Upper Motor Neuron (UMN): Cell bodies lie in the primary motor cortex (Betz cells of area pyramidalis) and brain stem; their axons form the corticospinal (pyramidal) and corticobulbar tracts, which descend to synapse on the anterior horn (motor) neurons of the spinal cord or cranial nerve nuclei.

Lower Motor Neuron (LMN): These are the anterior horn cells of the spinal cord (or cranial nerve motor nuclei) whose axons pass directly, via peripheral nerves, to innervate skeletal muscle fibers at the neuromuscular junction.

The primary motor cortex normally exerts a continual tonic stimulatory effect on the spinal motor neurons. According to Guyton and Hall, when a lesion destroys only the primary motor cortex (area pyramidalis) without damaging adjacent areas, there is loss of voluntary control of fine, discrete movements (especially of hands and fingers) but gross postural movements are preserved - this reflects the essential role of the area pyramidalis in voluntary fine motor control (Guyton and Hall Textbook of Medical Physiology, p. 691-692).

However, most real-life lesions (e.g., stroke) damage not just the primary motor cortex but also adjacent nonpyramidal motor areas and basal ganglia connections. These accessory pathways normally inhibit the vestibular and reticular brain stem motor nuclei. When cortical lesions destroy these inhibitory pathways, the vestibular/reticular nuclei become "disinhibited" and spontaneously overactive, producing excessive spastic muscle tone on the opposite side of the body (since motor pathways cross) - this is the mechanism of the spasticity that classically follows a stroke (Guyton and Hall, p. 692).

In contrast, damage to the LMN itself (anterior horn cell or its peripheral axon) removes the direct final motor pathway to muscle, so the muscle loses both voluntary and reflex innervation, causing flaccid paralysis, loss of reflexes, and rapid muscle wasting (denervation atrophy) because trophic influence from the nerve is lost.

UMN lesion = "spastic paralysis" with hyperreflexia, Babinski positive, no fasciculations. LMN lesion = "flaccid paralysis" with hyporeflexia/areflexia, wasting, and fasciculations.

This dichotomy arises because the UMN lesion removes descending cortical inhibition of brain stem reflex centers (causing disinhibition/spasticity), whereas an LMN lesion removes the final common pathway to the muscle itself, abolishing both voluntary movement and spinal reflexes at that segment.

Recent evidence check: I ran a search for recent systematic reviews/meta-analyses on this topic, but UMN/LMN lesion differentiation is stable, foundational neurophysiology - not an area with evolving clinical-trial evidence, so no contradicting recent literature applies here.