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Effect of Nimodipine on the Cerebral Circulation and Acute Ischemic Stroke

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New Trends in Diagnosis and Management of Stroke

Abstract

Current research suggests that cerebral ischemia induces a cascade of pathophysiological reactions, with a massive influx of calcium into the neuron as the “final common pathway”, resulting in catabolism and cell necrosis due to calcium overload. Treatment with calcium entry blockers, therefore, may be a new approach to arresting, and possibly preventing, destruction of cerebral tissue in stroke patients. The calcium entry blocker nimodipine was found to inhibit selectively spasms of the isolated cerebral arteries, produced either by depolarization or by receptor stimulation. In vivo experiments demonstrated that postischemic impairment of cerebral blood flow, which may be a major contributor to neuronal damage, is prevented.

After encouraging, although not conclusive, results of a single-blind pilot study, further clinical studies were undertaken and a double-blind, placebo-controlled, multicenter study was conducted. The data from this study strongly suggest that patients with acute ischemic stroke benefit from treatment with 120 mg nimodipine, started with 24 h after onset, combined with a “Standard” treatment, e. g., hemodilution by low molecular weight dextran. The conclusion so far is that calcium entry blockers such as nimodipine, may be useful in the treatment of patients with acute ischemic stroke.

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© 1987 Springer-Verlag Berlin Heidelberg

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Gelmers, H.J., Wiezer, J.H.A., de Weerdt, C.J., Gorter, K. (1987). Effect of Nimodipine on the Cerebral Circulation and Acute Ischemic Stroke. In: Poeck, K., Ringelstein, E.B., Hacke, W. (eds) New Trends in Diagnosis and Management of Stroke. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72996-6_11

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  • DOI: https://doi.org/10.1007/978-3-642-72996-6_11

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-18369-3

  • Online ISBN: 978-3-642-72996-6

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