Abstract

BackgroundAcute 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).MethodsPatients 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.ResultsAcute 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.ConclusionsThe 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.

Highlights

  • Acute posthypoxic myoclonus (PHM) can occur in patients admitted after cardiopulmonary resuscitation (CPR) and is considered to have a poor prognosis

  • In 30/67 (45%) patients, acute PHM persisted at 72 hours after CPR (Table 2)

  • In the majority of the patients, acute PHM was reported as focal myoclonus (47/79 patients (59%)), of whom 8 patients (17%) had a good outcome

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Summary

Introduction

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). Many patients remain comatose after successful cardiopulmonary resuscitation (CPR) due to brain damage caused by hypoxemia. Acute posthypoxic myoclonus (PHM) occurs in about 19-37% of these patients, typically within the first 24 hours after CPR, but knowledge about this illness is limited [1,2]. Lance-Adams syndrome, chronic PHM, occurs in patients after CPR, but usually arises in the post-intensive care unit period and it is mainly seen after hypoxia as primary cause of CPR [5,8]

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