mise à jour du
15 août 2002
The laryngoscope
The opercular syndrome - diagnostic trap in facial paralysis
Roger L Crumley San Francisco
voir imagerie de l'Opercule Rolandique


Case report : A 28-year-old black man was admitted to San Francisco General Hospital after being knocked out during an altercation. He was unconscious for an unknown period of time, but was subsequently taken home, where he slept for about 10 hours prier to admission. His initial complaints included headache, more severe on the left than on the right, and bloody drainage from the left car. He denied prior problems with his ears or facial paralysis.

Physical examination revealed an alert man with bloody otorrhea on the left. A tender boggy hematoma was present in the occipital area on the left, but there was no Battle's sign. Moderate swelling in the left parotid region was noted. The mandible deviated to the right on opening but the mandible and maxilla were intact. The left tympanic membrane was torn and a trickle of blood was seen coming from the middle ear. The Weber lateralized to the left, and the Rinne test was negative at 512 Hz on the left. A partial left facial paralysis was present, with inability to close the eye completely, wrinkle the nose, or smile. There appeared to be near normal voluntary movement in the forehead and platysma. The patient's mouth was noted to be nearly symmetrical at rest. The tongue deviated slightly to the left on protrusion. Skull X-rays were negative for fracture.

A diagnosis of left temporal bone fracture with facial nerve laceration or contusion was entertained, but the correct diagnosis became apparent when the patient laughed at a joke, exhibiting a normally symmetrical smile. He then yawned, and the upper and lower lips again moved symmetrically. Confirmation of the supranuclear contralateral location of the injury came when seizure activity was seen commencing in the left nasolabial fold area, and marching in true Jacksonian manner to involve the entire face on the left, masseter and temporalis muscles, tongue, sternocleidomastoid, and musculature of the upper arm on the left. The seizure lasted approxiniately 90 sec and resolved spontaneously. Postictally, the facial paralysis persisted to voluntary mimetic efforts, but emotional movements were normal. Eye blinking was normal in response to corneal stimulation, but the patient was unable to completely close the left eye voluntarily. One gram of phenytoin was given intravenously, and no further seizures were noted. The patient signed out of the hospital before an electroencephalogram or computed tomographic brain scan could be done. The patient has not returned for follow-up examination, but reported by telephone that the facial paresis resolved after a few days.

Comment : The paralysis of voluntary facial motion with retention of involuntary movement is easily explained by the neuroanatomy of the facial nucleus and its multiple supranuclear pathways. Volitional facial movements originate in the cerebral cortex of the precentral gyrus, and impulses pass through fibers in the internal capsule to synapse in the facial nucleus. The frontalis, corrugator supercilii and orbicularis oculi muscles are innervated by a clearly delimited area of the nucleus, the pars intermedia. The supranuclear innervation of this part of the nuclelis is both crossed and uncrossed, e.g., from both right and left sides of the cortex. This is why most central paralyses exhibit sparing of the upper face. (In this regard, May has shown that it is possible for a temporal bone fracture, or a stab wound of the parotid gland, to produce a facial paralysis with sparing of the upper face, due to the spatial orientation of fibers in the nerve trunk.) The "pseudo-peripheral" paralysis of the operculum syndrome does not usually spare the upper face, although in our patient this was not the case.

At least six other sites of innervation for the facial nucleus are known, each of which is responsible for a particular reflex or specific muscle stimulation. Fibers from the superior colliculus are responsible for the blink reflex in response to a bright light. Connections with the trigeminal nuclei produce a blink in the corneal reflex. Emotional smiles invoked by happiness or humor are the result of innervation of the facial nucleus by fibers front the thalamus and the globus pallidus. Tlie involuntary periodic blinking of both eyes is due to additional afferents from the reticular formation and/or basal ganglia. The stapedial acoustic reflex is mediated produced by fibers from the nucleus of tractus solitarius.

All of these "lower reflex" movements of muscles innervated by the facial nerve are preserved in patients with cortical or high corticobulbar lesions. Disorders of the brainstem and/or midbrain, on the other hand, may cause a paralysis of these reflexes, while voluntary movements (as the "social" smile) are preserved. There is evidence that a second cortical region located in the temporal lobe participates in the emotional smile pathway. A reciprocal picture, then, is seen in patients with lesions of these lower centers, e.g., in paralysis agitans or postencephalic Parkinsonism, voluntary or mimetic movements are normal while emotional facial responses are lost.

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