Trial of Ropinirole in Motor Recovery After Stroke - Full Text View

Sponsor:	University of California, Irvine
Collaborator:	GlaxoSmithKline
Information provided by:	University of California, Irvine
ClinicalTrials.gov Identifier:	NCT00221390

Purpose

The purpose of this study is to assess efficacy, as well as safety, of Ropinirole in improving movement among patients with chronic stroke.

Condition	Intervention	Phase
Cerebrovascular Accident Hemiparesis	Drug: Ropinirole (+ physical therapy) Drug: (vs.) Placebo + physical therapy	Phase II

Study Type:	Interventional
Study Design:	Allocation: Randomized Endpoint Classification: Safety/Efficacy Study Intervention Model: Parallel Assignment Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor) Primary Purpose: Treatment
Official Title:	Randomized, Placebo-Controlled, Double-Blind Pilot Trial to Evaluate the Safety and Efficacy of Ropinirole in Motor Recovery After Stroke

Resource links provided by NLM:

Drug Information available for: Ropinirole hydrochloride Ropinirole

U.S. FDA Resources

Further study details as provided by University of California, Irvine:

Secondary Outcome Measures:

Barthel Index [ Time Frame: Measured at weeks 1, 9, and 12 ] [ Designated as safety issue: Yes ]
Leg motor Fugl-Meyer scale [ Time Frame: Measured at baseline and weeks 1, 2, 4, 6, 7, 8, 9, and 12 ] [ Designated as safety issue: Yes ]
Stroke Impact Scale-16 [ Time Frame: Measured at weeks 1, 4, 7, 9, and 12 ] [ Designated as safety issue: Yes ]
Gait endurance [ Time Frame: Measured at weeks 1, 2, 4, 6, 7, 8, 9, and 12 ] [ Designated as safety issue: Yes ]
Hamilton Depression Scale [ Time Frame: Measured at baseline and weeks 1, 2, 9, and 12 ] [ Designated as safety issue: Yes ]
Safety [ Time Frame: 12 weeks ] [ Designated as safety issue: Yes ]

Estimated Enrollment:	52
Study Start Date:	October 2003
Study Completion Date:	May 2007
Primary Completion Date:	February 2007 (Final data collection date for primary outcome measure)

Detailed Description:

Stroke is a leading cause of disability. Current treatments target injury and must be delivered within hours. A body of literature suggests that there are processes ongoing days-months after stroke that can be targeted therapeutically, and improve function. The current study evaluates one such potential therapy, the dopamine agonist ropinirole. The current study tests the hypothesis that patients with chronic stroke randomized to ropinirole+physiotherapy will show improved gait velocity over the 12 weeks of study participation as compared to patients randomized to placebo+physiotherapy. A secondary aim is to test the hypothesis that ropinirole will improve three secondary endpoints at 12 weeks after study entry: the proportion of patients with no significant disability (Barthel Index ≥ 95); overall motor status, measured with the arm/leg FM score; and overall physical function, defined as the score on the Stroke Impact Scale-16 (SIS-16). This study will also evaluate the safety of ropinirole in patients recovering from stroke.

Eligibility

Ages Eligible for Study:	18 Years and older
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

Inclusion Criteria:

Stroke onset 4 weeks-12 months prior
Stroke is radiologically confirmed as either (a) ischemic or (b) hemorrhagic
Minimum age 18
No significant pre-stroke disability
No other stroke in previous 3 months
Absence of major depression
Fugl-Meyer (FM) motor score of 23-83 out of 100
Functional Independence Measure (FIM) ambulation-subscore of 3 or more, and 50 foot walk takes longer than 15 seconds

Exclusion Criteria:

Significant daytime somnolence or any substantial decrease in alertness, language reception, or attention
Pregnant or lactating
Advanced liver, kidney, cardiac, or pulmonary disease
Orthostatic hypotension
Current use of ciprofloxacin, a centrally acting dopamine agonist, or a centrally active dopamine antagonist
A terminal medical diagnosis consistent with survival < 1 year
Coexistent major neurological disease
Coexistent major psychiatric disease
A history of significant alcohol or drug abuse in the prior 3 years
A coexistent disease characterized by an abnormality of CNS dopaminergic tone
Current enrollment in another investigational study related to stroke or stroke recovery
Contraindication to ropinirole prescription

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00221390

Locations

United States, California
University of California, Irvine Medical Center
Orange, California, United States, 92868

Sponsors and Collaborators

University of California, Irvine

GlaxoSmithKline

Investigators

Principal Investigator:

Steven C Cramer, MD

University of California, Irvine

More Information

Publications:

1. Gresham GE, Duncan PW, Stason WB, Adams HP, Adelman AM, Alexander DN, Bishop DS, Diller L, Donaldson NE, Granger CV, Holland AL, Kelly-Hayes M, McDowell FH, Myers L, Phipps MA, Roth EJ, Siebens HC, Tarvin GA, Trombly CA. Post-Stroke Rehabilitation. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research, 1995. 2. Rathore SS, Hinn AR, Cooper LS, Tyroler HA, Rosamond WD. Characterization of incident stroke signs and symptoms: findings from the atherosclerosis risk in communities study. Stroke 2002;33:2718-21. 3. Dobkin BH. Neurologic Rehabilitation. Philadelphia: FA Davis, 1996. 4. Nudo RJ. Recovery after damage to motor cortical areas. Curr Opin Neurobiol 1999;9:740-7. 5. Cramer SC, Chopp M. Recovery recapitulates ontogeny. Trends Neurosci 2000;23:265-71. 6. Finklestein S, Campbell A, Baldessarini RJ, Moya KL, Haber SN. Late changes in cerebral monoamine metabolism following focal ventrolateral cerebrocortical lesions in rats. Brain Res 1985;344:205-10. 7. Finklestein S, Campbell A, Stoll AL, Baldessarini RJ, Stinus L, Paskevitch PA, Domesick VB. Changes in cortical and subcortical levels of monoamines and their metabolites following unilateral ventrolateral cortical lesions in the rat. Brain Res 1983;271:279-88. 8. Boyeson MG, Feeney DM. Striatal dopamine after cortical injury. Exp Neurol 1985;89:479-83. 9. Stroemer RP, Kent TA, Hulsebosch CE. Enhanced neocortical neural sprouting, synaptogenesis, and behavioral recovery with D-amphetamine therapy after neocortical infarction in rats. Stroke 1998;29:2381-95. 10. Cramer SC, Nelles G, Benson RR, Kaplan JD, Parker RA, Kwong KK, Kennedy DN, Finklestein SP, Rosen BR. A functional MRI study of subjects recovered from hemiparetic stroke. Stroke 1997;28:2518-27. 11. Feeney DM, Gonzalez A, Law WA. Amphetamine, Halperidol, and experience interact to affect the rate of recovery after motor cortex injury. Science 1982;217:855-857. 12. Gladstone DJ, Black SE. Enhancing recovery after stroke with noradrenergic pharmacotherapy: a new frontier? Can J Neurol Sci 2000;27:97-105. 13. Goldstein LB. Potential impact of drugs on poststroke motor recovery. In: L. B. Goldstein, ed. Restorative Neurology. Advances in pharmacotherapy for recovery after stroke. Armonk, NY: Futura Publishing Co., 1998:241-256. 14. Scheidtmann K, Fries W, Muller F, Koenig E. Effect of levodopa in combination with physiotherapy on functional motor recovery after stroke: a prospective, randomised, double-blind study. Lancet 2001;358:787-790. 15. Sullivan KJ, Knowlton BJ, Dobkin BH. Step training with body weight support: effect of treadmill speed and practice paradigms on poststroke locomotor recovery. Arch Phys Med Rehabil 2002;83:683-91. 16. Richards C, Malouin F, Dumas F, Tardif D. Gait velocity as an outcome measure of locomotor recovery after stroke. In: C. R and O. C, eds. Gait Analysis: Theory and Application. St. Louis: Mosby, 1995:355-364. 17. Potter JM, Evans AL, Duncan G. Gait speed and activities of daily living function in geriatric patients. Arch Phys Med Rehabil 1995;76:997-9. 18. Nieoullon A. Dopamine and the regulation of cognition and attention. Prog Neurobiol 2002;67:53-83. 19. Medico M, De Vivo S, Tomasello C, Grech M, Nicosia A, Castorina M, D'Agata MA, Rampello L, Lempereur L, Drago F. Behavioral and neurochemical effects of dopaminergic drugs in models of brain injury. Eur Neuropsychopharmacol 2002;12:187-94. 20. Bracha HS, Lyden PD, Khansarinia S. Delayed emergence of striatal dopaminergic hyperactivity after anterolateral ischemic cortical lesions in humans; evidence from turning behavior. Biol Psychiatry 1989;25:265-74. 21. Nutt JG, Fellman JH. Pharmacokinetics of levodopa. Clin Neuropharmacol 1984;7:35-49.

Additional publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):

Cramer SC, Dobkin BH, Noser EA, Rodriguez RW, Enney LA. Randomized, placebo-controlled, double-blind study of ropinirole in chronic stroke. Stroke. 2009 Sep;40(9):3034-8. Epub 2009 Jun 11.

Responsible Party:	Steven C. Cramer, MD, MMSc, University of California, Irvine
ClinicalTrials.gov Identifier:	NCT00221390 History of Changes
Other Study ID Numbers:	HS#2003-3096
Study First Received:	September 19, 2005
Last Updated:	June 19, 2008
Health Authority:	United States: Institutional Review Board

Keywords provided by University of California, Irvine:

stroke
Chronic stroke with hemiparesis

Additional relevant MeSH terms:

Paresis
Cerebral Infarction
Stroke
Neurologic Manifestations
Nervous System Diseases
Signs and Symptoms
Brain Infarction
Brain Ischemia
Cerebrovascular Disorders
Brain Diseases
Central Nervous System Diseases
Vascular Diseases

Cardiovascular Diseases
Ropinirole
Antiparkinson Agents
Anti-Dyskinesia Agents
Central Nervous System Agents
Therapeutic Uses
Pharmacologic Actions
Dopamine Agonists
Dopamine Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action
Physiological Effects of Drugs

ClinicalTrials.gov processed this record on February 12, 2012