Abstract The dorsal root (DR) carries afferent axons of primary sensory neurons in the DR ganglion (DRG), which relay sensory information to second order neurons in the spinal cord. Traumatic injuries to DRs include brachial plexus, lumbosacral plexus and cauda equina injuries. Brachial plexus injury (BPI), the most common form of DR injury, results from high-energy traction damaging cervical DRs. These injuries evoke chronic, often agonizing, pain and permanent loss of sensation. We have no effective therapies that can reduce the extent of the initial injury or, at a later stage, restore sensory connections. It is therefore extremely important to understand the full extent of the damage caused by traumatic injuries to DRs, especially cervical DRs, and the mechanisms by which the damage occurs. DR injury directly damages primary sensory axons, resulting in sensory loss by permanently eliminating primary afferent axons in spinal cord. It is widely believed, however, that second order neurons in spinal cord remain intact. In contradiction to this belief, we have serendipitously found in mice that cervical DR crush can provoke profound neural tissue loss in spinal cord that is far more severe than previously thought. Notably, the incidence and magnitude of the neural tissue damage vary widely among mice, and interestingly increase in males and outbred mice and after avulsing DRs, a clinically relevant model of DR injury. We hypothesize that DR injury can cause severe spinal cord damage by eliciting intense spinal cord ischemia, when it damages large radicular arteries in mice with vulnerable arterial organization. Aim 1 will determine if the spinal cord damage is indeed ischemic by testing if photothrombotic occlusion of large radicular arteries in intact DRs is sufficient to elicit severe neural tissue loss in spinal cord. Aim 2 will determine if wide variability of arterial organization among mice determines the incidence and severity of spinal cord ischemia, thus critically impacting the pathophysiological progression of DR injuries. Current understanding is that spinal cord ischemia in humans is caused by direct damage to spinal cord, but not by remote trauma to spinal roots or peripheral nerve. The blood supply of the spinal cord in humans is also highly variable. Therefore, elucidation of this novel form of spinal cord ischemia and concurrent spinal cord damage, in mice, may ultimately provide new directions in the diagnosis, treatment and prognosis of both sporadic and surgical DR injuries.