The patient's hemiparesis is produced by damage to either the motor cortex or the corticobulbar and corticospinal axons as they run through the deep white matter of the hemisphere toward the internal capsule. The leg area of cortex should not be affected since it is located on the medial aspect of the hemisphere and is in ACA territory. However the corticospinal axons for the leg must swing around to the lateral ventricle as they travel away from the cortex, and this puts them into superior branch MCA territory. Usually patients like this have less paralysis in the leg than in the arm and face. Presumably, the reason is that leg motor cortex is still intact and retains some additional functional connections. Sensory loss reflects milder damage to the somatosensory cortex for face and arm, which again is located on the lateral aspect of the hemisphere.
This patient has Broca's (expressive) aphasia, which is an intellectual or cognitive deficit in assembling or expressing ideas with language, whether spoken or written. These patients may also have difficulty enunciating words because of lower facial paralysis. Much of the inferior frontal and parietal as well as superior temporal lobes and insular cortex near the sylvian fissure is devoted to different aspects of language functions. Localization of specific aspects of language (speaking, reading etc.) is complex. A severe, lasting Broca's aphasia reflects damage to a large area of cortex that is centered in the inferior frontal gyrus.