The Hodgkin-Huxley (HH) model has dominated quantitative neuroscience since 1952. Its authors explicitly acknowledged its phenomenological character and called for a deeper mechanistic account. We propose that this account is the IMH model of nerve conduction. The model rests on three biophysical foundations: (1) the polyelectrolyte gel framework of Ling, in which intracellular K⁺ is adsorbed on protein sites and the resting ionic distribution is a thermodynamically stable Donnan equilibrium requiring no metabolic pump; (2) the Hofmeister ion series, which governs differential adsorption of K⁺ versus Na⁺; and (3) the hydraulic wave equation for a fluid-filled elastic tube, which predicts conduction velocity from myelin elastic modulus rather than sodium channel density. In this framework, the action potential is a coupled ionic-hydraulic phase transition propagating as a pressure wave in the periaxonal space. Electrical events are causally secondary — the electromagnetic shadow of the hydraulic wave, not its cause. We demonstrate that the model resolves a 75-year-old anomaly identified but left unexplained by Huxley and Stämpfli in 1949: positive current enters a node before the membrane potential reaches its maximum, a relation the authors themselves described as "impossible in a system of resistances and capacities." We present nine falsifiable predictions distinguishing the IMH model from HH, covering myelin mechanics, mechanoreceptor adaptation, terminal arborisation geometry as the physical substrate of the Umwelt, motor tremor as hydraulic interference, the temporal basis of conscious perception, and the coupled physical constraints that explain why large-diameter unmyelinated fibres do not exist in nature.