In many cerebral grey matter structures including the neocortex, spreading
depolarization (SD) is the principal mechanism of the near-complete breakdown
of the transcellular ion gradients with abrupt water influx into neurons.
Accordingly, SDs are abundantly recorded in patients with traumatic brain
injury, spontaneous intracerebral hemorrhage, aneurysmal subarachnoid
hemorrhage (aSAH) and malignant hemispheric stroke using subdural electrode
strips. SD is observed as a large slow potential change, spreading in the
cortex at velocities between 2 and 9 mm/min. Velocity and SD susceptibility
typically correlate positively in various animal models. In patients monitored
in neurocritical care, the Co-Operative Studies on Brain Injury
Depolarizations (COSBID) recommends several variables to quantify SD
occurrence and susceptibility, although accurate measures of SD velocity have
not been possible. Therefore, we developed an algorithm to estimate SD
velocities based on reconstructing SD trajectories of the wave-front's
curvature center from magnetic resonance imaging scans and time-of-SD-arrival-
differences between subdural electrode pairs. We then correlated variables
indicating SD susceptibility with algorithm-estimated SD velocities in twelve
aSAH patients. Highly significant correlations supported the algorithm's
validity. The trajectory search failed significantly more often for SDs
recorded directly over emerging focal brain lesions suggesting in humans
similar to animals that the complexity of SD propagation paths increase in
tissue undergoing injury
