Novel rat cardiac arrest model of posthypoxic myoclonus

Authors

  • Dr. Daniel D. Truong,

    Corresponding author
    1. Parkinson's and Movement Disorders Research Laboratory, Department of Neurology, California College of Medicine, University of California Irvine, Irvine, U.S.A.
    • University of California Irvine, College of Medicine, Department of Neurology, 154 Med Surge I, Irvine, CA 92717-4290, U.S.A.
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  • Rae R. Matsumoto,

    1. Parkinson's and Movement Disorders Research Laboratory, Department of Neurology, California College of Medicine, University of California Irvine, Irvine, U.S.A.
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  • Philip H. Schwartz,

    1. Parkinson's and Movement Disorders Research Laboratory, Department of Neurology, California College of Medicine, University of California Irvine, Irvine, U.S.A.
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  • Matthew J. Hussong,

    1. Parkinson's and Movement Disorders Research Laboratory, Department of Neurology, California College of Medicine, University of California Irvine, Irvine, U.S.A.
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  • Claude G. Wasterlain

    1. Departments of Neuroscience and Neurology, School of Medicine, University of California Los Angeles, Los Angeles, U.S.A.
    2. Epilepsy Research Laboratories, Veterans Administration Medical Center, Sepulveda, California, U.S.A.
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Abstract

We describe the time course of and pharmacology associated with auditory-induced muscle jerks following cardiac arrest in rats. The data indicate that several key features of this model mimic those of human posthypoxic myoclonus. Similar to the human form, the muscle jerks appear in the rats following an acute hypoxic episode (cardiac arrest). Initially, it is known that both spontaneous and auditory-induced myoclonus are present in these animals; some cardiac-arrested rats also exhibit seizures. Over the first few days after the arrest, episodes of both the seizure activity and spontaneous myoclonus disappear. The auditory-induced myoclonus continues to worsen, reaches a peak about 2 weeks after the arrest, then declines over time to subnormal levels. The auditory-induced muscle jerks exhibited by the cardiac arrested animals are attenuated by the typical antimyoclonic drugs 5-hydroxytryptophan, valproic acid, and clonazepam. In addition, the novel anticonvulsant felbamate was found to have antimyoclonic properties. The data suggest that this rat cardiac arrest model may be a valuable tool for investigating the pathophysiologic mechanisms of posthypoxic myoclonus and for developing new therapeutic strategies for treating the disorder.

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