Background: For more than a century, unusual and complex deficits in facial expression have been known to occur following localized brain damage. Some brain injuries leave the face with pronounced alterations in affect whereas others result in movement disorders such as blepharospasm and Meige syndrome. There is also a historic trail of clinical observations that document deficits in either voluntary or emotional control of the facial muscles following central nervous system damage.
Review summary: Recent studies in the nonhuman primate cerebral cortex reveal the existence of multiple cortical facial representations in the frontal lobe and adjacent anterior cingulate cortex. These comprise the facial representation of the primary motor cortex (M1), ventral lateral premotor cortex (LPMCv), supplementary motor cortex (M2), rostral cingulate motor cortex (M3), and caudal cingulate motor cortex (M4). Homologous facial representations reside in the human brain based on observations following cortical stimulation, functional neuroimaging, and localized surgical resection. In the nonhuman primate, all these facial representations have been found to be directly interconnected through topographically organized corticocortical connections, and each facial area has also been found to send direct corticobulbar projections to the facial motor nucleus. The facial representations of M2 and M3 are both located on the medial wall of the hemisphere, in the vascular territory of the anterior cerebral artery. Both preferentially give rise to bilateral projections to parts of the facial nucleus that innervate the upper facial musculature as demonstrated in the monkey. The facial representation of M1, LPMCv, and M4 preferentially give rise to contralateral axonal projections ending in parts of the facial nucleus that innervate the lower facial musculature. The facial representation of M1 and LPMCv both reside in the vascular territory of the middle cerebral artery (MCA). The classic clinical presentation of paralysis in the contralateral lower facial musculature and intact bilateral upper facial musculature following typical MCA in infarction in the human parallels this mapping pattern of corticobulbar connections found in the nonhuman primate.
Conclusions: Facial movements are undoubtedly under the powerful influence of the cerebral cortex and are essential for the appropriate execution of many important functions such as mastication, swallowing, and social interaction, including speech and nonverbal communication. This information provides a theoretic template for interpreting the clinical effects of neuropathologic disease and localized cortical trauma on facial movements.