In contrast, the unilateral form is rare and is caused by the formation of lesions on one side of the anterior or posterior region of the operculum.

[1] Lesions located in the anterior regions of the operculum are associated with motor deficits and anarthria, a total absence of the ability to form speech or language.

It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula formingFoix–Chavany– the gyri of the frontal, temporal, and parietal lobes.

[1] An individual affected with FCMS develops disabilities associated with voluntary movements using the facial, lingual, pharyngeal, and masticatory muscles.

The formation of bilateral lesions confined to the posterior operculum has a distinct symptom of word deafness, an inability to understand language.

However, less common causes that can eventually produce lesions to the operculum resulting in the FCMS syndrome include the following; tumors, trauma, encephalitis, neurodegenerative diseases, and vasculitis.

This causation results in the only reversible development of FCMS as it is the only cause that allows full recuperation from speech, swallowing, and mastication difficulties when treated.

[6] Anatomically, the word operculum is defined as the cortices encompassing the insula, which includes the pre and post-central, inferior-frontal, supramarginal, angular inferior parietal, and superior temporal convolutions.

Cerebral malformation, namely unilateral schizencephaly in association with contralateral polymicrogyria symmetrically in the perisylvian area is another known characteristic of FCMS.

Neurons that lie adjacently in the operculum project supranuclear fibers to the cranial nuclei for the voluntary movement of facial, pharyngeal, lingual, and masticatory muscles.

Emotional movement of these muscles is controlled by alternative pathways that run from the amygdala and lateral hypothalamus to the brainstem via the medial forebrain bundle and dorsal longitudinal fasciculus.

[1] In determining a diagnosis between with catatonia, akinetic mutism, and FCMS, a person must demonstrate their ability to perform voluntary function of the limbs.

In determining a diagnosis between Broca's aphasia and FCMS, a person must demonstrate their ability in voluntary movement of cranial musculature.

[1] In determining a diagnosis between pseudobulbar palsy, a person must demonstrate whether or not muteness is present, as well as the ability to move the facial, buccal, lingual, and pharyngeal muscles.

[9] In addition, brain scanning techniques are utilized to observe whether ischemic abnormalities or lesions are present within the operculum region of the cortices.

CT scans can also reveal, in patients with the syndrome, the bilateral cortical infarcts located in the posterior frontal region involving the opercular areas.

An electroencephalography (EEG) is also used in patients with the FCMS and it can reveal focal slowing and epileptic discharges from left fronto-temporal regions.

FCMS caused by epilepsy, specifically resulting in the development of lesions in the bilateral and subcortical regions of the brain can be treated using antiepileptic drugs to reverse abnormal EEG changes and induce complete neurological recovery.

Classical FCMS resulting in the decline of ones ability to speak and swallow can be treated using neuromuscular electrical stimulation and traditional dysphagia therapy.

Speech therapy further targeting dysphagia can strengthen oral musculature using modified feeding techniques and postures.