Neurologic Prognosis after Cardiac Arrest REPLY

Department of Clinical Neurological Sciences, University of Western Ontario, London, ON, Canada.
New England Journal of Medicine (Impact Factor: 55.87). 09/2009; 361(6):605-11. DOI: 10.1056/NEJMcp0903466
Source: PubMed


A 55-year-old man collapses while jogging through the park. A bystander finds him unconscious and without a pulse and initiates cardiopulmonary resuscitation (CPR) while an ambulance is summoned. On arrival in the emergency room, the patient is in ventricular fibrillation; the partial pressure of oxygen in arterial blood is 200 mm Hg, the pH is 7.25, and the bicarbonate level is 18 mmol per liter. Spontaneous circulation is reestablished, but he remains comatose with absent pupillary reflexes. He is then treated with hypothermia, achieving a core temperature of 34 degrees C in 4 hours, which is maintained for 24 hours, after which he remains unconscious. What would you advise regarding his neurologic prognosis?

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    • "In absence of rapid recovery of consciousness, it is of highest importance to evaluate the prognosis of comatose patients. Identifying those patients with no hope of recovery would allow considering withdrawal of support, both for ethical and economical reasons (Young, 2009; Howard et al., 2011). Currently, no single method is capable of adequate etiological diagnosis and prognostication. "
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    ABSTRACT: Objective: Our aim was to assess the diagnostic and predictive value of several quantitative EEG (qEEG) analysis methods in comatose patients. Methods: In 79 patients, coupling between EEG signals on the left–right (inter-hemispheric) axis and on the anterior–posterior (intra-hemispheric) axis was measured with four synchronization measures: relative delta power asymmetry, cross-correlation, symbolic mutual information and transfer entropy directionality. Results were compared with etiology of coma and clinical outcome. Using cross-validation, the predictive value of measure combinations was assessed with a Bayes classifier with mixture of Gaussians. Results: Five of eight measures showed a statistically significant difference between patients grouped according to outcome; one measure revealed differences in patients grouped according to the etiology. Interestingly, a high level of synchrony between the left and right hemisphere was associated with mortality on intensive care unit, whereas higher synchrony between anterior and posterior brain regions was associated with survival. The combination with the best predictive value reached an area-under the curve of 0.875 (for patients with post anoxic encephalopathy: 0.946). Conclusions: EEG synchronization measures can contribute to clinical assessment, and provide new approaches for understanding the pathophysiology of coma. Significance: Prognostication in coma remains a challenging task. qEEG could improve current multi-modal approaches.
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    • "Yet the outcome from global ischemia is often diffuse damage to the higher brain with sparing of the hypothalamus and brainstem. As a result, over several weeks many afflicted patients transition from coma to a persistent vegetative state [3]–[5], [12], [13], [47]. Neocortex, striatum, hippocampus and cerebellar cortex are particularly vulnerable to ischemia [17], [48]–[51]. "
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    ABSTRACT: Global ischemia caused by heart attack, pulmonary failure, near-drowning or traumatic brain injury often damages the higher brain but not the brainstem, leading to a ‘persistent vegetative state’ where the patient is awake but not aware. Approximately 30,000 U.S. patients are held captive in this condition but not a single research study has addressed how the lower brain is preferentially protected in these people. In the higher brain, ischemia elicits a profound anoxic depolarization (AD) causing neuronal dysfunction and vasoconstriction within minutes. Might brainstem nuclei generate less damaging AD and so be more resilient? Here we compared resistance to acute injury induced from simulated ischemia by ‘higher’ hippocampal and striatal neurons versus brainstem neurons in live slices from rat and mouse. Light transmittance (LT) imaging in response to 10 minutes of oxygen/glucose deprivation (OGD) revealed immediate and acutely damaging AD propagating through gray matter of neocortex, hippocampus, striatum, thalamus and cerebellar cortex. In adjacent brainstem nuclei, OGD-evoked AD caused little tissue injury. Whole-cell patch recordings from hippocampal and striatal neurons under OGD revealed sudden membrane potential loss that did not recover. In contrast brainstem neurons from locus ceruleus and mesencephalic nucleus as well as from sensory and motor nuclei only slowly depolarized and then repolarized post-OGD. Two-photon microscopy confirmed non-recoverable swelling and dendritic beading of hippocampal neurons during OGD, while mesencephalic neurons in midbrain appeared uninjured. All of the above responses were mimicked by bath exposure to 100 µM ouabain which inhibits the Na+/K+ pump or to 1–10 nM palytoxin which converts the pump into an open cationic channel.
    Full-text · Article · May 2014 · PLoS ONE
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    • "There is a well recognized but poorly understood caudal-to-rostral increase in the brain`s vulnerability to neuronal injury caused by metabolic stress [1][2][3] [4]. Global brain ischemia caused by heart attack or near-drowning can leave a functional brainstem while `higher` regions are severely compromised [4], leading to the persistent vegetative state (PVS). Maintained brainstem function with minimal higher brain activity in PVS patients is confirmed by case studies of global ischemia using MR imaging [5][6][7] as well as numerous studies measuring regional metabolism [8]. "
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    ABSTRACT: Higher brain regions are more susceptible to global ischemia than the brainstem, but is there a gradual increase in vulnerability in the caudal-rostral direction or is there a discrete boundary? We examined the interface between `higher` thalamus and the hypothalamus the using live brain slices where variation in blood flow is not a factor. Whole-cell current clamp recording of 18 thalamic neurons in response to 10 min O2/glucose deprivation (OGD) revealed a rapid anoxic depolarization (AD) from which thalamic neurons do not recover. Newly acquired neurons could not be patched following AD, confirming significant regional thalamic injury. Coinciding with AD, light transmittance (LT) imaging during whole-cell recording showed an elevated LT front that initiated in midline thalamus and that propagated into adjacent hypothalamus. However, hypothalamic neurons patched in paraventricular nucleus (PVN, n= 8 magnocellular and 12 parvocellular neurons) and suprachiasmatic nucleus (SCN, n= 18) only slowly depolarized as AD passed through these regions. And with return to control aCSF, hypothalamic neurons repolarized and recovered their input resistance and action potential amplitude. Moreover, newly acquired hypothalamic neurons could be readily patched following exposure to OGD, with resting parameters similar to neurons not previously exposed to OGD. Thalamic susceptibility and hypothalamic resilience were also observed following ouabain exposure which blocks the Na(+)/K(+) pump, evoking depolarization similar to OGD in all neuronal types tested. Finally, brief exposure to elevated [K(+)]o caused spreading depression (SD, a milder, AD-like event) only in thalamic neurons so SD generation is regionally correlated with strong AD. Therefore the thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus). In contrast hypothalamic neurons are comparatively resistant, generating weaker and recoverable anoxic depolarization similar to brainstem neurons, possibly the result of a Na/K pump that better functions during ischemia.
    Full-text · Article · Nov 2013 · PLoS ONE
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