into the eyelid anterior to the septum. In such cases, the septum can be misidentified as the levator aponeurosis.

Any restriction in the movement of the septum with the levator and orbicularis muscles, as with scarring from trauma or previous surgery, can result in a mechanical ptosis, retraction, or lagophthalmos.

The Preaponeurotic Fat Pockets

The preaponeurotic fat pockets in the upper eyelid and the precapsulopalpebral fat pockets in the lower eyelid are anterior extensions of extraconal orbital fat. These eyelid fat pockets are surgically important landmarks and help identify a plane immediately anterior to the major eyelid retractor, which is the levator aponeurosis. In the upper eyelid, there are typically two fat pockets: a medial pocket and a central one. Laterally, the lacrimal gland may be mistaken for a third fat pocket, although the color and texture are different, i.e., the lacrimal gland is more tan or pink in hue and firmer than the preaponeurotic fat. In the lower eyelid, there are three pockets: medial, central, and lateral. Occasionally, there is extensive fatty infiltration of Müller’s muscle. During ptosis surgery, it is important to recognize this since in these cases the aponeurosis lies anterior to this fatty layer and the next posterior layer is conjunctiva.

The Major Eyelid Retractors

The retractors of the upper eyelid consist of the striated levator palpebrae muscle and the smooth Müller’s sympathetic muscle. They function together to elevate the eyelid in a complex interplay relying on involuntary proprioceptive receptors mainly in Müller’s muscle, voluntary contractions of the levator coordinated with the vertical extraocular muscles, and voluntary and reflex arc movements of the orbicularis muscle.

The Levator Muscle

and Aponeurosis

In congenital ptosis, the levator muscle has been thought to be dystrophic. However, Edmonds et al. failed to find any histochemical differences between levator muscle fibers in normal individuals and those with congenital ptosis [10]. On the other hand, Iljin et al. [11] found that in congenital ptosis the levator muscle shows varying amounts of hypoplasia, decreased number and varying diameter of muscle fibers, collagen proliferation, mitochondrial loss, and hypoplasia in the endomysium and perimysium. They reported that the clinical severity of ptosis correlated with the degree of histopathologic changes.

In involutional ptosis, the pathology is generally thought to result from aponeurotic linkage failure, either disinsertion or more commonly redundancy. However, it has been shown that there is a correlation between degree of ptosis and reduced levator muscle function, suggesting levator muscle dysfunction as a possible additional contributing factor [12].

The levator muscle arises from the lesser sphenoid wing just above the annulus of Zinn. The muscle runs forward in the superior orbit just above the superior rectus muscle. Near the superior orbital rim, a condensation is seen in the muscle sheath [9], which forms the superior suspensory fascia of the levator system. This suspensory fascia is also referred to as Whitnall’s ligament. Its anterior component is formed by a thickening of the levator sheath, and its thicker posterior component represents a thickening of the common sheath separating the levator muscle from the underlying superior rectus muscle [13]. This posterior component has been referred to as the intermuscular transverse ligament by Lukas et al. [14] and appears to be the same structure referred to as the conjoint fascial sheath by Hwang et al. [15]. These fascial bands surrounding the levator muscle attach medially and ­laterally to the orbital walls and soft tissues, and fibers also blend with Tenon’s capsule below. These are important suspensory structures for the levator muscle/aponeurosis complex and

therefore should not be cut during ptosis surgery. A framework of fine fascial strands loosely suspends this fascial structure to the orbital roof. While the exact role of Whitnall’s ligament has been a matter of controversy, it appears to provide some support for the orbital fascial systems that maintain spatial relationships between a variety of anatomic structures in the superior orbit. However, the ligament does not correspond to the highest point of levator vector change, and MRI studies have shown that the ligament moves significantly with eyelid elevation, so that it clearly does not act as a fulcrum for the levator as the latter changes its vector from horizontal in the orbit to vertical in the eyelid (Fig. 3.4).

From Whitnall’s ligament, the muscle passes into its aponeurosis (Fig. 3.5). This structure has been shown to be made up of several layers. A thicker anterior layer terminates near the junction of the aponeurosis with the orbital septum. In the Caucasian double eyelid, this layer sends numerous delicate interconnecting slips forward and downward through the postorbicular fascial tissue to insert into the interfascicular septa of the pretarsal orbicularis muscle and subcutaneous tissue of the skin. These multilayered slips maintain the close approximation of the skin, muscle, aponeurosis, and tarsal lamellae, thus integrating the distal eyelid as a single functional unit. This relationship defines the upper eyelid crease of the western eyelid [16]. In the single

Asian eyelid, these anterior fibrous slips are less well developed or absent [17]. A thinner posterior layer of the aponeurosis is in contact with Müller’s supratarsal muscle and fuses with the anterior surface of the tarsus. Reid et al. [7] stressed that failure to recognize this layer could result in failure of ptosis surgery and postoperative lagophthalmos.

Both layers of the aponeurosis contain scattered smooth muscle fibers, more heavily concentrated in the posterior layer [18].

The levator aponeurosis is most firmly attached at about 3–4 mm above the eyelid margin [19, 20]. While the aponeurosis partially inserts onto the anterior surface of tarsus, most of its fibers insert onto the overlying orbicularis muscle interfascicular sheaths. As the aponeurosis passes into the eyelid from Whitnall’s ligament, it broadens to form the medial and lateral “horns.” The lateral horn forms a prominent fibrous sheet that indents the posterior aspect of the lacrimal gland, defining its orbital and palpebral lobes. It inserts through numerous slips onto the lateral orbital tubercle of the zygomatic bone, at the lateral retinaculum. The medial horn is less well developed. It blends with the intermediate layer of the orbital septum and inserts onto the posterior crus of the medial canthal tendon and the posterior lacrimal crest. Together, the two horns serve to distribute

the forces of the levator muscle along the aponeurosis and the tarsal plate.

In the lower eyelid, the capsulopalpebral fascia is a fibrous sheet arising from Lockwood’s ligament and the sheaths around the inferior rectus and inferior oblique muscles. It passes upward and generally fuses with fibers of the orbital septum about 4–5 mm below the tarsal plate. From this junction, a common fascial sheet continues upward and inserts into the lower border of tarsus. Fine fibrous slips pass forward from this fascial sheet to the orbicularis intermuscular septae and subcutaneous tissue, forming the lower eyelid crease and uniting the anterior and posterior lamellae into a single functional unit.

The Sympathetic Eyelid Retractors

Smooth muscles innervated by the sympathetic nervous system are present in both upper and lower eyelid and serve as accessory retractors [21]. In the upper eyelid, the supratarsal muscle of Müller originates abruptly from the under surface of the levator muscle just anterior to Whitnall’s ligament [22]. It runs downward, posterior to the levator aponeurosis, to which it is

adherent, and inserts onto the anterior edge of the superior tarsal border. Muscle fibers are intermixed with connective tissue, fat and blood vessels. Laterally, Müller’s muscle extends along with the levator aponeurosis between the orbital and palpebral lobes of the lacrimal gland, where it interdigitates with the ductules passing between the two lobes. These lateral fibers may contribute to the lateral flare commonly seen in patients with thyroid eye disease [23].

In the lower eyelid, the sympathetically innervated inferior tarsal muscle is less well defined. Fibers run behind the capsulopalpebral fascia to insert onto the lower border of tarsus, although they may end 2–5 mm below tarsus [24]. As noted above, the levator aponeurosis does not have any major attachment to the tarsus, and it is likely that Müller’s muscle helps transmit the levator force to the tarsal plate and conjunctiva [25]. In fact, it is theorized that the Müller’s muscle-conjunctival resection procedure for ptosis correction works by plicating levator and enhancing its effect.

Disruption of sympathetic innervation to these muscles results in Horner’s syndrome. This is characterized by the classic triad of ptosis, miosis, and ipsilateral anhidrosis of the face. Specific clinical findings vary according to the location of the lesion along the polysynaptic pathway. The upper eyelid ptosis and elevation (“reverse ptosis”) of the lower eyelid result from loss of sympathetic smooth muscle tone and therefore reduction in its action as an accessory eyelid retractor.

The Tarsal Plates

The tarsal plates consist of dense fibrous tissue, approximately 1–1.5 mm thick, that give structural integrity to the eyelids. Each measures about 25 mm in horizontal length and is gently curved to conform to the contour of the anterior globe. The central vertical height of the tarsal plate is 8–12 mm in the upper eyelid and 3.5–4.0 mm in the lower. Medially and laterally, they taper to 2 mm in height as they pass into

the canthal tendons. As these tarsal plates approach the canthal tendons, they widen toward the eyelid margin, thus assuming a more triangular cross­ -section. Within each tarsus are the Meibomian glands, approximately 25 in the upper lid and 20 in the lower lid. These are holocrine-secreting sebaceous glands not associated with lash follicles. Each gland is multilobulated and empties into a central ductule that opens onto the posterior eyelid margin behind the gray line. They produce the lipid layer of the precorneal tear film.

The Canthal Tendons

Medially, the tarsal plates pass into fibrous bands that form the crura of the medial canthal tendon. These lie between the orbicularis muscle anteriorly and the conjunctiva posteriorly. The superior and inferior crura fuse to form a stout common tendon that inserts via three limbs (Fig. 3.5) [2]. The anterior limb inserts onto the orbital process of the maxillary bone in front of and above the anterior lacrimal crest. It provides the major support for the medial canthal angle. The posterior limb arises from the common tendon near the junction of the superior and inferior crura and passes between the canaliculi. It inserts onto the posterior lacrimal crest just in front of Horner’s muscle. The posterior limb (Horner’s muscle) directs the vector forces of the canthal angle backward to maintain close approximation with the globe. The superior limb of the medial canthal tendon arises as a broad arc of fibers from both the anterior and posterior limbs. It passes upward to insert onto the orbital process of the frontal bone. The posterior head of the preseptal orbicularis muscle inserts onto this limb, and the unit forms the soft-tissue roof of the lacrimal sac fossa. This tendinous extension may function to provide vertical support to the canthal angle [26], but also appears to play a significant role in the lacrimal pump mechanism.

Laterally, the tarsal plates pass into fibrous strands that interdigitate and blend into the