, the valproic acid dose was increased to 1250 mg at bedtime, based on a subtherapeutic concentration of 27 L (normal range 50-100), and the quetiapine dose was increased to 200 mg every morning and 400 mg at bedtime. The physician noted that his patient's anxiety had decreased, but involuntary movements, including blinking, shoulder shrugging, and a vocal tic, manifested as coughing/throat clearing became more evident. The patient was diagnosed with a tic disorder not otherwise specified. On day 6, both vocal and motor tics decreased significantly.
Discussion. Quetiapine has been described as a clozapine-like atypical antipsychotic because of its low affinity for dopamine D2 receptors. Quetiapine is a weak antagonist of D2, with a low incidence of adverse reactions like extrapyramidal symptoms, tardive dyskinesia, and endocrine symptoms. Dopamine antagonism is thought to play a role in the treatment of tics. The mechanism of action of quetiapine in the treatment of tic disorders cannot be fully explained by dopamine antagonism. The blockade of receptor subtypes such as the D4 and/or serotonin (5-HT6) receptor5 or selective inactivation of mesolimbic cortical dopamine neurons producing an alteration in the expression of excitatory amino acids3 may explain quetiapine's benefit in Tourette's syndrome.
Limitations to our observations include the loss of the patient to
follow-up, concurrent use of valproic acid, waxing and waning of the tic
disorder, and subjective reports of improvement. Valproic acid is not used in
the treatment of tics, and the mechanism of action is generally unknown.
However, it may attenuate the inhibitory neurotransmitter 
-aminobutyric
acid and subsequently inhibit dopamine. When combined with quetiapine, this
action may enhance the inhibition of tics. The use of quetiapine in the
management of tic disorders is controversial but may have the advantage of a
lower incidence of adverse reactions, compared with traditional dopamine
antagonists used in tic disorders.
Footnotes
Dr. Kissack is on the AstraZeneca Speaker's Bureau.
We thank Diane Nykamp PharmD for her editorial comments.
References
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