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(Stroke. 1999;30:1417-1423.)
© 1999 American Heart Association, Inc.

Original Contributions

Nimodipine and Perfusion Changes After Stroke

Presented in part at the 1996 Annual Scientific Meeting of the Stroke Society of Australasia, Adelaide, Australia, October 2–4, 1996, and at the 1997 Annual Scientific Meeting of the Australian Association of Neurologists and Association of British Neurologists, Sydney, Australia, April 29 to May 2, 1997.

Bernard Infeld, MB, BS, FRACP; Stephen M. Davis, MD, FRACP; Geoffrey A. Donnan, MD, FRACP; Masahiro Yasaka, MD; Meir Lichtenstein, MB, BS, FRACP; Peter J. Mitchell, MB, BS, FRACR Gregory J. Fitt, MB, BS, FRACR

From the Departments of Neurology (B.I., S.M.D.), Nuclear Medicine (M.L.), and Radiology (P.J.M.), Royal Melbourne Hospital; and Departments of Neurology (G.A.D., M.Y.) and Radiology (G.J.F.), Austin and Repatriation Medical Center, Melbourne, Australia.

Background and Purpose—Meta-analysis of previous trials of oral nimodipine in acute stroke has suggested a benefit when commenced within 12 hours of onset. We sought to study the effect of oral nimodipine on reperfusion after acute stroke and the relation between reperfusion and outcome.

Methods—Fifty patients with acute middle cerebral artery territory cortical infarction were blindly randomized within 12 hours of onset to either oral nimodipine (30 mg every 6 hours) or placebo. Treatment was continued for 2 weeks. Cerebral blood flow was assessed with the use of ^99mTc–hexamethylpropyleneamine oxime single-photon emission CT before therapy, 24 hours later, and at 3 months. Hypoperfusion was measured by a validated volumetric technique. Neurological impairment and functional outcome were assessed with the Canadian Neurological Scale and Barthel Index, respectively. Tissue loss was measured with CT at 3 months. Four patients were excluded from analysis for technical reasons.

Results—Twenty-three patients received nimodipine, and 23 received placebo. In the nimodipine group, there was early reperfusion that was not maintained at outcome (P=0.01). In the placebo group, mean infarct hypoperfusion volumes showed no overall change. Nonnutritional reperfusion in nimodipine-treated patients was associated with adverse neurological (P=0.05) and functional outcome (P=0.06). There was, however, no difference in clinical outcome between the 2 groups.

Conclusions—Oral nimodipine administered within 12 hours enhanced acute reperfusion, but this was largely nonnutritional. Larger studies using a shorter treatment delay are required to evaluate the clinical efficacy of nimodipine in acute ischemic stroke.

Key Words: calcium channel blockers • cerebral blood flow • cerebrovascular disorders • nimodipine • reperfusion • tomography, emission computed

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