Prognosis following Postanoxic Myoclonus Status epilepticus

Hui, Andrew; Cheng, Claudia; Lam, Anita; Mok, Vincent; Joynt, Gavin M.

doi:10.1159/000086755

Cited by 75 publications

(54 citation statements)

References 45 publications

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“…When persistent, acute post-hypoxic myoclonus is sometimes termed myoclonic status epilepticus or myoclonus status. The prognosis of patients with myoclonus status is extremely poor and must influence the decision to withdraw life support when present in comatose patients after cardiac arrest, 18,19 but careful evaluation allowed for more cautious optimistic outcome in this case. The development of myoclonus can also occur well after the initial insult, which has been known as Lance-Adams syndrome.…”

Section: Discussionmentioning

confidence: 94%

Generalized Myoclonus

Inoa

McCullough

2013

The Neurohospitalist

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Movement disorders have been reported as rare complications of stroke. The basal ganglia have been implicated in the pathophysiology of most post-stroke dyskinesias. We outline different types of post-stroke myoclonus and their possible pathophysiology. A middle-aged man developed generalized myoclonus after an ischemic stroke in the superior midbrain and subthalamic nuclei. Spontaneous resolution was seen by 72 hours. A lesion to the subthalamic nuclei disrupted the normal thalamic inhibition, which likely led to the involuntary movements seen in our patient. In this case, myoclonus was generalized, which, to the best of our knowledge, has not been reported in the literature as a direct consequence of focal stroke.Keywords stroke, cerebrovascular disorders, movement disorders, clinical specialty, stroke and cerebrovascular disease, clinical specialty Movement disorders are rare complications of stroke. These can manifest as either long-term sequelae (usually after motor function has been partially or totally regained) or, less commonly, an immediate consequence of brain ischemia or hemorrhage. We report a case of a 61-year-old man with controlled hypertension on metroprolol who was found unresponsive in his home. He was initially transferred by ambulance to an outside hospital, where a nonenhanced head computed tomography (CT) was negative. He was given phenytoin 1000 mg intravenously (IV) and decadron 20 mg IV prior to arrival at our center. On our initial neurologic examination performed 3.5 hours after he was found unresponsive, he was stuporous and not responding to commands. He was withdrawing to pain in all 4 extremities and an extensor plantar reflex was noted on the right. Cranial nerves showed fixed and unequal pupils (right 5 mm and left 2 mm), left eye hypertropia, and right eye exotropia. Corneal and gag reflexes were present. No involuntary movements were appreciated. His National Institutes of Health Stroke Scale score was 22. General examination revealed an irregular heart rate and a blood pressure of 131/76 mm Hg. His electrocardiography showed atrial fibrillation. He was intubated immediately for airway protection after apneic breathing episodes were noted. Rocuronium was used for intubation, and he was premedicated with lidocaine and etomidate. After intubation, a single propofol bolus was given for transient hypertension and agitation. His oxygen saturation remained over 95% at all times. Urine toxicology and serum biochemistry that included a basic metabolic panel, cardiac, and liver enzymes were normal, except for the serum creatine kinase level that was found to be elevated (ie, 748 IU/L). A repeat nonenhanced head CT showed areas of hypoattenuation in the brain stem. Subsequent CT angiography was normal, with no evidence of large-vessel stenosis or embolus. Brain magnetic resonance imaging (MRI) showed clear evidence of restricted diffusion in the right and superior aspects of the midbrain, extending bilaterally upward into the subthalamic nuclei, which was also seen on fluidatten...

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Section: Discussionmentioning

confidence: 94%

Generalized Myoclonus

Inoa

McCullough

2013

The Neurohospitalist

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“…We've demonstrated a 100% mortality rate in NCSE post-cardiac arrest, independent of various treatment efforts such as hypothermia (39%) and IV anaesthetic infusions (72%). Others have also shown that patients with NCSE following cerebral anoxia almost invariably have a fatal outcome [36][37][38][39]. The same holds true for postanoxic generalized myoclonus, despite the successful use of propofol infusions to control elecographic seizure activity [40].…”

Section: Discussionmentioning

confidence: 97%

A Descriptive Analysis of Prognostic Indicators in Patients with Non-Convulsive Status Epilepticus in a Tertiary Hospital Population

Hrazdil¹,

Alroughani²,

Javidan³

2012

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Background: Non-convulsive status epilepticus (NCSE) is defined as a change in mental state of at least 30 minutes associated with continuous or nearly continuous epileptiform discharges. Identification of prognostic indicators can guide decision making surrounding the use of poorly established treatment interventions in this heterogeneous population. Methods: We identified 66 consecutive inpatients with NCSE. Data surrounding clinical, electrographic, and treatment factors were collected via a retrospective systematic review of medical records and electronic EEGs, and were correlated with discharge outcome (return to baseline, new disability, or death). Results: Of all subjects, 21% returned to baseline, 26% acquired new disability, and 53% died, of whom half had anoxic encephalopathy. On univariate analysis, seventeen variables correlated significantly with death, although multivariate logistic regression analysis subsequently identified only comatose state and number of life threatening comorbidities as independent predictors of mortality. Of survivors, comatose state, critical care environment, length of hospital stay, and acute symptomatic seizures predicted new disability, with the latter two showing independent significance. Following exclusion of cases with anoxic encephalopathy, the use of an anaesthetic infusion was also an independent predictor of mortality. Conclusions: NCSE is associated with variable morbidity and mortality. While one fifth of our NCSE patients returned to baseline, those comatose with acute structural/metabolic seizures, anaesthetic infusions, and life threatening comorbidities were unlikely to survive without disability at discharge.

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“…Myoclonus in the first few days after hypoxic brain damage is in general considered to predict an unfavorable prognosis in patients who remain comatose after cardiopulmonary resuscitation (CPR) 1, 2, 3. The incidence of posthypoxic myoclonus (PHM) in resuscitated patients with postanoxic encephalopathy (PAE) is 19%, and only 9–14% of these patients recover with mild to no cognitive deficits 4, 5, 6…”

Section: Introductionmentioning

confidence: 99%

The interrelation between clinical presentation and neurophysiology of posthypoxic myoclonus

Zijl

Beudel

Jong

et al. 2018

Ann Clin Transl Neurol

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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.

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Prognosis following Postanoxic Myoclonus Status epilepticus

Cited by 75 publications

References 45 publications

Generalized Myoclonus

Generalized Myoclonus

A Descriptive Analysis of Prognostic Indicators in Patients with Non-Convulsive Status Epilepticus in a Tertiary Hospital Population

The interrelation between clinical presentation and neurophysiology of posthypoxic myoclonus

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