According to Flowers, 1 one must appreciate that the eye will open quite normally with total disconnection of the aponeurosis, as long as there is an intact and properly functioning Mueller’s muscle. Although this can be demonstrated clearly on live patients at surgery, supine and seated, it could be that prolonged absence of insertion by the leathery aponeurosis allows fraying and attenuation of Mueller’s muscle, and in time leads to ptosis. We propose a hypothetical mechanism for involuntary tonic contraction of the levator muscle for keeping the palpebral fissure open (Fig 1B). 2 According to this hypothesis, Mueller’s muscle may function as a large muscle spindle of the levator muscle, so that stretching of this muscle by voluntary phasic contraction of type II fibers of the levator muscle may evoke an afferent impulse to the mesencephalic trigeminal nucleus. Subsequently, this nucleus may stimulate a part of the central caudal nucleus of the oculomotor nuclear complex, leading to involuntary contraction of type I fibers of the bilateral levator muscles, which results in involuntary retraction of the bilateral upper eyelids. This study investigated how and why aponeurotic blepharoptosis develops in terms of the relationship between the levator aponeurosis and Mueller’s muscle functioning as the muscle spindle of the levator muscle.
Materials and Methods
A total of 200 consecutive patients with acquired blepharoptosis who underwent surgery between 1993 and 1996 were evaluated. The average age of the 161 women and 39 men was 56.1 years (age range, 31–79 years). Their ptosis was graded as moderate to severe according to the upper eyelid position in the primary gaze position and the upper eyelid excursion, which ranged from less than 5 to 7 mm. Patients completed questionnaires regarding their history of physical irritation to the eyelids, trauma, contact lens usage, cataract surgery, and so on. We always incise the orbital septum horizontally to open the preaponeurotic fat space, which allows us to observe the levator aponeurosis, levator muscle, and Mueller’s muscle. Intraoperative photographs were taken to document the condition of the levator aponeurosis and that of the Mueller’s muscle behind it (Figs 1B and C). Informed consent for this study was obtained in writing from all patients.
Several kinds of physical irritations to the eyelids were reported, such as habitual rubbing of the eyelids (182 patients), contact lens usage (117 patients), 3,4 cataract surgery (23 patients), 5 and continuous rubbing of the eyelids while crying all night (5 patients). Habitual rubbing of the eyelids was found to cause aponeurotic blepharoptosis at any age, regardless of the history of contact lens usage. The rubbing was caused by arousal stimulation (182 patients), removal of makeup in female patients (143 patients), crying (17 patients); and itching (192 patients) resulting from dryness immediately after removal of contact lenses (117 patients), allergic conjunctivitis and dermatitis (76 patients), atopic dermatitis (14 patients), dry eyes (81 patients), cilial irritation (23 patients), and the contact lenses themselves (1 patient). 6 Hard contact lens users forcefully pulled the eyelid skin on removal of the lenses. 7 Hard contact lenses were used by 55 patients, soft contact lenses were used by 38 patients, and both types of contact lenses were used by 117 patients. The duration of contact lens use ranged from 3 months to 31 years, and the severity of blepharoptosis depended on the duration of contact lens usage, regardless of the lens material. Patients who both habitually rubbed their eyelids and used contact lens experienced aponeurotic blepharoptosis within a short period of time.
There were two main findings regarding aponeurosis. First, the aponeurosis was disinserted from the tarsus, resulting in a large amount of play between the aponeurosis and the tarsus (Figs 2 and 3), but there was no disconnection of the aponeurosis from the tarsus (Fig 4C). Disinsertion was observed to a greater or lesser degree in patients of all ages. Second, the aponeurosis and Mueller’s muscle behind it were attenuated and elongated (Fig 4) in older patients and in younger patients with a long history of habitual rubbing of the eyelids and contact lens usage. No dehiscence or fraying of the aponeurosis was observed.
The reported etiologies of aponeurotic blepharoptosis include acquired dehiscence, 8 disinsertion, 9 or stretching 10 of the aponeurosis, which connects the levator muscle to the tarsal plate. Intraoperative examination revealed that the etiologies of aponeurotic blepharoptosis consisted of disinsertion and attenuation of the levator aponeurosis. Dehiscence may be caused iatrogenically by surgical dissection via a difficult route. These findings suggest the following pathogenesis (Table): Nothing but the small terminal fibers of the levator aponeurosis are inserted onto the tarsus (Fig 1A), 11,12 so that rubbing of the eyelids as a result of itching and crying may disinsert the fibers from the tarsus, resulting in a moderate amount of play between the levator aponeurosis and the tarsus at a young age (see Fig 1B). 13 After disinsertion, the levator muscle retracts the pretarsal fascia via the levator aponeurosis and the tarsus via Mueller’s muscle. Under these circumstances, the levator muscle and Mueller’s muscle act as a continuous two-belly muscle, 14,15 which means that the levator muscle and its muscle spindle (Mueller’s muscle) are arranged in series in the physiological sense. The mechanoreceptor in Mueller’s muscle may then be controlled easily by contraction of the levator muscle, resulting in a wider palpebral fissure at adolescence. Further rubbing because of removal of makeup, in addition to itching and crying, and forceful pulling of the eyelid skin on removal of hard contact lenses 7 may cause loosening of the pretarsal fascia, resulting in a large amount of play between the levator aponeurosis and the tarsus. Because this play causes transmission failure between the levator muscle and the tarsus via the levator aponeurosis, it may require not only excessive voluntary contraction of the levator muscle (glaring) but also sympathetic contraction of Mueller’s muscle to retract the tarsus. Therefore, the sympathetic tone to Mueller’s muscle—which travels via the noncardiovascular sympathetic center in the hypothalamus, the ciliospinal tract of Budge, and the superior cervical ganglion—is important both to maintain retraction of the upper eyelid and to control sensitivity of the mechanoreceptor of Mueller’s muscle. However, it is not known what controls the activity of the noncardiovascular sympathetic center in the hypothalamus.
The cornea is smaller in curvature than the eyeball, and Mueller’s muscle and the anteriorly located aponeurosis are softer than the tarsus. Interactive movement between the cornea and the eyelid during closing and opening of the eye may therefore attenuate and elongate Mueller’s muscle and the aponeurosis in front of it through these differences in shape and consistency as a consequence of the natural aging process (see Figs 1A and C). This process may be accelerated by the contact lens, which projects onto the surface of the cornea. It may also be accelerated by habitual rubbing of the eyelids toward the cornea. This attenuation and elongation combined with disinsertion may cause transmission failures between the levator muscle and the tarsus as well as between the levator muscle and the mechanoreceptor of Mueller’s muscle despite excessive voluntary contraction of the levator muscle and sympathetic contraction of Mueller’s muscle. This condition then results in clinical blepharoptosis (see Fig 1C).
Based on another point of view, aponeurotic blepharoptosis can be classified into compensated and decompensated stages (see the Table). During the compensated stage, involuntary contraction of the levator muscle cannot compensate for transmission failures, but voluntary contraction (glaring) can. During the decompensated stage, even voluntary contraction of the levator muscle can no longer compensate for transmission failures, resulting in the clinical manifestation of blepharoptosis in the primary gaze position.
Presented at the 14th annual meeting of the Japan Society of Cranio-Maxillo-Facial Surgery; Yokohama, Japan; November 8, 1996.
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