The motor nucleus of the facial nerve receives supranuclear inputs from different areas of the brain that mediate facial muscle contractions in different contexts. The main examples are the corticonuclear fibers that originate in the primary motor cortex, which mediates volitional (voluntary) movements of the face, and limbic pathways, that originate in diverse areas of the cortex such as the medial surface of the prefrontal cortex, the insula, and the cingulate gyrus, that mediate involuntary emotional facial expressions [1,2,3].

Lesions of these supranuclear pathways may result in selective impairment of the contraction of facial muscles depending on whether the patient is smiling volitionally (such as when the doctor asks for it) or spontaneously (such as seeing a loved one or hearing a joke). In cases of supranuclear facial palsy, there may be volitional paralysis that spares the emotional smile with lesions affecting only the corticonuclear pathways, emotional paralysis that spares the volitional smile with lesions affecting solely the limbic pathways, or paralysis during both the volitional and emotional smiling with lesions affecting both pathways [4]. Georg Herman Monrad-Krohn (1884-1964) was the first to describe that in some cases of selective volitional paralysis, the emotional movements of the face may not only be spared but may even be accelerated and exaggerated, such as seen in the present case [5]. This phenomenon suggests that when volitional pathways are impaired, emotional ones may become more active – the extreme example is the uncontrolled emotional expressions that patients with bilateral lesions of the corticonuclear pathways can exhibit (called pseudobulbar palsy).