Background Magnesium mitigates several mechanisms involved in secondary brain injury after cardiac arrest. Because systemically administered magnesium crosses the blood–brain barrier poorly, it may be unsuitable for early post‐cardiac arrest neuroprotection. We tested whether intrathecal magnesium (IT‐Mg), which bypasses the blood–brain barrier, improves neurologic outcomes in a porcine model of asphyxial cardiac arrest. Methods Twenty‐four pigs underwent asphyxial cardiac arrest and cardiopulmonary resuscitation. Thirty minutes after return of spontaneous circulation, the IT‐Mg group received 75 mg of magnesium via cranial intrathecal catheters; the control group received no IT‐Mg treatment. Animals were observed for up to 72 hours post return of spontaneous circulation. Results Survival duration and cumulative survival did not differ significantly between groups. In controls, the mean amplitude‐integrated electroencephalography amplitude remained depressed for 24 hours, whereas it increased in the IT‐Mg group (group×time interaction P <0.001). Compared with controls, the IT‐Mg group demonstrated superior neurologic function (lower overall performance category, group effect P =0.039; lower neurologic deficit score, group effect P =0.013) and reduced histologic injury (lower temporal cortical P =0.038 and total P =0.041 histologic damage scores). Conclusions Intrathecal administration of magnesium after return of spontaneous circulation mitigated histologic injury and improved neurologic function in a porcine model of asphyxial cardiac arrest.
Lee et al. (2026) studied this question.