Ptosis is a common ophthalmology condition that is more common in children and older adults. With social development and changes in lifestyle, the incidence of ptosis in young people is increasing each year. In this article, we review the etiology, pathogenesis, diagnosis, and treatment of various types of ptosis that occur in young adults. Ptosis is a common ophthalmologic condition with two main types, congenital and acquired, and is most common in children and older adults. In recent years, with social development and changes in lifestyle, the incidence of ptosis in young people has increased year by year, with a variety of causes and corresponding treatment options. On the basis of this classification, we present a review of the etiology, pathogenesis, and treatment of acquired ptosis in young people. (a) Contact lens-induced ptosis In 1981, Epstein and Putterman first discovered that contact lens wear could cause ptosis. In 1995, Kersten looked at 91 young adults with acquired ptosis and found that 47% of them had no possible causative factors other than the possibility of ptosis from contact lens wear. In all of these studies, it was confirmed during surgery that ptosis was caused by thinning of the levator aponeurosis and separation of the lid attachment of the aponeurosis, suggesting that rough handling and repeated pulling of the upper lid during contact lens wear and removal can cause damage to the levator aponeurosis. The youth population is the largest group of contact lens wearers, and long-term contact lens wear, especially rigid contact lenses, is likely to damage the levator aponeurosis and cause ptosis. Studies have found that contact lens-induced ptosis usually presents with a widening of the upper lid crease and moderate ptosis with good levator muscle strength. Treatment is based on physical examination, and in cases where the upper lid can be elevated after a 10% drop of neuflexin, this can be corrected by partial excision of the lid-Müller muscle, and the remainder can be corrected by external levator shortening. (ii) Lid laxity Lid laxity occurs in young adults with bilateral onset and is characterized by recurrent episodes of painless upper lid edema. 80% of patients have onset before the age of 20 years and the number of episodes decreases as the patient ages and enters a quiescent phase. collin observed 30 patients with lid laxity and described the main symptoms as excessive skin laxity and thinning, prolapse of the lacrimal gland, and fat herniation with a range of complications. Grassegger et al. found a significant loss of elastic fibers in the diseased eyelid tissue and a high level of IgA deposition around the remaining elastic fibers, suggesting that autoimmune lysis of the elastic fibers is a possible causative factor. Lid laxity is often associated with ptosis, and surgery confirms that this type of ptosis is primarily due to thinning of the levator aponeurosis, which may occur due to passive dilatation of the tendon membrane from recurrent eyelid edema. The lid laxity must generally be treated surgically, and surgery is more effective in the resting phase.Custer [4] et al. suggested that transcutaneous levator shortening can be used, and Collin suggested that the choice of ptosis procedure and the amount of surgical correction should be determined by the degree of ptosis, and that the ptosis should be corrected with simultaneous excision of the excess skin and repositioning of the prolapsed lacrimal gland. Injury ptosis (a) Medically induced ptosis can occur after endophthalmic surgery, but is mostly seen in the elderly, especially in cataract surgery where pulling on the eyelid can damage the otherwise weakened levator muscle tendon membrane and produce ptosis. Linberg et al. found that approximately 10% of patients, with an average age of 34 years, developed ptosis after a radial corneal incision. During the procedure, the patient’s eyelid was held open by a metal lid opener and subsequently developed a widening of the blepharoplasty crease, but the levator muscle strength was good. Corrective surgery was performed on this group of patients, and intraoperative separation of the levator aponeurosis was confirmed. Therefore, Linberg suggests that rough use of the lid opener is the cause of ptosis and that detachment of the tendon membrane is the likely mechanism, with the use of a rigid device to pull the eyelid and the stimulated eyelid appearing to close forcibly, thereby damaging the tendon membrane. Surgical treatment is usually performed with an epicanthalmos tendon repair. (ii) Eyelid laxity In 1981, Culberston and Ostler first described eyelid laxity. It is characterized by chronic progressive upper eyelid laxity and chronic papillary conjunctivitis. It is characterized by extreme laxity of the conjunctival surface of the upper eyelid and relatively normal skin surface, with recurrent epicanthalmia. It is currently hypothesized that the onset of ptosis is related to chronic injury to the eyelid. If a patient with obesity is habitually oriented to one side when lying in bed, the lid on that side is chronically injured due to long-term gravitational relationships, lid integrity is destroyed, spontaneous eyelid flip during sleep occurs, secondary to chronic papillary conjunctivitis, and the above factors combine to cause ptosis. Conservative treatment includes the use of eye shields and lubricating eye drops. Dutton recommends total upper eyelid shortening and, in patients with ptosis, both levator muscle shortening and enhancement of horizontal eyelid tension. The parasympathetic fibers of the articular nerve originate from the unilateral central caudate nucleus and primarily innervate the levator aponeurosis. Before entering the orbit, the nerve is divided into superior and inferior branches, with the superior branch fibers mainly distributing to the levator palpebrae and superior rectus muscles and the inferior branch mainly innervating the internal rectus, inferior rectus, inferior oblique muscles, and pupil. Injury to any part of the nerve distribution that governs the levator muscle can cause ptosis. Ptosis due to an injury to the motoneurotic nerve usually presents with different symptoms depending on the site of injury. Injury to the superior branch results in ptosis and difficulty in upward eye gaze; damage to the trunk results in pupillary dilation and external downward slanting of the eye. Therefore, careful examination of eye movement and pupil condition is necessary in patients with actinic nerve palsy. Second, microangiopathy is very rare in young people, and the presence of these symptoms should first exclude intracranial and orbital occupying lesions and intracranial hemorrhage. In 1981, Beyer and McCarthy reported on the surgical treatment of ptosis due to ophthalmic nerve palsy, suggesting that the ptosis could be treated with a combination of the levator muscle, the superior rectus muscle, the frontalis muscle, and the crura muscle. In 1996, Carter et al. reported the use of silicone strips for frontalis suspension to correct this type of ptosis, comparing silicone to other suspension materials and concluding that silicone was flexible and stretchable compared to fascia, and that silicone suspension not only allowed easy adjustment of the eyelid height through a small incision in the center of the brow, but also allowed the patient to partially This increases postoperative upper lid mobility while maintaining good upper lid height, which is particularly beneficial in patients with actinic nerve palsy who have lost Bell’s phenomenon. In Carter’s report, all patients developed varying degrees of postoperative exposure keratitis, but only one developed irreversible pathology and the rest were cured by conservative treatment. 1980, Putterman used a stepwise lid margin suture to treat exposure keratitis, a method that allowed the patient’s cornea to gradually adapt to the postoperative exposure, thereby adequately correcting the actinic nerve palsy upper This approach allows the patient’s cornea to gradually adapt to the postoperative exposure, thus adequately correcting the actinic nerve palsy ptosis and avoiding the previous correction in multiple surgeries. (ii) Horner syndrome The Müller muscle of the eyelid is sympathetically innervated, and sympathetic nerve injury can cause Horner syndrome, which is characterized by ipsilateral ptosis, pupillary narrowing, decreased lid height, absence of sweating, and increased accommodation. The etiology of this condition is unknown, and if it occurs a neuro-ophthalmologist should be consulted for a collaborative examination and diagnosis. Acute, painful Horner’s syndrome in young adults should be given high priority because it may be a manifestation of carotid artery dissection. In 1990, Glatt et al. reported the use of conjunctival Müller muscle resection for the treatment of ptosis in Horner syndrome, which is now the first-line procedure for the treatment of this condition and is generally considered to be used for a positive neoflavin test. putterman described the specific treatment, which begins with the neoflavin test by the patient leaning back and raising the head, with the eye gazing downward, in 1 After 5 minutes, the patient returns to a seated position and the height of the upper lid margin to the center of the pupil is measured and compared to the pre-test level, and the upper lid height is largely restored as positive. It can also be adjusted by the following rule, with each 1 mm of resection raising the upper eyelid 0.5 mm. Myasthenia Gravis (MG) is an autoimmune disease that occurs in young people, mainly due to autoantibodies attacking the postsynaptic acetylcholine receptors at the neuromuscular junctions, and the pathogenesis is not completely clear. Studies have found that 84% of patients with MG have ocular symptoms as the first symptom, and 90% of patients have ocular symptoms of varying degrees of severity during the course of the disease, with ptosis and recurrence being the most predominant ocular symptoms. Therefore, it is important to be vigilant in young people with unexplained ptosis. The clinical presentation of MG is fluctuating, with ptosis generally being mild in the morning and heavy in the afternoon or worsening with exercise. Cogan observed upper eyelid flutter in MG patients who changed from a downward gaze to an upward gaze, and diagnostic tests for MG include the sleep test, electromyography, anti-acetylcholine receptor antibody test, and the Tensilon test. They found that 80% of patients diagnosed with MG had an increase in upper eyelid height of at least 2 mm after receiving an ice pack on the drooping eyelid for 2 min. Therefore, a positive freezing test in their patients was diagnostic of MG. Treatment for MG is primarily non-surgical and includes oral immunosuppressants and acetylcholinesterase inhibitors. Surgical treatment may be considered for medication failure. bradley et al. performed corrective surgery on 16 cases of ptosis in refractory MG and found that 87.5% of patients could be corrected in a single procedure. The surgical approach includes frontalis suspension and levator shortening, which is determined by the patient’s preoperative levator muscle strength and the amount of eyelid ptosis; Carter et al. performed frontalis suspension in 2 patients with MG and obtained satisfactory correction after surgery. （Chronic Progressive External Ophthalmoplegia (CPEO) is a chronic progressive ophthalmoplegia of unknown etiology in young adults, often bilateral, with a slow onset that gradually causes paralysis of the levator palpebrae, external ophthalmoplegia, and reduced orbicularis muscle function. Due to the chronic onset, patients usually present with a peculiar head position, chin elevation, and rely on the strength of the frontalis muscle to elevate the upper lid. Physical examination may reveal severe ptosis with poor levator muscle strength, which may be associated with extraocular muscle paralysis, incomplete eyelid closure, loss of Bell’s phenomenon, and decreased basal tear production. Some patients present with lower eyelid laxity and lower lid ectropion, which exacerbates the possibility of postoperative corneal exposure. Potential patients with ptosis as the first symptom are difficult to diagnose due to the slow course of the disease, but CPEO patients may have the following concomitant symptoms, such as uveitis and dysphagia. CPEO should be highly suspected in young patients with progressively worsening ptosis with these concomitant symptoms. There are many ways to treat ptosis in patients with CPEO, but conservative treatment is the mainstay, and Callahan and Beard noted that these patients not only have loss of Bell’s phenomenon due to limited extraocular muscle activity, but also have an ineffective blink reflex due to atrophy of the orbicularis muscle, which will cause serious surgical complications. Daut et al. performed ptosis correction in three patients with CPEO, all of whom developed postoperative exposure keratitis and required readmission for corneal ulcer treatment. The surgical approach can be based on shortening of the levator muscle, autologous fascia, allograft fascia, frontalis flap, and silicone frontalis suspension.Burnstinehe and Putterman reported the use of total upper lid skin-muscle excision, which is equivalent to physical suspension, and partial postoperative improvement in upper lid height without the development of exposure keratitis.Postoperative follow-up of CPEO is extremely important and the course of the disease should be closely monitored. To reduce the incidence of postoperative complications, in patients with lower lid laxity, horizontal shortening of the lower lid can be performed at the same time as upper lid surgery to prevent postoperative corneal exposure. (iii) Upper lid ptosis due to botulinum toxin Botulinum toxin is a neuromuscular toxin used to treat idiopathic blepharospasm and is now also used in cosmetic procedures such as wrinkle reduction. Local injections of botulinum toxin for cosmetic purposes are now very popular among young people abroad. Complications arise because the toxin can move from the original injection site to other surrounding areas, the most common of which is ptosis. According to Botox’s botulinum toxin product usage records, 11% of the 1,684 patients treated with botulinum toxin experienced ptosis. Botox-induced ptosis is primarily treated conservatively. It is important to take a detailed history in these patients, especially in young women, to prevent misdiagnosis. Because the toxin usually does not act for more than 3 to 4 months, these patients do not require surgery and most recover on their own.