Open Access Highly Accessed Research article

Acute posthypoxic myoclonus after cardiopulmonary resuscitation

Aline Bouwes12*, Daniël van Poppelen1, Johannes HTM Koelman3, Michael A Kuiper14, Durk F Zandstra5, Henry C Weinstein26, Selma C Tromp7, Eveline GJ Zandbergen8, Marina AJ Tijssen39 and Janneke Horn1

Author Affiliations

1 Department of Intensive Care, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, The Netherlands

2 Department of Neurology, Sint Lucas Andreas Hospital, Amsterdam, The Netherlands

3 Department of Neurology and Clinical Neurophysiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

4 Department of Intensive Care, Medical Center Leeuwarden, Leeuwarden, The Netherlands

5 Department of Intensive Care, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands

6 Alzheimer Center, Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands

7 Department of Clinical Neurophysiology, St. Antonius Hospital, Nieuwegein, The Netherlands

8 Department of Neurology, Rijnstate Hospital, Arnhem, The Netherlands

9 Department of Neurology, University Medical Center Groningen, Groningen, The Netherlands

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BMC Neurology 2012, 12:63  doi:10.1186/1471-2377-12-63

Published: 1 August 2012



Acute posthypoxic myoclonus (PHM) can occur in patients admitted after cardiopulmonary resuscitation (CPR) and is considered to have a poor prognosis. The origin can be cortical and/or subcortical and this might be an important determinant for treatment options and prognosis. The aim of the study was to investigate whether acute PHM originates from cortical or subcortical structures, using somatosensory evoked potential (SEP) and electroencephalogram (EEG).


Patients with acute PHM (focal myoclonus or status myoclonus) within 72 hours after CPR were retrospectively selected from a multicenter cohort study. All patients were treated with hypothermia. Criteria for cortical origin of the myoclonus were: giant SEP potentials; or epileptic activity, status epilepticus, or generalized periodic discharges on the EEG (no back-averaging was used). Good outcome was defined as good recovery or moderate disability after 6 months.


Acute PHM was reported in 79/391 patients (20%). SEPs were available in 51/79 patients and in 27 of them (53%) N20 potentials were present. Giant potentials were seen in 3 patients. EEGs were available in 36/79 patients with 23/36 (64%) patients fulfilling criteria for a cortical origin. Nine patients (12%) had a good outcome. A broad variety of drugs was used for treatment.


The results of this study show that acute PHM originates from subcortical, as well as cortical structures. Outcome of patients admitted after CPR who develop acute PHM in this cohort was better than previously reported in literature. The broad variety of drugs used for treatment shows the existing uncertainty about optimal treatment.

Coma; Anoxic; Myoclonus; Adult; Electroencephalography; Evoked potentials