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Mechanism of ítowí-Cinnamic Acid Dibromide to 8-Bromostyrene 2639 furic acid gave in the usual way a black crude phenol. Two treatments of this material in benzene solution with charcoal gave, in turn, a gray, waxy solid, which was sublimed to give 2,3-dimethyl-5-phenylphenol as colorless needles of m.p. 51-52°.

Recent electrophysiological studies have suggested surges in electrical correlates of consciousness (i.e., elevated gamma power and connectivity) after cardiac arrest (CA). This study examines electrocorticogram (ECoG) activity and coherence of the dying brain during asphyxial CA. Male Wistar rats (n = 16) were induced with isoflurane anesthesia, which was washed out before asphyxial CA. Mean phase coherence and ECoG power were compared during different stages of the asphyxial period to assess potential neural correlates of consciousness. After asphyxia, the ECoG progressed through four distinct stages (asphyxial stages 1–4 [AS1-4]), including a transient period of near-electrocerebral silence lasting several seconds (AS3). Electrocerebral silence (AS4) occurred within 1 min of the start of asphyxia, and pulseless electrical activity followed the start of AS4 by 1–2 min. AS3 was linked to a significant increase in frontal coherence between the left and right motor cortices (p < 0.05), with no corresponding increase in ECoG power. AS3 was also associated with a significant posterior shift of ECoG power, favoring the visual cortices (p < 0.05). Although the ECoG during AS3 appears visually flat or silent when viewed with standard clinical settings, our study suggests that this period of transient near-electrocerebral silence contains distinctive neural activity. Specifically, the burst in frontal coherence and posterior shift of ECoG power that we find during this period immediately preceding CA may be a neural correlate of conscious processing.

Spreading depolarization (SD) accompanies numerous neurological conditions, including migraine, stroke, and traumatic brain injury. There is significant interest in understanding the relationship between SD and neuronal injury. However, characteristics underlying SD and repolarization (RP) induced by global cerebral ischemia (e.g., cardiac arrest (CA)) and reperfusion are not well understood. Quantifying features of SD and RP during CA and cardiopulmonary resuscitation (CPR) may provide important metrics for diagnosis and prognosis of neurological injury from hypoxia-ischemia. We characterized SD and RP in a rodent model of asphyxial CA+CPR using a multimodal platform including electrocorticography (ECoG) and optical imaging. We detected SD and RP by (1) alternating current (AC), (2) direct current (DC), and (3) optical imaging of spreading ischemia, spreading edema, and vasoconstriction. Earlier SD (r=-0.80; p<0.001) and earlier RP (r=-0.71, p<0.001) were associated with better neurological recovery after 24hrs. SD+RP onset times predicted good vs poor neurological recovery with 82% sensitivity and 91% specificity. To our knowledge, this is the first preclinical study to link SD and RP characteristics with neurological recovery post-CA. These data suggest that SD and RP may be ultra-early, real-time prognostic markers of post-CA outcome, meriting further investigation into translational implications during global cerebral ischemia.