The management of spinal cord cavernous malformations (SCCMs) involves critical decisions between surgical and conservative treatments, informed by the patient’s preoperative neurological status, lesion characteristics, and timing of intervention (early or delayed surgery). Surgery remains an option for symptomatic patients, especially those with significant or progressive neurological deficits and large lesions, aiming for gross total excision to prevent (re)hemorrhage and improve outcomes. Conversely, conservative management is appropriate for small, asymptomatic lesions, with regular monitoring to detect changes necessitating surgery. Studies highlight the benefits and risks of both approaches. Surgical resection typically leads to neurological recovery, although worse preoperative status and larger lesions predict poorer outcomes. Other factors influencing surgical success include lesion location and timing of surgery, with early surgery (within 3 months) generally yielding better long-term outcomes. Future research should focus on the optimal timing of surgery, particularly the benefits of urgent intervention.

Cardiopulmonary bypass (CPB) has been linked with the introduction of particulate matter and gaseous microemboli, which are believed to contribute to neurologic dysfunction after cardiac surgery. During CPB, microemboli can originate in the aorta from manipulation, valve decalcification, cardiotomy suction, cavitation, and air entrainment into the extracorporeal circuit. Perfusion factors including pump flow, perfusion pressure, venous drainage, cannulation site turbulence, and temperature may also alter embolic load. Anesthetic manipulation can modulate cerebral autoregulation, vascular tone, and neuroinflammation and may also play a role in determining brain vulnerability to injury. Despite relatively low risk for clinically evident stroke after CPB, diffusion‐weighted MRI reveals silent cerebral infarcts in up to 50% of patients, which have been linked with cognitive dysfunction and delayed postoperative neurocognitive recovery. This review will focus on the relationship between embolic sources, perfusion factors, and physiologic effects of anesthesia that influence cerebral embolic injury during CPB, as well as practical methods to minimize microembolic load.