Upper motor neuron lesions cause hyper-reflexia and spasticity primarily by interrupting descending pathways and removing normal inhibitory influences on spinal circuits.
The retrieved literature consistently supports the physiological mechanism that upper motor neuron lesions and spinal cord injuries disrupt descending control, leading to a loss of inhibitory inputs (such as GABAergic or general synaptic inhibition) and resulting in hyperreflexia and spasticity.