Elsevier

The Lancet

Volume 343, Issue 8913, 25 June 1994, Pages 1642-1643
The Lancet

Letters to the Editor
Myoclonus status in comatose patients after cardiac arrest

https://doi.org/10.1016/S0140-6736(94)93100-3Get rights and content

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    Our results indicate that anoxic long-term potentiation of excitatory synapses is a plausible mechanism underlying certain pathological EEG patterns observed in postanoxic encephalopathy. It is compatible with the apparent network hyperexcitability in patients with severe postanoxic encephalopathy, reflected by a frequent observation of epileptiform discharges (Wijdicks and Young, 1994; Young et al., 1990). Since anoxic long-term potentiation is independent of Ca2+ dependent presynaptic neurotransmitter release, there is no paradox between synaptic depression and a rise in extracellular glutamate levels (Ikeda et al., 1989; Martin et al., 1994).

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    The names and definitions used for status myoclonus vary among those studies. While the presence of myoclonic jerks in comatose survivors of cardiac arrest is not consistently associated with poor outcome (FPR 9%),145,272 a status myoclonus starting within 48 h from ROSC was consistently associated with a poor outcome (FPR 0 [0–5]%; sensitivity 8%) in prognostication studies made in non-TTM-treated patients,276,289,290 and is also highly predictive (FPR 0% [0–4]; sensitivity 16%) in TTM-treated patients.144,156,291 However, several case reports of good neurological recovery despite an early-onset, prolonged and generalised myoclonus have been published.

  • Predictors of poor neurological outcome in adult comatose survivors of cardiac arrest: A systematic review and meta-analysis. Part 2: Patients treated with therapeutic hypothermia

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    According to recent recommendations,61 generalised myoclonus appearing during the first 24 h after cardiac arrest is usually, but not always,62 a sign of unfavourable prognosis in patients treated with TH. Indeed, in studies performed in patients not treated with TH presence of myoclonus63–65 (mostly generalised and multifocal) in the first 24–48 h was associated almost invariably with a poor outcome,8 except in a few case reports.66–69 In TH-treated patients detection of myoclonus during the first 24 h is difficult, due to the combined presence of neuromuscular blocking and sedation.49,70

  • Predictors of poor neurological outcome in adult comatose survivors of cardiac arrest: A systematic review and meta-analysis. Part 1: Patients not treated with therapeutic hypothermia

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    Myoclonus, a series of sudden, involuntary, brief jerks of peripheral or axial musculature,66 was a relatively infrequent, but early and highly specific predictor of poor outcome in studies included in our review. Characteristics of myoclonus in studies included in our review were inconsistent: three over five studies18,21,63 reported status myoclonus, defined in one of these studies as myoclonus persisting for at least 30 min. Others20,62 described myoclonus as intermittent or even single myoclonic jerks.

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