ORIGINAL ARTICLE Tetrabenazine Treatment in Movement Disorders D. Paleacu, MD,* N. Giladi, MD,† O. Moore, RN, MA,† A. Stern, MD,‡ S. Honigman, MD,‡ and S. Badarny, MD‡ Abstract: Tetrabenazine (TBZ) is a catecholamine depletor used for the treatment of a variety of movement disorders. The purpose of this study was to assess the efficacy of TBZ in a retrospective chart review in 3 tertiary care movement disorders centers over long-term treat- ment. Of 150 patients to whom TBZ was prescribed, 118 were fol- lowed up and assessed using the Clinical Global Impression of Change (CGIC), (-3 to +3), a composite grade from a patient and caregiver scale over variable periods. The patients had a variety of hyperkinetic movement disorders including dystonia (generalized and focal: axial, Meige syndrome, torticollis, blepharospasm, brux- ism), Huntington disease (HD) or other choreas, tardive dyskinesia (TD) or akathisia, and Tourette syndrome. Mean patient age was 48.8 ± 18.7 years; 48 were men (40.7%) with a mean disease duration of 93 months. The mean follow-up time was 22 months and the mean TBZ dose was 76.2 ± 22.5 mg/d (median 75 mg, range 25–175 mg/d). The mean CGIC score was +1 (mild improvement). The group of patients who scored +3 on the CGIC (very good improvement) rep- resented 18.6% (n = 22) of all patients. They had HD or other types of chorea 7.6% (n = 9), facial dystonia/dyskinesia (n = 7, 5.9%), 1 with TD, 2 with trunk dystonia, 2 with Tourette syndrome, and 1 with tar- dive akathisia. This group had the longest treatment duration and re- ceived a mean TBZ dose of 70.5 mg/d (median 75 mg/d) for a mean of 25.4 ± 21.3 months. The report concludes that TBZ is a moderately effective treatment of a large variety of hyperkinetic movement dis- orders, with excellent effects in a subgroup with chorea and facial dystonia/dyskinesias. Key Words: movement disorders, treatment, tetrabenazine (Clin Neuropharmacol 2004;27:230–233) M ost hyperkinetic movement disorders benefit from treat- ment with antidopaminergic therapy, mainly dopamine receptor blockers, whose deleterious influence, expressed as tardive syndromes during long-term therapy, is well known. From this derives the need for drugs with other mechanisms of action. Tetrabenazine (TBZ), a benzoquinolizine derivative, is a catecholamine depletor 1 used in the treatment of a variety of movement disorders. Initially it was used as an antipsychotic drug in schizophrenia but it was later superseded by the phe- nothiazines 2 and reappraised in the late 1960s as an antidyski- netic drug. During the past 2 decades TBZ has been used in a mul- titude of movement disorders: tardive dyskinesia (TD), 3–6 dys- tonia 7–9 and tremor, 10 choreic syndromes, 11,12 primary 8,9,13–15 or secondary dystonia, 16 and tic disorders. 17–22 We report our experience of a long-term treatment and follow-up with TBZ from 3 tertiary movement disorders clin- ics. Our goal was to assess the efficacy of TBZ as an add-on or single therapy in patients with various hyperkinetic movement disorders. PATIENTS AND METHODS TBZ was prescribed to 150 patients during the period of December 1998–December 2002, who were assessed at 1 of 3 tertiary clinics (the Neurology Service at Abarbanel Mental Health Center; the Movement Disorders Unit, Department of Neurology, Tel Aviv Medical Center; and the Movement Dis- orders Clinic, Department of Neurology, Carmel Medical Cen- ter). TBZ was prescribed using a special form (29G) approved by the Israeli Ministry of Health that enables a patient by name to receive a drug that is not listed in the Israeli Pharmacopoeia. TBZ was prescribed at a starting dose of 12.5 mg BID, augmenting the daily dose in increments of 25 mg once a week to a target dose of 150 mg/d in 2 or 3 divided doses daily. Augmentation above this dose was considered if no favorable effects were reported and no side effects were observed. It is worthwhile mentioning that in most patients TBZ was the 2nd or 3rd line of treatment following treatment with anticholiner- gics or benzodiazepines. None of our patients received botuli- num toxin before TBZ treatment was instituted. All eligible patients (n = 121) were interviewed (by tele- phone, n = 38; or at their follow-up visit, n = 83) regarding treatment duration, dose, effect of treatment, and the cause for interrupting the treatment or side effects. The effect of treat- ment was assessed by the Clinical Global Impression of Change (CGIC), where -3 was marked worsening, -2 moder- From the *Neurology Service and Memory Clinic, Abarbanel Mental Health Center, Bat-Yam, affiliated to the Sackler School of Medicine, Tel Aviv University; †Movement Disorders Unit, Department of Neurology, Tel Aviv Medical Center and Sackler School of Medicine, affiliated to the Tel Aviv University; and ‡Movement Disorders Clinic, Department of Neu- rology, Carmel Medical Center, Haifa, affiliated to the Rappoport Faculty of Medicine, Technion, Haifa, Israel. Reprints: Diana Paleacu, MD, Neurological Service and Memory Clinic, Abarbanel Mental Health Center, 15 Keren Kayemet, 59110 Bat Yam, Israel (e-mail: paleacu@post.tau.ac.il). Copyright © 2004 by Lippincott Williams & Wilkins 230 Clin Neuropharmacol • Volume 27, Number 5, September - October 2004