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. 2016 Aug;80(2):175-84.
doi: 10.1002/ana.24697. Epub 2016 Jun 28.

Clinically distinct electroencephalographic phenotypes of early myoclonus after cardiac arrest

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Clinically distinct electroencephalographic phenotypes of early myoclonus after cardiac arrest

Jonathan Elmer et al. Ann Neurol. 2016 Aug.

Abstract

Objective: We tested the hypothesis that there are readily classifiable electroencephalographic (EEG) phenotypes of early postanoxic multifocal myoclonus (PAMM) that develop after cardiac arrest.

Methods: We studied a cohort of consecutive comatose patients treated after cardiac arrest from January 2012 to February 2015. For patients with clinically evident myoclonus before awakening, 2 expert physicians reviewed and classified all EEG recordings. Major categories included: Pattern 1, suppression-burst background with high-amplitude polyspikes in lockstep with myoclonic jerks; and Pattern 2, continuous background with narrow, vertex spike-wave discharges in lockstep with myoclonic jerks. Other patterns were subcortical myoclonus and unclassifiable. We compared population characteristics and outcomes across these EEG subtypes.

Results: Overall, 401 patients were included, of whom 69 (16%) had early myoclonus. Among these patients, Pattern 1 was the most common, occurring in 48 patients (74%), whereas Pattern 2 occurred in 8 patients (12%). The remaining patients had subcortical myoclonus (n = 2, 3%) or other patterns (n = 7, 11%). No patients with Pattern 1, subcortical myoclonus, or other patterns survived with favorable outcome. By contrast, 4 of 8 patients (50%) with Pattern 2 on EEG survived, and 4 of 4 (100%) survivors had favorable outcomes despite remaining comatose for 1 to 2 weeks postarrest.

Interpretation: Early PAMM is common after cardiac arrest. We describe 2 distinct patterns with distinct prognostic significances. For patients with Pattern 1 EEGs, it may be appropriate to abandon our current clinical standard of aggressive therapy with conventional antiepileptic therapy in favor of early limitation of care or novel neuroprotective strategies. Ann Neurol 2016;80:175-184.

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Conflict of interest statement

Conflicts of interest: The authors have no conflicts of interest to report.

Figures

Figure 1
Figure 1
A) This is the initial recording for Pattern 1 on post-arrest day 0. Note the bursts of high amplitude polyspikes with rapid decrescendo in amplitude. Bursts are superimposed onto a suppressed background. Clinical myoclonus is apparent in lock-step with the initial polyspikes. B) Post-arrest-day 1, stage 2 of Pattern 1. Bursts lengthen in duration and high amplitude polyspikes are decreasing in amplitude. Background remains suppressed. C) Hospital day 2, Stage 3 of Pattern 1. Bursts are “softening” and have lost the polyspikes and variation in amplitude and variable frequencies, instead becoming more uniform in frequency and amplitude. Periods of suppression are still appreciated. D) Hospital day 3, Stage 4 of Pattern 1. Amplitude and variability rapidly decrease, ultimately progressing to a featureless, attenuated background. (30mm/second, 10uV/mm, bipolar longitudinal montage)
Figure 1
Figure 1
A) This is the initial recording for Pattern 1 on post-arrest day 0. Note the bursts of high amplitude polyspikes with rapid decrescendo in amplitude. Bursts are superimposed onto a suppressed background. Clinical myoclonus is apparent in lock-step with the initial polyspikes. B) Post-arrest-day 1, stage 2 of Pattern 1. Bursts lengthen in duration and high amplitude polyspikes are decreasing in amplitude. Background remains suppressed. C) Hospital day 2, Stage 3 of Pattern 1. Bursts are “softening” and have lost the polyspikes and variation in amplitude and variable frequencies, instead becoming more uniform in frequency and amplitude. Periods of suppression are still appreciated. D) Hospital day 3, Stage 4 of Pattern 1. Amplitude and variability rapidly decrease, ultimately progressing to a featureless, attenuated background. (30mm/second, 10uV/mm, bipolar longitudinal montage)
Figure 2
Figure 2
A) Post-arrest day 0, recording suggestive of Pattern 2 with a continuous background of various frequencies and narrow spikes and polyspikes with midline with a parasagittal predominance. Myoclonus observed with spikes. B) Recording taken 1 month after arrest, with persistent parasagittal spike-wave discharges and action myoclonus typical of Lance Adams syndrome. Note improved background rhythms
Figure 3
Figure 3
A) Post-arrest day 0, another example of Pattern 2 with continuous background though of low amplitude with narrow small polyspikes. B) Post-arrst day 4, persistent spike-wave discharges with persistent myoclonus indicative of a patient likely to fulfill criteria for Lance Adams syndrome after awakening.
Figure 4
Figure 4
The progression of patients with PAMM and Pattern 1 on their initial EEG is generally predictable, although a minority of patients do go on to develop fast seizure activity on the second and third day of monitoring.

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