Motor control of the limbs starts with a motor plan being developed in association motor cortices; this probably occurs bilaterally, but more so contralateral to the limbs to be moved than ipsilateral. Motor planning involves input from sensory cortices, the cerebellum, and the basal ganglia. The motor plan is sent to the primary motor cortex, contralateral to the limbs to be moved, for execution. Upper motor neurons in the parts of the primary motor cortex that control the arm (lateral) and the leg (medial) send axons into the corticospinal tract that descends through the deep cerebrum and brainstem.
Most of these axons decussate at a place called the pyramidal decussation, which is at the junction of the brainstem and the spinal cord. These axons then continue to descend in the lateral column of the spinal cord, where they are called the lateral corticospinal tract, until they synapse, directly or via interneurons, on lower motor neurons in the anterior gray horn of levels connected to the limbs. These levels are in the upper spinal cord for the arms and the lower spinal cord for the legs. Because of the pyramidal decussation, most of the control of limb movements is from the contralateral brain.
Upper motor neurons that control limb movements appear to have more redundant innervation for muscles groups of the arms that are proximal, flexor, and pronator; the same is true for muscles groups of the legs that are proximal, extensor, and plantarflexor. These patterns are presumed because the opposite pattern of weakness often appears with corticospinal tract dysfunction. This pattern often caused a distinctive posture after a unilateral lesion of the corticospinal tract: the arm is flexed and the hand is pronated, while the leg is extended and the ankle is plantarflexed. This is usually most noticeable when walking, when the patient often swings the foot around laterally to avoid catching the toes on the ground, which is called circumduction. This overall pattern when walking is called the hemiparetic gait.