Case reportNeurologic recovery after therapeutic hypothermia in patients with post-cardiac arrest myoclonus☆
Introduction
Early myoclonus in comatose survivors of cardiac arrest, even when it is not myoclonic status epilepticus (MSE), is considered a sign of severe global brain ischemia and has been associated with high rates of mortality and poor neurologic outcomes.1, 2, 3 A previous prospective cohort of 114 comatose cardiac arrest survivors found that all seven patients with “status myoclonus other than MSE” died prior to hospital discharge.1 In addition, Levy et al. showed that 90% of comatose survivors of cardiac arrest with myoclonus either died or had poor functional outcomes (persistent vegetative state or conscious but unable to independently care for themselves).2
With the advent of induced hypothermia and increased attention to the post-arrest period of care, clinical findings previously believed to have prognostic significance may need to be reevaluated or reconsidered. Two recent studies did evaluate myoclonus as an outcome predictor after induced hypothermia. One of these investigations found that 35 of 36 (97%) patients with early myoclonus had Glasgow-Pittsburgh Cerebral Performance Category (CPC) scores of 3, 4, or 5 (CPC scores: 1 = conscious, alert, able to work, might have mild neurologic or psychologic deficit; 2 = conscious and alert with moderate disability; 3 = conscious with severe disability; 4 = comatose or in a persistent vegetative state; 5 = brain death). In another cohort of comatose cardiac arrest survivors treated with TH, all five patients with early “status myoclonus” (defined as massive myoclonus of the axial musculature not accompanied by ictal activity on electroencephalography [EEG]) died.4, 5, 6, 7 While these investigations do suggest poor outcomes in patients with early myoclonus even after induced hypothermia, the relative sample size remains low and the potential for survival with good neurological outcome for a number of patients in this population may go undetected.
We report on three survivors of cardiac arrest who had massive myoclonus in the first 4 h after return of spontaneous circulation (ROSC) and, after treatment with TH, experienced good neurologic outcomes (two patients with a CPC score = 1 and one patient with a CPC score = 2).
Section snippets
Patient 1
A 76-year-old woman with a history of hypertension was transferred to Beth Israel Deaconess Medical Center (BIDMC) after she suffered a ventricular tachycardia (VT) cardiac arrest while undergoing cardiac catheterization for an ST-segment elevation myocardial infarction (STEMI) at another hospital. Successful ROSC was achieved after defibrillation. An amiodarone drip was initiated, an intra-aortic balloon pump (IABP) was inserted, and she was transferred directly to the intensive care unit
Discussion
Previous research has shown that patients with myoclonus in the early post-cardiac arrest period, even when it is not MSE, have high rates of mortality and severe neurologic impairment.1, 2, 3 In a prospective analysis of comatose, cardiac arrest survivors by Krumholz et al., 100% of the seven patients with “status myoclonus other than MSE” and 84% of the 19 patients with MSE died prior to hospital discharge, while Levy et al. found that 90% of those with post-arrest myoclonus either died or
Conclusion
Although the presence of early myoclonus in cardiac arrest survivors has traditionally been considered a poor prognostic sign, we report on three patients with early, massive myoclonus who had good neurologic outcomes after treatment with mild therapeutic hypothermia. These cases suggest that mild therapeutic hypothermia may improve outcomes in patients with early, massive myoclonus. The concept that myoclonus heralds a poor prognosis may need to be reconsidered in the era of post-cardiac
Funding sources
This study was funded, in part, by American Heart Association grant # 0735533T.
Conflict of interest statement
The authors have no conflicts of interest to report.
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Cited by (83)
To Treat or Not to Treat: Ethics of Management of Refractory Status Myoclonus Following Pediatric Anoxic Brain Injury
2023, Seminars in Pediatric NeurologyEuropean Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2021: Post-resuscitation care
2021, ResuscitationCitation Excerpt :It typically develops during the first 1–2 days after the arrest and is often transient during the first days-week. It is associated with a poor prognosis but some patients survive with a good outcome.181,182 Most post-hypoxic myoclonus has a cortical origin183 and the EEG shows synchronous time-locked discharges or burst-suppression in a substantial proportion of patients.181
Improvement of consciousness before initiating targeted temperature management
2020, ResuscitationCitation Excerpt :Standard post-resuscitation care after ROSC includes target temperature management (TTM),1–3 but TTM is costly and is likely unnecessary in cases with rapid awakening.4–6 Spontaneous neurological recovery after ROSC does occur in some patients.7–9 However, up until now, we have lacked knowledge of the percentage of patients who do experience spontaneous recovery before TTM, the time interval from the ROSC to full recovery, and the predictive factors for recovery.
Anoxic-Ischemic Brain Injury
2017, Neurologic ClinicsClinical classification of post anoxic myoclonic status
2017, ResuscitationCitation Excerpt :Much of the early literature on cardiopulmonary arrest had suggested that myoclonic status was universally predictive of poor outcome [1,2]. However, several cases of post anoxic myoclonic status with good neurological recovery have been published even in the setting of early-onset, prolonged and generalized myoclonus, features previously felt to be most ominous [3–12]. Thus, it is now clear that the presence of myoclonic status does not preclude recovery after cardiac arrest.
Early Lance–Adams syndrome after cardiac arrest: Prevalence, time to return to awareness, and outcome in a large cohort
2017, ResuscitationCitation Excerpt :LAS can appear a few days to few weeks after injury [6], but also while the patient is still in coma [7], as we observed. Status myoclonus usually starts also early, within the first 24–48 h following CA [11], but “resists” to sedation during targeted temperature management [1]. As opposed to the present series, previous reports [12,13] described LAS developing rather in patients with respiratory causes of CA; this suggests that LAS may not be preferentially linked to a specific pathophysiology.
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A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2011.09.017.