Bilateral anterior opercular syndrome is also known as Foix-Chavany-Marie syndrome (FCMS). FCMS is characterized by a loss of voluntary control of facial, lingual, pharyngeal and masticatory muscles, in the presence of preserved reflexive and automatic functions (automatic-voluntary dissociation) of the same muscles. The lesions are usually located at the anterior part of the operculum. Here, we report the case of a patient in whom FCMS developed following right putamen and corona radiata stroke.
Case report
A 62 - year old man with manifesting left hemiparesis, anarthria and hypomimia visited our clinic. He had a past history of hospitalization with left basal ganglia infarction in same year. Understanding of spoken and written language was preserved and there were no apraxia or agnosia. The mouth was closed, but the patient could open his mouth about 2 finger breath. On neurologic examination, corneal reflex was preserved. There was no limitation of eyeball movement, but he could not completely close his both eyes. Bilateral facial paralysis was observed, severe in the left side, but sensory of face was preserved. The gag reflex was diminished, and he was unable to initiate swallowing due to severe clumsiness of tongue. On the other hand, swallowing reflex was preserved. The tongue was immobile, did not show fibrillate, with slightly right side deviation. He had a severe left upper and lower limb paresis (upper - MRC grade 1/5, lower- MRC grade 2/5). He had a generalized hyperreflexia in left upper and lower limb, and Babinski reflex was not observed. He had bilateral lip, tongue, and pharyngeal weakness with automatic-voluntary dissociation of the lower face.
These symptoms were the hallmark of FCMS and also referred to as bilateral opercular syndrome. Brain MRI performed on the day of symptom onset showed acute cerebral infarction in the right putamen and corona radiata and encephalomalacia due to old infarct in left putamen and corona radiata. The subcortical lesion causes an automatic-voluntary dissociation because the corticobulbar tract from the fronto-parietal cortex passes through the corona radiata and posterior limb of internal capsule. This suggests that the subcortical lesion could lead to FCMS due to the failure of the connection between cortical and subcortical structures.
Conclusion
In this case, the brain MRI finding did not demonstrate bilateral opercular lesions. We suggest that a unilateral corona radiata lesion may lead to FCMS in a patient who already has contralateral subcortical dysfunction although bilateral opercular lesions is the main etiology of FCMS.
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