Around 30 minutes in, Henderson explains how stretching of the spinal cord or brain stem could cause CNS dysfunction. Such stretching can be a result of various structural anomalies, such as: CCI, spinal stenosis, basilar invagination, cranial settling, etc. It seems that when neurons are subjected to stretching forces they take in excessive amounts of calcium.
I did some more research and found this study:
In this study, primary cortical neurons were cultured on an elastic substrate and subjected to graded levels (0%, 10%, 30%, 50%) of either uniaxial (cells stretched in one direction only) or biaxial (cells simultaneously stretched in two directions) stretch. We found that neurons stretched in either injury paradigm exhibited immediate increases in intracellular free calcium ([Ca2+]i), but the magnitude of the ([Ca2+]i) rise was nearly an order of magnitude higher in biaxially stretched neurons compared to uniaxially stretched neurons. Moreover, while the ([Ca2+]i) transient after uniaxial stretch was blocked with specific channel antagonists (APV, CNQX, nimodipine, TTX), a substantial ([Ca2+]i) transient persisted in biaxially stretched neurons.
Other practitioners, such as Jay Goldstein, also trialed nimodipine with patients, but if a positive response was not seen immediately, they did not continue the trial. Goldstein rated nimodipine the third best of his top 23 drugs for ME/CFS.