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A widened palpebral fissure has been regarded as one of the hallmarks of peripheral facial nerve palsy.1Contrary to this textbook description, however, peripheral facial nerve palsy often causes narrowing of the palpebral fissure on the affected side.2 This narrowing probably results from drooping of the upper eyelid because of weakness of the frontal muscle, but the anatomical basis has not been clear. We report here a bedside test which is very helpful in differentiating two types of palpebral narrowing—that is, one caused by weakness of the frontal muscle and the other by weakness of the levator palpebrae superioris.
Ptosis—palpebral narrowing—in the present communication was defined as drooping of the upper eyelid to cover one third or more of the cornea, according to the criteria described by Caplan.3Its severity was classified into three grades: (1) mild ptosis if the upper eyelid covered more than one third of the cornea, (2) moderate ptosis if it covered more than one half of the cornea, and (3) severe ptosis if the palpebral fissure was nearly closed.
The subjects were six patients with peripheral facial nerve palsy with palpebral narrowing but with no abnormality of the pupils and eye movements (five men, one woman; age range, 33 to 72 years; mean age 60.3 years) and five patients with oculomotor nerve palsy having ptosis but without facial palsy (two men, three women; range 45 to 64 years; mean age 59.5 years). In all subjects peripheral facial nerve palsy or oculomotor nerve palsy developed acutely or suddenly. The palpebral narrowing was confirmed by the patient or family by comparison with the previous state. The aetiologies of peripheral facial nerve palsy consisted of peripheral facial nerve injury at craniotomy (one patient), sarcoidosis (one patient), and Bell’s palsy (four patients), and those of oculomotor nerve palsy consisted of oculomotor nerve injury due to aneurysmal surgery at the top of the basilar artery (two patients), cavernous sinus syndrome (one patient), IC-PC aneurysm (one patient), and midbrain infarction (one patient). The patient with peripheral facial nerve palsy and sarcoidosis and the patient with oculomotor nerve palsy and midbrain infarction had bilateral palsy.
On neurological examination at their acute stage all were alert and cooperative. All showed drooping of the upper eyelid. No patient showed excessive contraction of the orbicularis oculi muscles as occurs in blepharospasm. All of the peripheral facial nerve palsy group were unable to close their eye tightly. All of the oculomotor nerve palsy group had either a dilated or normal sized pupil, but no weakness of the upper face on the affected side. With the patient looking straight ahead, the following items were evaluated: (1) severity of palpebral narrowing (ptosis), (2) position of the eyebrow on the affected side, and (3) change of palpebral narrowing when the eyebrow on the affected side was lifted manually by the examiner (“eyebrow lifting test”).
Of the patients with unilateral peripheral facial nerve palsy, two showed severe, two moderate, and one mild palpebral narrowing. One patient with bilateral peripheral facial nerve palsy showed severe palpebral narrowing on one side and moderate narrowing on the other side. Of the patients with unilateral oculomotor nerve palsy, three showed severe and one mild palpebral narrowing. One patient with bilateral oculomotor nerve palsy showed severe narrowing on both sides.
In four patients with peripheral facial nerve palsy and unilateral palsy, the position of the eyebrow on the affected side was much lower than the non-affected side, whereas in two patients with unilateral oculomotor nerve palsy, it was much higher. In the remaining three patients with unilateral peripheral facial nerve palsy or oculomotor nerve palsy and two with bilateral palsy, there was no remarkable laterality of the position of the eyebrows. However, on closer inspection the eyebrow on the narrower side of the palpebral fissure in two patients with peripheral facial nerve palsy (one unilateral and one bilateral) was definitely lower although the degree was slight.
In all of the peripheral facial nerve palsy group palpebral narrowing disappeared when the eyebrow on the affected side was lifted slightly, whereas in all of the oculomotor nerve palsy group palpebral narrowing remained unchanged, even when the eyebrow was lifted to its maximal extent (figure). In two of the patients with unilateral or bilateral peripheral facial nerve palsy, and in two of the patients with unilateral oculomotor nerve palsy, lifting of the eyebrow on the affected side led to drooping of the contralateral eyelid, although this phenomenon was not found in the others (figure).
Elevation of the upper eyelid is served chiefly by the levator palpebrae superioris innervated by the oculomotor nerve, and accessorily by Müller’s muscle via the oculosympathetic pathway and by the frontal muscle via the facial nerve.4 The frontal muscle participates in eyelid elevation indirectly through the attachments into the eyebrow.4 Therefore, the palpebral narrowing due to frontal muscle weakness occurs as a result of drooping of the eyebrow, and is essentially different from palpebral narrowing caused by weakness of the eyelid muscles.2
We applied this difference to an “eyebrow lifting test”. As was described, the result of this test was clear cut. All the palpebral narrowing due to peripheral facial nerve palsy disappeared, and all the narrowing caused by oculomotor nerve palsy remained unchanged. This implied that the peripheral facial nerve palsy related narrowing was attributable to weakness of the frontal muscle but not of the levator palpebrae superioris.
In patients with drooping of the contralateral eyelid elicited by lifting of the eyebrow, their attempts to overcome palpebral narrowing may have induced an increase in innervation in both levator palpebrae superioris muscles resulting in elevation of the contralateral eyelid, because Hering’s law of equal innervation to agonist muscles applies to the levator palpebrae superioris as well as to the extraocular muscles.5 Therefore, it is plausible that in the two patients with peripheral facial nerve palsy resolution of palpebral narrowing on one side led to a decrease in levator palpebrae superioris innervation with resultant drooping of the contralateral eyelid. It remained to be determined, however, why this phenomenon occurred in some patients with peripheral facial nerve palsy and not in others, and why it also did in the two patients with oculomotor nerve palsy without resolution of palpebral narrowing.
Palpebral narrowing associated with peripheral facial nerve palsy showed a varying degree of drooping of the eyebrow. There were patients with a severe degree of narrowing. This indicates that the frontal muscle which has been considered as an accessory muscle, occasionally plays a very important part in eyelid elevation. We suspect that this is closely related to the skin condition of the upper face. Some Japanese people, especially elderly ones, have excessively loose skin of the upper eyelid or forehead, resulting in “masked” palpebral narrowing. In such a situation, occurrence of frontal muscle weakness can produce severe palpebral narrowing.
In conclusion, the “eyebrow lifting test” is simple but very helpful in differentiating between two types of palpebral narrowing due to weakness of the frontal muscle and levator palpebrae superioris.
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