Jockin, Yvette M. MD
Blepharoptosis (ptosis) in childhood varies in etiology and severity. While the majority of children with ptosis are otherwise healthy, ptosis can also be a presenting sign in a wide variety of clinical conditions. The management of pediatric ptosis can be a challenge, not only in achieving normal cosmetic appearance but also in maximizing visual potential by addressing associated amblyopia and strabismus. Examination techniques, common clinical presentations and surgical options are reviewed.
Blepharoptosis in the pediatric population is a relatively common condition with a wide variety of presentations. A recent large review of 408 eyes of 336 children presenting with ptosis at a tertiary care hospital revealed a mean age at presentation of 3.2 years and a positive family history in 19.4% of cases. Isolated congenital ptosis was noted to be the most common cause (68.9%), followed by blepharophimosis syndrome (16.7%).1
Evaluation of the child with ptosis begins with a thorough history and careful observation. History should include birth history, family history, and any history of systemic conditions, surgery, or trauma. Review of old photographs can be helpful to determine whether the ptosis is new or only newly noticed, variable, or progressive. While obtaining the history, the child is observed from a nonthreatening distance. Children with ptosis will often be observed to assume a chin-up head posture throughout the examination to peek under the ptotic eyelid(s). They will also often chronically arch the brow, engaging frontalis muscle to compensate for poor levator function (Fig. 1). Brow arching and head positioning is particularly common in children with bilateral ptosis, though it can be an encouraging sign in children with unilateral ptosis. The absence of chin-up posturing and/or brow arching in a child with significant unilateral ptosis is an indication that the child has likely developed amblyopia on the affected side.
When examining a child with ptosis, the eyelids are observed for the presence or absence of a well-formed eyelid crease, any redundancy or doubling of the crease, and lid margin contour abnormalities. The face is assessed for overall symmetry, and the lids, brow, and orbital rim are palpated to assess for mass lesions. Obtaining accurate measurements is often a challenge in the pediatric population, but every effort should be made to assess the eyelid height and degree of levator muscle function.
The severity of ptosis is most commonly graded by judging the marginal reflex distance (MRD1), the distance between the upper lid margin and the central corneal light reflex. If the child naturally assumes a chin-up posture, the head should be held to eliminate the posture when assessing for MRD1 (Figs. 2A, B). The brow must also to immobilized to eliminate any effect of brow arching on the level of the lid. This can be achieved by the examiner placing their palm against the side of the head and using the thumb to exert gentle pressure on the brow. Normal MRD1 in children is approximately +4.0 mm. If the lid margin is at the level of the corneal reflex, the MRD1 is 0 mm. Lids that ride lower than the corneal reflex are described with a negative value for MRD1. The vertical palpebral fissure height should also be recorded, as well as the horizontal palpebral fissure length, which may be abnormally short (eg, blepharophimosis syndrome) or long (eg, Kabuki syndrome).
Assessment of levator function is a crucial element of the ptosis evaluation as it will determine what surgical intervention may be appropriate. With the brow immobilized, the amount of vertical lid excursion from extreme downgaze to upgaze is measured in millimeters. In young children it is helpful to present a visually interesting target and repeatedly move it up and down to best estimate the levator function. Levator function is determined to be excellent if the lid rises 13 mm or more, good if it rises 8 to 12 mm, fair if it rises 5 to 7 mm, and poor if it rises 4 mm or less.2
A significant percentage of children with ptosis also have ocular misalignment. A careful evaluation of ocular motility is indicated at every clinical visit, as strabismus may become apparent over time. The reported incidence of strabismus in children with ptosis is between 7% and 37%.1,3,4 Strabismus may be associated with the ptosis itself (eg, limitation of elevation on the affected side), or be sensory in nature due to amblyopia. Strabismus is noted more frequently in children with occlusion of the visual axis and in those with unilateral ptosis.5
All children with ptosis require close monitoring of visual function. Fixation preference and visual behavior are recorded in the nonverbal child. Arguably the most important component of managing patients with childhood ptosis is the prevention, timely detection, and treatment of amblyopia. Although the treatment of ptosis itself can often be delayed depending on the clinical circumstances, amblyopia has a treatment window that shrinks with each passing year. Amblyopia is common in this population, reported incidence ranges from 17% to 70%, the lowest incidence being reported in children with good levator function and no evidence of strabismus.4–6 The cause of amblyopia in the patient with ptosis is often multifactorial. Severe ptosis with obscuration of the visual axis is an obvious risk for amblyopia, particularly in the unilateral case (Fig. 3). Left untreated these children can develop dense amblyopia, and early intervention to clear the visual axis is indicated. It is important to recognize, however, that amblyopia can occur in absence of visual axis occlusion. The amblyopia in these cases is often the result of anisometropia, strabismus, or a combination of the 2. Anisometropia is frequently encountered in this population and may progress over time. In unilateral ptosis, astigmatism is more common on the ptotic side, though spherical anisometropia may also be present. The risk for amblyopia persists throughout the many years of visual development. The child with ptosis therefore deserves frequent assessment of visual function and refractive error, timely correction of anisometropia, and a low threshold for instigating amblyopia treatment.
The majority of childhood ptosis is present at birth. An analysis of all patients with ptosis up to age 0 to 19 years in the Olmstead County population study revealed close to 89.7% of childhood ptosis to be congenital, with a birth prevalence of 1 in 842 births.7 The most common form of congenital ptosis, termed simple or isolated congenital ptosis, is not associated with other systemic abnormalities. Simple congenital ptosis may be unilateral or bilateral, unilateral cases representing roughly ¾ of all cases. Interestingly, unilateral ptosis seems to have a propensity to involve the left eyelid.1,8 This left-side predominance has been suggested in 1 pedigree to result from a modifier gene determining laterality.8
Isolated congenital ptosis may be sporadic or familial. The inheritance pattern of congenital ptosis is often autosomal dominant with incomplete penetrance, though a family with severe bilateral ptosis inherited in an X-linked dominant manner has also been described.9 Several genes have been identified that lead to simple congenital ptosis, including PTOS1, PTOS2, and ZFH-4.10,11
Simple congenital ptosis is a myogenic form of ptosis involving hypoplasia, fibrosis, and fatty infiltration of the levator superiorus muscle or tendon with markedly decreased muscle function.12 The absence of an eyelid crease is common. The muscle is less elastic than normal, so in addition to the limitation of elevation of the lid, lid lag in downgaze and nocturnal lagophthalmos is common in this population. Early surgery is often indicated, particularly in severe and unilateral cases.
Blepharophimosis ptosis epicanthus syndrome (BPES) is a well-described congenital disorder with a characteristic pattern of 4 eyelid abnormalities: blepharophimosis (shortening of the horizontal palpebral fissure), ptosis (bilateral with poor levator function), epicanthus inversus (a fold of skin emanating from the medial lower lid and coursing upward and medially), and telecanthus (decreased intercanthal distance with normal interpupillary distance) (Fig. 4). Two types of BPES have been described, type I includes the characteristic eyelid findings plus female infertility due to premature ovarian failure, and type II with eyelid findings only. BPES can be associated with developmental delay, but patients typically have a normal lifespan. BPES may occur sporadically or be inherited in an autosomal dominant pattern. An abnormality of the FOXL2 gene, located at 3q23, can be identified in 88% of cases of BPES diagnosed clinically.13 Patients with larger FOXL2 deletions present more frequently with associated clinical findings, such as developmental delay.14
Surgical intervention for the eyelid abnormalities in BPES is performed in stages. If ptosis is severe, early intervention to clear the visual axes may be indicated. If not, correction of the epicanthus is recommended at 3 to 4 years of age, followed by ptosis surgery at a later date. The ophthalmologist caring for female patients with BPES must bear in mind the possibility of ovarian failure and alert the family to seek appropriate consultation.
Marcus Gunn Jaw Winking Ptosis
Marcus Gunn jaw winking synkinesis (MGJWS) is a result of aberrant innervation of the levator palpebrae superioris muscle by a branch of the trigeminal nerve that normally supplies the muscles of mastication. MGJWS is often associated with ptosis on the affected side. Parents will report observing rhythmic movement of the eyelid when the child is eating or suckling. MGJWS can be elicited in the office by asking the child to open their mouth or move the jaw from side to side (Figs. 5A, B). In some cases, the synkinesis also involves the extraocular muscles, resulting in ocular misalignment with movement of the jaw.15 Some degree of MGJWS has been reported in 2% to 13% of children with congenital ptosis.16 MGJWS generally occurs in isolation and is not associated with ocular or systemic abnormalities. Although MGJWS is mostly unilateral, few bilateral cases have been reported. Shah et al17 recently reported a case of bilateral MGJW with asymmetric ptosis and unilateral ocular elevation deficit.
Ptosis associated with jaw winking may be minimal to severe and levator function is generally moderate to good, though voluntary control of the levator may be poor. Prudence is indicated in managing these cases as the child is often able to gain some measure of control over the jaw wink as they get older. If ptosis is of primary concern and the jaw wink is mild, standard ptosis surgery, either levator resection or frontalis suspension, may be performed. It is important to educate the family that standard surgery will address the ptosis only, and not the jaw wink. If surgery is considered to eliminate the jaw wink, it is necessary to disable to levator muscle on the affected side, followed by frontalis suspension. To gain symmetry in the postoperative appearance, particularly in downgaze, frontalis suspension is often also performed on the unaffected side. Demirci and colleagues reported on a series of 48 patients with MGJW, 30 of which underwent surgery with unilateral disabling of the levator and either unilateral or bilateral frontalis suspension. Though postoperative lid height symmetry was good in both groups, those operated unilaterally had significant differences in lid height in downgaze.18 Some surgeons prefer bilateral frontalis suspension with disabling of the levator on both sides.19
Horner syndrome results from interruption of sympathetic innervation to the eye and eyelid, resulting in characteristic combination of signs. The classic triad of the Horner syndrome is ptosis, miosis, and anhidrosis on the affected side. Anhidrosis (absence of sweating) is difficult to or impossible to determine in the child. A more obvious a sign is anisochromia, which is often a prominent feature of the Horner syndrome in the pediatric population: the iris on the affected side is lighter in color (Fig. 6). A useful diagnostic test in children suspected of the Horner syndrome involves topical sympathetic stimulation. The ptosis in the Horner syndrome will resolve or improve significantly in response to instillation of 10% phenylephrine drops (2.5% in infants) (Figs. 7A, B).
Instances of the Horner syndrome in the pediatric population are split roughly equally between congenital and acquired cases. Analysis of individuals younger than 19 years of age in the Olmstead County population study revealed an incidence of pediatric Horner syndrome of 1.42 per 100,000 and a birth incidence of 1 in 6250; 62% of which had a history of birth trauma.20 Patients with acquired Horner syndrome will also often have a history of surgical or nonsurgical trauma. A review of 73 patients with pediatric Horner syndrome by Jeffery and colleagues identified neuroblastoma in 1 patient with congenital Horner syndrome and in 2 patients with acquired Horner syndrome. Other pathology identified in this study included rhabdomyosarcoma (1 case) and brainstem vascular malformation (1 case).21 Mahoney and colleagues reported on a series of 56 children with the Horner syndrome at a large pediatric neuro-ophthalmology referral center; 28 of whom had no previously identified cause. Of the 20 patients that underwent imaging of the brain, neck, and chest, 4 had neuroblastoma, 1 had Ewing sarcoma, and 1 had juvenile xanthogranuloma. They concluded that a child of any age with the Horner syndrome and no history of trauma or surgery requires imaging to exclude a mass lesion.22 In contrast, Smith et al20 reported no instances of an underlying mass in 20 patients with pediatric Horner syndrome in a large population study, and suggested a need to reevaluate the recommendation for extensive evaluations in these patients.
Myasthenia gravis must be considered in the evaluation of ptosis in childhood, particularly if the ptosis is variable, intermittent, and associated with ocular misalignment. Juvenile myasthenia gravis (JMG) is an autoimmune disorder caused by antibody components of the postsynaptic membrane of the neuromuscular junction. Isolated ocular symptoms are frequent at onset. The clinical signs and course of disease in children differs from that in adults, often leading to delay in diagnosis. Castro and colleagues recently reported their 20-year experience with JMG. Of 58 patients, 50% were African American and 58.6% were female. Age of onset was 11 months to 17 years and 84% were acetylcholine receptor antibody (AchR-Ab) positive.23 If myasthenia is suspected by history, the ice test is a reliable and useful evaluation that can be performed in the office. After the lids are carefully assessed for the severity of ptosis, an ice pack is held against the eyelids for 2 minutes. Any improvement in eyelid position is observed and recorded. A recent retrospective cohort study without selection bias reported the ice test to have a sensitivity of 0.92, specificity of 0.79, a positive predictive value of 0.73, and a negative predictive value of 0.94.24
Treatment of ocular myasthenia begins with management of the underlying disease. Medical therapy includes the use of pyridostigmine with or without steroids. Thymectomy results in clinical improvement in the majority of children and should be considered a treatment option early in the disease process, particularly in children with generalized AchR-Ab positive JMG.25 Ptosis surgery may be indicated for patients with myasthenia gravis whose ptosis is stable and persistent despite medical management.
Other Conditions Associated With Childhood Ptosis
Ptosis can be a component of a variety of genetic conditions including Smith-Lemli-Opitz syndrome, Noonan syndrome, Kabuki syndrome, and Dubowitz syndrome.26 Mechanical ptosis may occur in the form of plexiform neurofibroma in patients with neurofibromatosis type I. The most common lid mass resulting in ptosis in the pediatric population is infantile (capillary) hemangioma. If ptosis is acquired and progressive one must suspect myotonic dystrophy or Kearns Sayre syndrome, both of which have associated ocular findings. Myotonic dystrophy is characterized by distinct lenticular changes, and Kearn Sayre with pigmentary retinal degeneration and possibly cataract. Ptosis may also be the result of trauma, including birth trauma. Unlike patients with simple congenital ptosis, patients with congenital ptosis as the result of birth trauma generally have good levator function and normal levator morphology. Additional conditions presenting with both ptosis and strabismus include CN III palsy, congenital fibrosis of the extraocular muscles, and Moebius sequence.
Surgical intervention is often indicated for children with ptosis. Surgery may be indicated early in life to maximize visual potential and aid in normal overall development. A retrospective review by Gazzola et al27 reported that early surgery for congenital ptosis decreased the rate of amblyopia from 34% to 8%. In a recently described series of children with severe ptosis, torticollis (head posture), and subjective developmental motor delay, the developmental motor delay was reported to rapidly reverse after ptosis surgery.28
Several surgical options are available to elevate the ptotic lid in childhood. The choice of procedure is largely driven by levator function, as well as surgeon comfort level and preference. More than one surgery is often necessary. A large retrospective review reported an overall undercorrection rate after pediatric ptosis surgery of 36.5%, with a mean number of procedures performed of 1.5 (range, 1 to 4).1 A recent review of 162 patients operated for congenital ptosis at a mean age of 10 months reported an overall reoperation rate of 19.8% (29.3% for frontalis suspension, 10.4% for levator resection).29
Resection and advancement of the levator aponeurosis can be an effective way to treat childhood ptosis with reasonable levator function. It can be performed unilaterally or bilaterally under a single anesthesia (Figs. 8A–D). This technique is unlikely to have adequate effect if levator function is <3 to 5 mm. Levator resection is often performed through an anterior (external) approach, though it can also be performed transconjunctivally or through a small skin incision.30 In the external approach an incision is created along the length of the eyelid crease, and blunt dissection is directed beneath the orbicularis muscle superiorly to identify the orbital septum. The orbital septum is violated, exposing the levator aponeurosis that is clamped, excised, and reopposed to the superior anterior aspect of tarsus. Depending on the anatomy of the individual patient, excision of some orbital fat and or a section of skin can also be performed to improve postoperative appearance. The amount of levator resection is gauged based on preoperative lid height, levator function, and intraoperative findings. Wu and colleagues recently reported a series of 85 patients treated with unilateral levator resection for congenital ptosis with an 84.5% surgical success rate. Severe ptosis and surgery performed under 2 years of age were significant contributors to surgical failure.6 Complications of levator resection include undercorrection, overcorrection, loss of the eyelid crease with overhanging skin, and eyelid margin contour abnormalities.
Frontalis suspension ptosis surgery augments the lid elevating effect of the frontalis muscle by creating a physical connection between the musculature of the brow and the eyelid. Frontalis suspension is often the procedure of choice for children with poor levator function (Figs. 9A, B). It can also be used as a temporizing measure in young children with moderate levator function who may ultimately benefit from surgery on the levator, allowing for growth before the levator complex is addressed surgically.
A variety of materials are used for frontalis suspension surgery. The procedure was first described using autogenous fascia lata, and this remains a reliable option in older children and adults, though fascia harvesting may lay outside the realm of surgical expertise for many ophthalmologists. Donor preserved fascia lata is a good alternative and well tolerated. Commonly used synthetic brow-suspension materials include monofilament polypropylene (Prolene), sheathed braided polyamide (Supramid Extra II), silicone frontalis suspension rod (Visitec Seiff frontalis suspension set), woven polyester (Mersilene mesh), and expanded polytetrafluoroethylene (Ptose-Up). Silicone rod has gained popularity in recent years, and has the advantage of greater elasticity, which minimizes postoperative lagophthalmos. Kwon et al31 recently evaluated the microstructural and mechanical properties of several synthetic brow-suspension materials and silicone rod compared favorably to other materials. Silicone rod also does not become incorporated into surrounding tissues, which allows it to be adjusted easily even long after surgery. This same property, however, sometimes results in cheese wiring of the silicone through surrounding tissues over time with gradual recurrence of ptosis, or extrusion of the silicone through the skin. Trauma to the brow may also result in disruption of the silicone and its suspensory power, resulting in sudden and dramatic recurrence of ptosis. Rizvi et al32 recently evaluated 46 patients (56 eyelids) with severe congenital ptosis treated with silicone rod frontalis suspension, reporting satisfactory eyelid elevation in 93%, with a 4% complication rate.
Frontalis suspension may be performed as a closed or open technique. The closed technique involves creating stab incisions and threading the suspension material beneath skin and orbicularis without the creation of an eyelid incision. The open technique involves the creation of an eyelid crease incision with direct visualization and attachment of the frontalis suspension material to tarsus. The open technique has the advantage of allowing the surgeon better opportunity to create an eyelid crease in patients without a native crease.33
Complications of frontalis suspension include postoperative lagophthalmos with corneal exposure, overcorrection, undercorrection, and contour abnormalities. Foreign body granulomas of the brow and eyelid may occur in response to synthetic materials, particularly in my experience with polytetrafluoroethylene (Fig. 10).
Whitnall sling is an alternative to frontalis suspension in patients with poor levator function. Whitnall ligament is a suspensory ligament of the eyelid and lacrimal gland that acts as a pulley off of which the levator muscle gains support and direction. The Whitnall sling procedure involves resecting the levator aponeurosis up to the point of the Whitnall ligament followed by suturing of the ligament to the superior tarsal plate. Anderson reported on a series of 69 patients who underwent Whitnall sling without tarsectomy. Over a period of 1 year postoperatively, 30.7% of eyelids which were initially judged to have adequate correction had recurrent ptosis requiring reoperation.34 Tarsectomy (resection of some portion of tarsus before attaching it to the Whitnall ligament) augments the effect of this procedure.35
Frontalis Muscle Flap
Frontalis muscle flap is another surgical option for patients with levator function <4 mm. This procedure evolved from frontalis suspension, and has the advantage of using the patient’s own native tissue. A flap of innervated frontalis muscle is passed near the insertion of the orbital septum at the superior orbital rim, then downward to tarsus.36 Complications include temporary forehead anesthesia and brow asymmetry.
Posterior Lamellar Surgery
Posterior lamellar ptosis repair is performed through the posterior aspect of the lid. Several variants of this procedure have been described, including the Müller muscle-conjunctiva resection and the Fasanella-Servat procedure, which involves resection of some portion of the superior aspect of tarsus. Posterior lamellar ptosis repair is the procedure of choice for patients with the Horner syndrome and a positive phenylephrine test. It can also be quite effective in patients with mild ptosis and a negative phenylephrine test.37 Complications include corneal abrasion secondary to posterior eyelid suture material, hemorrhage, infection overcorrection, and undercorrection.
Children with ptosis deserve thorough medical evaluation, as well as prolonged close monitoring and timely intervention. More than one surgery may be necessary to obtain optimal results. Maximizing visual function is of primary concern in this challenging population.
1. El Essawy R, Elsada MA .Clinical and demographic characteristics of ptosis in children: a national tertiary hospital study.Eur J Ophthalmol. 2013; 23:256–260.
2. Heher KL, Katowitz JA. Katowitz JA .Pediatric ptosis.Pediatric Oculoplastic Surgery. 2002 .New York:Springer-Verlag; 253–288.
3. Anderson RL, Baumgartner SA .Strabismus in ptosis.Arch Ophthalmol. 1980; 98:1062–1067.
4. Berry-Brincat A, Willshaw H .Paediatric blepharoptosis: a 10-year review.Eye (Lond). 2009; 23:1554–1559.
5. Gusek-Schneider GC, Martus P .Stimulus deprivation amblyopia in human congenital ptosis: a study of 100 patients.Strabismus. 2008; 4:261–270.
6. Wu SY, Ma l, Huang HH, et al .Analysis of visual outcomes and complications following levator resection for unilateral congenital blepharoptosis without strabismus.Biomed J. 2013; 36:179–187.
7. Griepentrop GJ, Diehl NN, Mohney BG .Incidence and demographics of childhood ptosis.Ophthalmology. 2011; 118:1180–1183.
8. Pavone P, Barbagallo M, Parano E, et al .Clinical heterogeneity in familial congenital ptosis: analysis of fourteen cases in one family over five generations.Pediatr Neurol. 2005; 33:251–254.
9. McMullan TF, Tyers AG .X linked dominant congenital isolated bilateral ptosis: the definition and characterization of a new condition.Br J Ophthalmol. 2001; 85:70–73.
10. Engle EC, Castro AE, Macy ME, et al .A gene for isolated congenital ptosis maps to a 3-cM region within 1p32-p34.1.Am J Hum Genet. 1997; 60:1150–1157.
11. McMullan TF, Robinson DO, Tyers AG .Toward an understanding of congenital ptosis.Orbit. 2006; 25:179–184.
12. Guercio JR, Martyn LJ .Congenital malformations of the eye and orbit.Otolaryngol Clin North Am. 2007; 40:113–140.
13. Beysen D, De Paepe A, De Baere E .FOXL2 mutations and genomic rearrangements in BPES.Hum Mutat. 2009; 30:158–169.
14. Zahanova S, Meaney B, Labieniec B, et al .Blepharophimosis-ptosis-epicanthus inversus syndrome plus: deletion 3q22.3q23 in a patient with characteristic facial features and with genital anomalies, spastic diplegia and speech delay.Clin Dysmorphol. 2012; 21:48–52.
15. Kassem IS, Kodsi SR .Marcus Gunn jaw winking with trigemino-oculomotor synkinesis on the inferior division of the oculomotor nerve.J AAPOS. 2009; 13:315–316.
16. Carman KB, Ozkan S, Yakut A, et al .Marcus Gunn jaw winking synkinesis: report of two cases.BMJ Case Rep. 2013; ■:■
17. Shah AD, Kuar AB, Kothari K .Bilateral Marcus Gunn jaw winking synkinesis with monocular elevation deficiency: a case report and literature review.Int Ophthalmol. 2012; 32:199–201.
18. Demirci H, Frueh BR, Nelson CC .Marcus Gunn jaw-winking synkinesis: clinical features and management.Ophthalmology. 2010; 117:1447–1452.
19. Cates CA, Tyers AG .Results of levator excision followed by fascia lata brow suspension in patients with congenital and jaw-winking ptosis.Orbit. 2008; 27:83–89.
20. Smith SJ, Diehl N, Leavitt JA, et al .Incidence of pediatric Horner syndrome and the risk of neuroblastoma: a population-based study.Arch Ophthalmol. 2010; 128:324–329.
21. Jeffery AR, Ellis FJ, Repka MX, et al .Pediatric Horner syndrome.J AAPOS. 1998; 2:159–167.
22. Mahoney NR, Liu GT, Menacker SJ, et al .Pediatric Horner syndrome: etiologies and roles of imaging and urine studies to detect neuroblastoma and other responsible mass lesions.Am J Ophthalmol. 2006; 142:652–659.
23. Castro D, Derisavifard S, Anderson M, et al .Juvenile myasthenia gravis: a twenty-year experience.J Clin Neuromuscul Dis. 2013; 14:95–102.
24. Fakiri MO, Tavy DL, Hama-Amin AD, et al .Accuracy of the ice test in the diagnosis of myasthenia gravis in patients with ptosis.Muscle Nerve. 2013; 48:902–904.
25. Heng HS, Lim M, Absoud M, et al .Outcome of children with acetylcholine receptor (AChR) antibody positive juvenile myasthenia gravis following thymectomy.Neuromuscul Disord. 2014; 24:25–30.
26. Jones KL .Smith’s Recognizable Patterns of Human Malformation, ed 6. 2006 .Philadelphia:Elsevier.
27. Gazzola R, Piozzi E, Lanfranchi AL, et al .Congenital ptosis and blefarophimosis: retrospective analysis of the effectiveness of correction with levator resection and frontalis suspension.Pediatr Med Chir. 2011; 33:129–133.
28. Bohnsack BL, Bhatt R, Kahana A .Non-ophthalmic symptoms secondary to ocular torticollis from severe blepharoptosis: an underappreciated but treatable condition.Ophthal Plast Reconstr Surg. 2012; 28:e36–e39.
29. Skaat A, Fabian D, Spierer A, et al .Congenital ptosis repair- surgical, cosmetic and functional outcome: a report of 162 cases.Can J Ophthalmol. 2013; 48:93–98.
30. Baroody M, Holds JB, Sakamoto DK, et al .Small incision transcutaneous aponeurotic repair for blepharoptosis.Ann Plast Surg. 2004; 52:558–561.
31. Kwon KA, Shipley RJ, Edirisinghe M, et al .Microstructure and mechanical properties of synthetic brow-suspension materials.Mater Sci Eng C Mater Biol Appl. 2014; 1:220–230.
32. Rizvi SA, Gupta Y, Yousuf S .Evaluation of safety and efficacy of silicone rod in tarsofrontalis sling surgery for severe congenital ptosis.Ophthal Plast Reconstr Surg. 2014; 30:11–14.
33. Yagci A, Egrilmez S .Comparison of cosmetic results in frontalis sling operationis: the eyelid crease incision versus the supralash stab incision.J Pediatr Ophthalmol Strabismus. 2003; 40:213–216.
34. Anderson RL, Jordan DR, Dutton JJ .Whitnall’s sling for poor function ptosis.Arch Ophthalmol. 1990; 108:1628–1632.
35. Holds JB, McLeish WM, Anderson RL .Whitnall’s sling with superior tarsectomy for the correction of severe unilateral blepharoptosis.Arch Ophthalmol. 1993; 111:1285–1911.
36. Ramirez OM, Pena G .Frontalis muscle advancement: a dynamic structure for the treatment of severe congenital eyelid ptosis.Plast Reconstr Surg. 2004; 113:1841–1849
37. Samimi DB, Erb MH, Lane CJ, et al .The modified fasanella-servat procedure: description and quantified analysis.Ophthal Plast Reconstr Surg. 2013; 29:30–34.