For a variety of reasons, new radiological imaging techniques are supplanting traditional cadaver dissection in the teaching of human anatomy. The authors briefly review the historical forces behind this transition, and then explore the advantages and drawbacks of each approach. Cadaver dissection offers an active, hands-on exploration of human structure, provides deep insights into the meaning of human embodiment and mortality, and represents a profound rite of passage into the medical profession. Radiological imaging permits in vivo visualization, offers physiologic as well as anatomic insights, and represents the context in which contemporary practicing physicians most frequently encounter their patients' otherwise hidden internal anatomy. Despite its important strengths, radiology cannot simply substitute for cadaver dissection, and the best models for teaching gross anatomy will incorporate both cadaver dissection and radiological imaging.

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Cortical spreading depression (CSD) is a slow-moving ionic and metabolic disturbance that propagates in cortical brain tissue. In addition to massive cellular depolarizations, CSD also involves significant changes in perfusion and metabolism—aspects of CSD that had not been modeled and are important to traumatic brain injury, subarachnoid hemorrhage, stroke, and migraine. In this study, we develop a mathematical model for CSD where we focus on modeling the features essential to understanding the implications of neurovascular coupling during CSD. In our model, the sodium-potassium–ATPase, mainly responsible for ionic homeostasis and active during CSD, operates at a rate that is dependent on the supply of oxygen. The supply of oxygen is determined by modeling blood flow through a lumped vascular tree with an effective local vessel radius that is controlled by the extracellular potassium concentration. We show that during CSD, the metabolic demands of the cortex exceed the physiological limits placed on oxygen delivery, regardless of vascular constriction or dilation. However, vasoconstriction and vasodilation play important roles in the propagation of CSD and its recovery. Our model replicates the qualitative and quantitative behavior of CSD—vasoconstriction, oxygen depletion, extracellular potassium elevation, prolonged depolarization—found in experimental studies. We predict faster, longer duration CSD in vivo than in vitro due to the contribution of the vasculature. Our results also help explain some of the variability of CSD between species and even within the same animal. These results have clinical and translational implications, as they allow for more precise in vitro, in vivo, and in silico exploration of a phenomenon broadly relevant to neurological disease.