The interrelation between clinical presentation and neurophysiology of posthypoxic myoclonus

Abstract

ObjectivePosthypoxic myoclonus (PHM) in the first few days after resuscitation can be divided clinically into generalized and focal (uni‐ and multifocal) subtypes. The former is associated with a subcortical origin and poor prognosis in patients with postanoxic encephalopathy (PAE), and the latter with a cortical origin and better prognosis. However, use of PHM as prognosticator in PAE is hampered by the modest objectivity in its clinical assessment. Therefore, we aimed to obtain the anatomical origin of PHM with use of neurophysiological investigations, and relate these to its clinical presentation.MethodsThis study included 20 patients (56 ± 18 y/o, 68% M, 2 survived, 1 excluded) with EEG‐EMG‐video recording. Three neurologists classified PHM into generalized or focal PHM. Anatomical origin (cortical/subcortical) was assessed with basic and advanced neurophysiology (Jerk‐Locked Back Averaging, coherence analysis).ResultsClinically assessed origin of PHM did not match the result obtained with neurophysiology: cortical PHM was more likely present in generalized than in focal PHM. In addition, some cases demonstrated co‐occurrence of cortical and subcortical myoclonus. Patients that recovered from PAE had cortical myoclonus (1 generalized, 1 focal).InterpretationHypoxic damage to variable cortical and subcortical areas in the brain may lead to mixed and varying clinical manifestations of myoclonus that differ of those patients with myoclonus generally encountered in the outpatient clinic. The current clinical classification of PHM is not adequately refined to play a pivotal role in guiding treatment decisions to withdraw care. Our neurophysiological characterization of PHM provides specific parameters to be used in designing future comprehensive studies addressing the potential role of PHM as prognosticator in PAE.

Brain injury after cardiac arrest: from prognostication of comatose patients to rehabilitation

“…It is generally taught that massive, axial jerks might be associated with highly malignant EEG patterns, whereas brief, mostly multifocal jerks do not always herald a poor prognosis; however, the clinical-neurophysiological association of myoclonus appears unreliable. 16,17 EEG showing underlying continuous, reactive patterns suggests a treatable post-anoxic myoclonus, most likely representing early forms of Lance-Adams syndrome. 6,14,18 This syndrome might be incapacitating initially, but responds to treatment and is compatible with a good long-term outcome.…”

Negative Myoclonus: Neurophysiological Study and Clinical Impact in Progressive Myoclonus Ataxia

“…Power spectrum was estimated based on 1‐second segments with overlap of 50%, according to Welch's method. CMC was considered positive if its values exceeded a 95% confidence level for at least four consecutive frequency bins, 24 within a 10–40 Hz range 19 . The 95% confidence limit was calculated according to the following formula: 1−(0.05) 1/(L−1) , where L is the number of analyzed segments 21 .…”

Neurophysiological and Clinical Correlates of Acute Posthypoxic Myoclonus

“…Some have also proposed that defining SSEP amplitudes are key in defining acute PHM. Giant SSEPs, which can signify cortical myoclonus, may predict a better outcome, 12,28 although the cortical and subcortical dichotomy for prognosis is controversial, as will be discussed later. Giant SSEPs are not specific for cortical myoclonus and can be seen in other neurological disorders.…”

“…12,27 Therefore, the dichotomy between acute and chronic PHM in the literature is not sufficient to differentiate cases with good or poor prognosis and thus in defining PHM for prognostic and management decisions. 8,23,28 The differentiation between "malignant," which implies a poor outcome, from less malignant or "benign" acute PHM is crucial given these prognostic implications because acute PHM itself may lead to the withdrawal of life-sustaining therapy. It has been suggested that clinical features and ancillary neurophysiological testing hold the key to better defining outcomes when acute PHM is present.…”

“…12,27 Therefore, the dichotomy between acute and chronic PHM in the literature is not sufficient to differentiate cases with good or poor prognosis and thus in defining PHM for prognostic and management decisions. 8,23,28…”