Key points

Introduction

Blepharoptosis is one of the most common problems presenting to the ophthalmic plastic surgeon. Most ptosis surgery involves some combination of resecting and advancing or plicating the eyelid retractors (the levator muscle/aponeurosis or Mueller muscle) with the intention of elevating the upper eyelid margin. Excluded from this paradigm are bypass procedures, such as frontalis suspension, which is not a focal topic of this discussion. Although ptosis surgery may conceptually appear straightforward, it requires a detailed knowledge of relevant eyelid anatomy, understanding of the pathophysiology of the cause of ptosis, and careful surgical planning to execute effectively. Even with these considerations, ptosis surgery can be frustratingly unpredictable, signifying that major gaps exist in our knowledge as it relates to ptosis physiology, mechanisms of repair, and the biological healing process.

Current surgical management of ptosis is typically by 1 of 2 approaches, anterior and posterior, mostly defined by the respective eyelid elevators surgically addressed: the levator anteriorly and Muller muscle posteriorly. The anterior/external approach involves advancement or resection of the levator aponeurosis, and for consistency in this discussion this will be referred to as an external levator resection (ELR). Posterior/internal approach ptosis surgery involves resection of the Muller muscle and conjunctiva, and for consistency this will be referred to as Muller muscle conjunctival resection (MMCR). It should be noted that neither of these surgeries is likely pure, and in each case some manipulation of the other elevator is expected. It is also important to differentiate the conceptual approach from surgical access. The incision does not define the approach. Techniques in which a posterior incision is used to plicate the levator are considered anterior approaches. Vice versa, methods in which an anterior incision is used to plicate the Muller muscle would be considered posterior approaches. We refer to anterior and posterior as they relate to the elevators primarily involved in the surgery, not the position of the incision or surgical access. Thus, whether the skin or conjunctiva is incised is not particularly relevant for this discussion of anterior and posterior ptosis surgery.

The decision of whether to perform anterior or posterior ptosis surgery in many ways ultimately depends on surgeon preference, although there are circumstances in which one approach may be preferred over the other. In this article, we discuss relevant anatomy, pathophysiology, surgical techniques, and our decision-making process for selecting the appropriate ptosis surgery.

Anatomic considerations

The 2 primary retractors of the upper eyelid are the levator palpebrae superioris (LPS) muscle and Muller muscle. The frontalis muscle is often considered a secondary retractor of the eyelid; however, recent investigations suggest that the mechanical action of the frontalis (elevating the brow) does not transmit to the eyelid under normal circumstances. The frontalis is thus not considered an eyelid elevator for this discussion.

The LPS is a skeletal muscle, originating from the lesser wing of the sphenoid bone superolateral to the optic canal. ^, Its muscular portion is approximately 36 mm long and fans out as it courses anteriorly from a width of 4 mm posteriorly to 18 mm at the level of the superior transverse (Whitnall) ligament. The Whitnall ligament consists of a band of fibrous tissue extending from the lacrimal gland fossa laterally to the trochlea medially. Whitnall’s ligament is believed to function as a pulley for the LPS, allowing the muscle to change direction.

Anterior to the Whitnall ligament, the LPS courses inferiorly as a fibrous aponeurosis. Microscopically, the transition from LPS to aponeurosis is gradual with muscular fibers present in diminishing amounts as it travels distally into the eyelid. The levator aponeurosis expands medially to form the medial horn, which coalesces with the posterior portion of the medial canthal tendon and inserts onto the posterior lacrimal crest. Similarly, a lateral horn is formed laterally, which divides the lacrimal gland into orbital and palpebral lobes and attaches to the lateral orbital (Whitnall) tubercle. ^{, ,}

The levator aponeurosis has been classically thought to insert inferiorly onto the lower half of the anterior surface of the tarsus in white eyelids. Histopathological evidence suggests though that this insertion may be more diffuse and variable, effectively anywhere along the tarsus. This is particularly evident in Asian eyelid configurations. Fibers of the aponeurosis additionally extend anteriorly through the orbicularis oculi muscle and insert onto the skin, which is believed to form the eyelid crease. ^,

The Muller muscle is a smooth muscle. Its origin is found within the Whitnall ligament, where the LPS undergoes muscle-aponeurosis transition. Histologic studies demonstrate interweaving smooth and striated muscle fibers at this position. ^, The Muller muscle is approximately 8 to 12 mm in length and courses deep to the levator aponeurosis, in what some consider to be a potential “postaponeurotic” space. Distally, there is some controversy regarding the insertion of the Muller muscle. Classically it is described as inserting onto the superior border of the tarsus. Other investigations have suggested that it may insert more inferiorly onto the anterior surface of the tarsus. Some have further proposed that the Muller muscle terminates above the tarsus within a complex network of elastic and collagen fibers involving the levator aponeurosis, Muller muscle, and orbicularis. ^, It is likely that this insertion is variable across populations, and may even change over time. Interestingly, the LPS-Muller configuration is somewhat unique in the body, with the skeletal LPS and smooth Muller muscle being arranged in series without a fixed anchor point.

The Muller muscle receives sympathetic innervation, a finding that has been confirmed clinically by its involvement in Horner syndrome, experimentally by immunostaining of sympathetic receptors, and pharmacologically by using sympathetic agonists and antagonists. Although it is known to be sympathetically innervated, the precise nervous pathway within the orbit is poorly understood. It is likely that innervation is derived from multiple sympathetic roots. The Muller muscle is responsible for approximately 3 mm of upper eyelid excursion. This has been confirmed experimentally in healthy subjects where from a neutral position, the eyelid can be lowered 1.5 mm with sympathetic antagonists and raised 1.5 mm with agonists.

There is some controversy regarding the function of the Muller muscle. Some suggest it is a transmitter of the levator aponeurosis action, whereas others propose it is a stretch receptor for the LPS, providing a primarily proprioceptive role. The most widely accepted hypotheses suggest that it functions to maintain tonic eyelid position, allowing for responses based on sympathetic stimulation, or that it maintains a 3 mm “fine tuning” role in upper eyelid position. It is additionally possible (and plausible) that the Muller muscle is multifunctional.

Pathophysiology

The determination of eyelid position likely involves a comprehensive maintenance system with afferent inputs, central processing, and efferent outputs. Dysfunction anywhere in this system may lead to ptosis, and ptosis surgery is theorized to modify this system, leading to a re-setting of static eyelid position.

Potential afferent inputs to this system include vision, touch sensation, and proprioception. Although it is well-documented that functional visual field impairment due to ptosis can be reversible with surgery, visual stimuli may not be a critical component in the development of ptosis, as patients with anophthalmic sockets can demonstrate ptosis and respond to both anterior and posterior ptosis surgery. Simple touch sensation also may be a less relevant input, as it is well known that an anesthetic eye, for instance after topical proparacaine use, is not reliably associated with ptosis. Proprioceptive stimuli are of keen interest as potential vital inputs ; however, much of the evidence for this pathway is speculative at this point. Further research is needed to determine the influence of these various afferent factors.

The flow of afferent information is also incompletely understood. Presumably these signals follow the trigeminal system. The trigeminal sensory pathway passes through the trigeminal ganglion, synapses in the main sensory trigeminal nucleus, decussates, and travels along the contralateral ventral trigeminal lemniscus before synapsing in the ventral posteromedial (VPM) nucleus of the thalamus. The proprioceptive signals from the extraocular muscles and eyelid elevators presumably follow this pathway; however, animal data suggest that at least some of the extraocular muscle proprioceptive input travels directly to the lateral geniculate nucleus with retinal ganglion cells and even with motor nerves, including the oculomotor nerve. From the thalamus, these signals travel diffusely throughout the brain to visual, sensory, and balance centers. Indirect evidence of eyelid position signals traveling through the thalamus can be drawn from studies in which thalamic injury (infarct, hemorrhage) can be associated with ptosis. These afferent systems are relatively poorly understood; however, they clearly play a role in eyelid position homeostasis.

Output systems are more completely characterized. Motor innervation to the LPS via the superior division of the third cranial nerve is well-established. ^, Muller muscle innervation is part of the sympathetic system. There is some controversy as to the precise anatomic projection of efferent intraorbital pathways to the Muller muscle, and the motor control could perhaps have input from other related extraorbital systems. However anatomically transmitted, much evidence of sympathetic innervation exists.

The integration and coordination of the afferent and efferent signals is the most sparsely investigated and consequently most poorly understood aspect of eyelid position physiology. Some have proposed a reflex arc involving afferent stretch receptors in the Muller muscle and efferent output via the LPS and frontalis muscles. ^, This work is theoretic, yet perhaps it does provide some framework for conversion of afferent to efferent signals, though without central processing.

There is, however, much emerging evidence of integration capacity, and thus central processing, in the eyelid position maintenance system. For instance, eyelid position is relatively preserved when gravitational forces are altered. We examined photographs of astronauts both on Earth and in space and found zero gravity does not significantly change marginal reflex distance 1 (MRD1). We have also shown that in healthy individuals, changing postural position was also associated with relative preservation of eyelid position. In addition, reducing protracting forces in facial palsy is in most cases associated with maintenance of normal eyelid position, although it should be noted that more severe facial weakness is associated with a breakdown in this system and eyelid position abnormalities. ^, These results together suggest there is adaptive capacity within the eyelid position maintenance system. However, at present the capacity, functionality, and neural basis for this system are each very poorly characterized. Clearly, more research in this area is needed to more accurately understand the determinants of eyelid position, particularly as it relates to central processing and proprioception.

Mechanisms of repair

Surgical technique