## 4 Discussion  
This study demonstrates for the first time the relationship between intramedullary stress/strain and neurological dysfunction in degenerative cervical myelopathy. Intramedullary stress and strain at the level of maximum spinal cord compression during neck flexion were significantly correlated with sensorimotor hand dysfunction and disease severity. The results of this study highlight the potential clinical utility of spinal cord biomechanics for the diagnoses of degenerative cervical myelopathy. There is increasing evidence that intrinsic spinal cord forces due to the stress and strain of the cord during neck motion are important contributors to neural injury in DCM [2]. Human cadaver studies have shown that longitudinal stretch (strain) along the spinal cord during flexion is accentuated in the presence of spinal cord compression or kyphosis [25]. Neck motion creates chronic, repetitive stretch injuries that produce neural injury. Evidence for cellular pathways that mediate stretch-associated axonal [26] and myelin [27] injury further supports a larger role for intramedullary stress and strain in the pathophysiology of DCM. The contribution of spinal cord biomechanics to the structural spinal cord suggests a possible mechanism by which intramedullary stress and strain relate to neurological dysfunction in DCM. Although extrinsic spinal cord compression contributes to spinal cord damage, there is increasing evidence that intrinsic spinal cord forces due to the stress and strain of the cord during neck motion are important contributors to neural injury in DCM [2]. During neck flexion, increased spinal cord strain at the level of maximum cord compression is noted in the dorsal half of the spinal cord affecting the dorsal column-medial lemniscus pathway, which relates to light touch sensation and proprioception relative to the brain. We found that flexion-related intramedullary stress and strain were correlated to hand sensation, and this link is potentially due to the effect of neck flexion on the dorsal columns. In addition, we found that higher pre-surgical intramedullary stress and strain are linked to decreased hand dexterity and prolonged dexterity time. The corticospinal tracts, which control hand dexterity, are located in the dorsal half of the spinal cord, and these tracts experience increased spinal cord tension during neck flexion. Increased tension or deformation in these tracts may disrupt the precision and speed of neural transmission necessary for coordinated hand movements. Together, neck flexion is correlated with sensorimotor dysfunction in DCM due to increased intramedullary stress and strain at the level of maximum cord compression. There are several possible pathophysiological mechanisms that affect the dorsal spinal cord during neck flexion in DCM patients. Vascular disruption occurs as neck flexion induces elongation and tension in the posterior spinal arteries, leading to a zigzagging pattern and transient reductions in lumen size, which diminish blood flow and increase the risk of ischemic damage to the dorsal columns [28; 29; 30]. This is compounded by increased intramedullary pressure due to the flexion-related deformation of the spinal cord, which impedes microcirculatory efficiency and could provoke ischemia within the dorsal neural tissues, disrupting the functionality of the dorsal columns and corticospinal tracts [31; 32; 33]. Moreover, the mechanical tension exerted on the dorsal spinal cord can distort mechanosensitive ion channels [34] and the axonal and myelin [35; 36] structures within these pathways, impairing axoplasmic transport and leading to sensory and motor dysfunctions. Additionally, shear stresses from pathological flexion or torsional movements significantly impact the dorsal spinal cord, misaligning or displacing neural tissues, which adversely affects the integrity and function of the dorsal columns and associated neural pathways [37, 38]. The findings of this study highlight the potential clinical utility of spinal cord biomechanics in DCM.