Blepharitis is a chronic inflammation of the eyelid margin that is mediated by the immune system. It is one of the common ocular surface diseases and often leads to serious sequelae that threaten vision, such as dry eye syndrome due to insufficient tear secretion, corneal neovascularization, and stubborn chalazion. Elucidating its precise etiology is therefore imperative. Emerging high-throughput sequencing and metagenomic analyses have unveiled a quantitative and qualitative disruption of the periocular microbiome (dysbiosis), characterized by the expansion of specific bacterial species such as Staphylococcus aureus, coupled with episodic blooms of Demodex. These perturbations are no longer considered epiphenomena. In this review, we reveal the possible mechanisms of the role of blepharitis and microbiota dysbiosis.

Ophthalmomyiasis is a rare condition caused by the infestation of ocular or periocular tissues by fly larvae. It is typically reported in tropical regions, rural settings, or among individuals with animal exposure. This report presents a unique case of ophthalmomyiasis externa in a 2-year-old girl from upstate New York. The patient presented with persistent left lower eyelid edema, erythema, and discharge following an insect bite that was unresponsive to antibiotic therapy. A botfly larva was expressed with digital pressure. The case underscores the diagnostic challenges of ophthalmomyiasis in unlikely regions and raises important questions about the ecological and environmental shifts facilitating the spread of parasitic diseases. Early recognition and intervention, including larval extraction and systemic therapy, proved effective. This report highlights the need for vigilance and broader differential diagnoses in regions where such infestations are uncommon.

Kabuki syndrome (KS) is characterized by typical facial features (long palpebral fissures with eversion of the lateral third of the lower eyelid; arched and broad eyebrows; short columella with depressed nasal tip; large, prominent, or cupped ears), minor skeletal anomalies, persistence of fetal fingertip pads, mild-to-moderate intellectual disability, and postnatal growth deficiency. Other findings may include: congenital heart defects, genitourinary anomalies, cleft lip and/or palate, gastrointestinal anomalies including anal atresia, ptosis and strabismus, and widely spaced teeth and hypodontia. Functional differences can include: increased susceptibility to infections and autoimmune disorders, seizures, endocrinologic abnormalities (including isolated premature thelarche in females), feeding problems, and hearing loss.

Naltrexone is a competitive opioid receptor antagonist that is FDA-approved for the treatment of alcohol and opioid use disorders. It is also used as an off-label treatment for a plethora of conditions spanning multiple specialties, including multiple sclerosis, chronic pain, Crohn's disease, and compulsive disorders. Naltrexone has also been used off-label for the treatment of pruritus in patients with burn injuries, atopic dermatitis, cholestatic dermatitis, chronic urticaria, and immunotherapy-induced pruritus. Naltrexone is thought to alleviate pruritus through its antagonist effect on the µ-opioid receptor at pain-transmitting and pruritoceptive dorsal horn neurons. This case report explores the treatment of persistent surgical scar pruritus following endoscopic brow lift and bilateral upper eyelid blepharoplasties under general anesthesia. After trialing first-line treatments of oral antihistamines and topical antipruritics, naltrexone was initiated. The treatment dose was titrated between 25 and 100 mg daily, and the pruritus is currently well-controlled with a dose of 25 mg twice a day. While our case report supports the limited available data for the use of naltrexone as treatment for pruritus in certain conditions, more research is warranted to further establish efficacy, safety, and specific diagnosis indications. Naltrexone is not currently FDA-approved to treat pruritus.

Dysregulated lipid metabolism and chronic inflammation are hallmarks of aging, yet their interplay in age-related tissue disorders remains poorly defined. In the ocular surface, age-related meibomian gland dysfunction (ARMGD) is highly prevalent but mechanistically unclear, leading to significant visual impairment without targeted therapies. To identify key molecular drivers of ARMGD, we performed integrated multi-omics screening of aging mouse meibomian glands (MGs) and identified DHCR24, a key cholesterol metabolism enzyme, as a critical regulator of gland homeostasis. Single-cell sequencing identified age-associated downregulation of Dhcr24 predominantly in meibocytes. Based on this finding, we generated a meibocyte-specific Dhcr24 knockout (cKO) model, which exhibited typical ARMGD pathology including glandular atrophy, disrupted lipid homeostasis, and inflammatory activation. Further in vitro studies using SZ95 sebocytes demonstrated that DHCR24 deficiency induces mitochondrial dysfunction and cytosolic mitochondrial DNA (mtDNA) leakage, triggering cGAS/STING-dependent inflammatory senescence. Notably, AAV-mediated restoration of DHCR24 in mice reversed age-related gland pathology. Our findings establish DHCR24 as a dual-target regulator that maintains cholesterol metabolic homeostasis while suppressing mtDNA-driven inflammation via the cGAS-STING pathway, highlighting its therapeutic potential for ARMGD and related disorders characterized by lipid-inflammatory imbalance.

Apraxia of lid opening (ALO), synonymous with apraxia of eyelid opening, is a nonmotor abnormality characterized by the patient's difficulty in eyelid elevation bilaterally. There is an inability of voluntary eye reopening without an orbicularis oculi spasm despite sustained frontalis contraction. In other words, ALO is a disorder characterized by a patient's difficulty in voluntarily opening their eyes despite an ability to do so and the absence of any ocular motor or muscular abnormalities. The definition is a misnomer, given that it rarely represents pure and true apraxia. On rare occasions, it can occur as an isolated idiopathic phenomenon. Max Heinrich Lewandowsky, a renowned German physician and academician, first described ALO in his 1907 essay "Über apraxie des Lidschlusses." Later, Schilder, in 1927, reported 2 patients (1 with Huntington chorea), and Riese, in 1930, 1 patient with frontotemporal injury from a bullet. No other reports were found in the literature until 1965, when Goldstein and Cogan reported 4 patients (Huntington disease, parkinsonism, parkinsonian syndrome after cyanide attempted suicide, and cerebral diplegia). ALO is often misdiagnosed due to its clinical subtlety and the lack of overt pathognomonic signs. ALO is distinct from blepharospasm, where involuntary muscle contraction forces the eyelids closed, and from ptosis, where a droop in the eyelid occurs due to muscle weakness or mechanical issues. The eyelid opening mechanism involves a complex interaction of muscles and nerves. The levator palpebrae superioris muscle is primarily responsible for lifting the upper eyelid, and it is innervated by the superior division of the oculomotor nerve (cranial nerve III). The Müller's muscle, innervated by the sympathetic nervous system, also assists in eyelid elevation. Voluntary eyelid control is modulated by neural pathways that connect the basal ganglia, frontal lobes, and supplementary motor area, which are areas involved in initiating and planning voluntary movements. In ALO, the dysfunction appears to lie within these neural pathways rather than in the muscles themselves. The disorder is believed to originate from a disruption in the communication between the brain's intention to open the eyelid and the execution of that action. While the exact pathophysiological mechanism is not fully understood, it is associated with neurodegenerative conditions such as Parkinson disease, progressive supranuclear palsy, and other diseases that affect the basal ganglia. Patients with ALO typically demonstrate effortful attempts to open their eyelids, often engaging in compensatory maneuvers such as manually lifting the eyelids or using exaggerated facial expressions. These actions suggest a disconnect between the intention to open the eyelids and the actual movement, a hallmark of apraxia. The condition can fluctuate throughout the day and may be influenced by factors such as fatigue, stress, or concentration. While ALO can be an isolated phenomenon, it is often seen as part of a broader neurological syndrome. It may initially present in conjunction with other Parkinsonian features before spreading to involve more extensive areas of motor control. In Parkinson disease, ALO is thought to be a manifestation of the widespread motor planning disruptions that characterize the disease. The diagnosis of ALO is clinical, relying on the recognition of its characteristic features during examination. There are no specific tests to confirm ALO, and its diagnosis is one of exclusion. It is vital to distinguish ALO from other eyelid movement disorders, as the treatment and prognosis differ significantly. The management of ALO is challenging and is best approached with a multidisciplinary team, including neurologists and ophthalmologists. Treatment strategies may include optimizing therapy for underlying neurological conditions, using botulinum toxin injections to facilitate eyelid opening, or employing surgical interventions in refractory cases. Understanding ALO's natural history and anatomical basis is crucial for proper diagnosis and treatment. Given its association with neurodegenerative diseases and its impact on patient's quality of life, ALO represents a significant clinical challenge that requires further research and education within the medical community. By increasing awareness and knowledge of this condition, healthcare professionals can better identify and manage this disabling and often overlooked disorder.

The term “ptosis” is derived from the Greek word falling and refers to drooping of a body part. Blepharoptosis is upper eyelid drooping with the eyes in the primary position of gaze. The shape of one's eyes along with the position of the eyelids, shape, and position of the eyebrow determines one's identity. Hence, drooping of the eyelids may produce a functional or a cosmetic deficit. Ptosis can occur in all age groups and is the result of various factors. One must remember that when a patient presents with complaints of drooping, it is a mere symptom and not the diagnosis. A thorough evaluation is of utmost importance to determine the cause. Ptosis can classify as true ptosis or pseudoptosis. True ptosis is further classified based on the age of presentation into congenital ptosis and acquired ptosis.[1] Acquired adult ptosis is further classified based upon the etiological factors as: 1. Aponeurotic ptosis. 2. Neurogenic ptosis. 3. Myogenic ptosis. 4. Mechanical ptosis. 5. Traumatic ptosis. Aponeurotic ptosis Aponeurotic ptosis is the most prevalent form of adult ptosis and usually presents in the 5th or 6th decade of life. It is also known as involutional ptosis. However, it can occur in young individuals following trauma, recent eyelid swelling, ocular surgery or prolonged use of contact lenses. The pathogenesis of aponeurotic ptosis is most often due to dehiscence or disinsertion of the levator aponeurosis.[2] In involutional cases, true dehiscence is sometimes absent, and ptosis occurs due to stretching or thinning of the aponeurosis. Rarely the levator muscle shows fatty infiltration. Characteristic features of this type of ptosis are that patients have a good levator function with a high lid crease, affected eyelid appears lower on down gaze and a thin upper eyelid with redundant skin. Neurogenic ptosis Neurogenic ptosis results from any condition which disrupts the innervation of either the levator muscle or muller’s muscle. The varieties most commonly encountered by an ophthalmologist are 3rd cranial nerve palsy and Horner syndrome. Third cranial nerve palsy Lesions along the oculomotor nerve present with ptosis and restriction of adduction, elevation and depression movements of the eyeball. Pupillary involvement may or may not be present. Bell's phenomenon is usually poor. Pupil-involving third nerve palsy is considered a neurological as it is most often due to a posterior communicating artery aneurysm compressing the nerve. Pupil-sparing third nerve palsy is most often due to an ischemic vascular cause and usually resolves spontaneously in 3 months. Other causes include inflammation, trauma or tumors along the course of the nerve. Lesions of the superior orbital fissure, orbital apex, or cavernous sinus, present in combination with other cranial nerve palsies. Treatment is challenging as the patients have a poor or absent Bell’s phenomenon placing them at high risk of developing exposure keratopathy post-surgery. Ideally, strabismus surgery is done first to correct the deviation followed by ptosis correction via the frontalis sling technique with planned under-correction. Horner syndrome (Oculosympathetic paresis) Horner syndrome consists of mild ptosis, pupillary miosis, apparent enophthalmos, and anhidrosis. It occurs due to interruption of the sympathetic nerve supply to the muller’s muscle and dilator pupillae muscle. Pupillary anisocoria can be well demonstrated in dim illumination. Patients with Horner’s syndrome occurring during childhood also have iris heterochromia due to decreased melanin production in melanocytes which is controlled by the sympathetic pathway. The diagnosis of Horner syndrome is often made clinically. Pharmacological tests using 4% cocaine, 1% hydroxyamphetamine or 2.5% phenylephrine help confirm the diagnosis. Myogenic ptosis Myogenic ptosis arises due to an abnormality in the levator muscle itself. These patients usually present with reduced levator action along with restricted extraocular motility and facial expression. Myasthenia gravis Myasthenia gravis is an autoimmune disorder characterized by the presence of antibodies to acetylcholine receptors located at the neuromuscular endplates of voluntary muscles.[3] This leads to decreased action of acetylcholine which results in muscle weakness and fatigue. Myasthenia may be generalized or localized to the eye (ocular myasthenia). The most common presenting feature is variable ptosis associated with diplopia. Symptoms may be unilateral or bilateral. Patients with myasthenia initially have a good levator function. Prolonged upgaze will cause a worsening of ptosis in these patients due to muscle fatigue. Cogan lid twitch sign: Rapid saccadic eye movements from downgaze to primary position results in rapid upshoot of the lid followed by a gradual drop to the primary position. Other tests which help confirm the diagnosis include ice test, serum acetylcholine receptor antibody assay, single fiber electromyography, and repetitive nerve stimulation test. Treatment of such patients involves administration of acetylcholinesterase drugs, oral steroids or immunosuppressants. In patients with severe ptosis, ptosis correction with planned under-correction may be an option. Myotonic dystrophy Myotonic dystrophy is an autosomal dominant disorder which presents with gradually progressing ptosis and external ophthalmoplegia. The pathologic process is a failure of muscle to relax after contraction. It also involves muscles of facial expression, neck, and limbs. Ocular examination in these patients also shows pupillary light-near dissociation, chromatic cataracts (Christmas tree cataract), and retinal pigmentary degeneration. Males develop a frontal pattern of balding and testicular atrophy. Chronic progressive external ophthalmoplegia (CPEO) CPEO is a mitochondrial myopathy causing bilateral symmetrical involvement of the extraocular muscles. Manifestations begin in childhood or adolescent age and progress slowly during adulthood. Bilateral symmetrical involvement is the first symptom followed by bilateral ophthalmoplegia. Due to the symmetric involvement of extraocular muscles, patients often do not complain of diplopia. As the muscles of facial expression are involved, patients develop an expressionless face (Hutchinson's face) Diagnosis is confirmed by muscle biopsy which shows ragged red fibers due to enlarged mitochondria. Kearns-Sayre syndrome: A variant of CPEO which shows retinal pigmentary degeneration, cardiac conduction defects, complete heart block, ataxia, neuropathy, endocrine dysfunction, and occurs in young adults. There is no treatment to date for CPEO. Ptosis surgery to clear the visual axis can be done in severe cases keeping in mind the high risk of exposure keratopathy. Oculopharyngeal muscular dystrophy This autosomal dominant disorder manifests in the 4 to 5 decade of life with bilateral ptosis, progressive external ophthalmoplegia, dysphagia, dysarthria, facial muscle weakness, and proximal limb weakness. Mechanical ptosis Ptosis secondary to any tumor producing an increased weight on the lids, cicatrization or scarring of the conjunctiva, and blepharochalasis. Traumatic ptosis Ptosis occurs due to direct or indirect trauma to the levator muscle. Penetrating injuries involving the levator can be repaired immediately. However, ptosis secondary to blunt trauma may resolve spontaneously over time. Ptosis which does not improve after 6 months can have surgical repair. Pseudoptosis It is not true ptosis but apparent ptosis due to abnormalities in structures other than the levator muscle. Causes include dermatochalasis, brow ptosis, hypotropia, microphthalmos, anophthalmos, phthisis bulbi, and contralateral eyelid retraction. It is very important to distinguish true ptosis from a pseudoptosis before embarking upon any surgical correction for drooping. Clinical presentation Patients usually complain of: 1. Drooping of eyelids. 2. Feeling of heaviness in the eyes. 3. Visual obscuration due to drooping. 4. Cosmetic complaints. Assessment A thorough history taking and clinical examination help determine the etiology of ptosis and plan appropriate treatment. History History taking should include the age of onset of ptosis, progression, duration, and any aggravating or relieving factors. Any associated symptoms such as diplopia, diurnal variation, pain, lid swelling, dysphagia or muscle weakness help provide a provisional diagnosis. Predisposing factors such as trauma, ocular or eyelid surgery, contact lens use, and botulinum toxin injection should be carefully ruled out. A family history of ptosis should be looked for to rule out hereditary disorders. In patients where the history is inconclusive, assessment of old photographs gives an idea about the time of onset. Any systemic illness, mental health issues, and medication history require documentation. Patients on blood thinners such as aspirin should be advised to stop medications 1 week before surgery. Clinical examination Clinical examination starts from the moment the patient walks into the doctor's clinic. It is essential to look for any facial asymmetry, frontalis overaction, chin up or head tilt posture. Ocular examination : 1. Visual acuity and refraction. 2. Cover test to look for any hypotropia and rule out any component of pseudoptosis. 3. Extraocular motility disturbance and any aberrant eyelid movements. 4. Pupillary examination to look for Horner syndrome or 3rd cranial nerve palsy. 5. Examination to look for any giant papillary conjunctivitis or symblepharon. 6. Corneal sensation and dry eye evaluation as they can predispose to post-operative keratopathy. 7. Fundus examination for features of retinal pigmentary degeneration. Specific examination of ptosis  Lid measurements should be done positioning the face in the frontal plane, negating the action of frontalis muscle with the thumb, and eyes in the primary position of gaze. The examiner should be seated at the eye level of the patient to avoid parallax error.  1. Palpebral fissure height (PFH): It is the vertical palpebral aperture height between the upper and lower eyelid margin in the pupillary plane with eyes in the primary position of gaze. Average PFH is around 10mm.  2. Marginal reflex distance 1 (MRD 1): MRD 1 is the distance between the upper lid margin and the corneal light reflex. Normal MRD 1 is 4-5mm. The difference in MRD 1 between the two eyes helps classify ptosis as mild, moderate or severe in patients presenting with unilateral ptosis. The difference in MRD 1 between two eyes: 2mm – Mild ptosis. 3mm – Moderate ptosis. 4mm – Severe ptosis  3. Marginal reflex distance 2 (MRD 2): MRD 2 is the distance between the corneal light reflex and lower eyelid margin. Normally MRD 1 + MRD 2 = PFH.  4. Levator action: It is the amount of excursion measured with a millimeter scale when the eyelid moves from extreme downgaze to extreme upgaze with frontalis action negated. Normal levator action is greater than 15mm. It is the single most important measurement in a patient with ptosis as its value determines the choice of surgical procedure. Grading of levator action[4]: Less than 4 mm – Poor. 5 to 9 mm – Fair. 9 to 11 mm – Good. Greater than 12 mm – Excellent. In patients with poor levator action (less than 4mm), frontalis sling surgery is the preferred procedure.  5. Margin crease distance (MCD): It is the distance between the lid margin and skin crease in downgaze. Normal MCD is 7 to 8mm in men and 8 to 10 mm in women. In congenital ptosis, MCD is usually absent or faint, whereas in aponeurotic ptosis MCD is higher than normal. During surgery, it is very important to reform the crease identical to the contralateral eye to maintain symmetry and achieve good cosmesis.  6. Bell’s phenomenon: This is another very important factor to be considered before ptosis correction. The patient is asked to close the eyes gently, and an attempt is made to open them. In patients with poor bell’s, ptosis correction should be avoided or undercorrected to avoid the risk of post-operative exposure keratopathy.  7. Assess presence of lagophthalmos and lid lag on downgaze which if present will worsen post-surgery.  8. Any brow ptosis or dermatochalasis if present should be documented. In involutional ptosis, blepharoplasty procedure is often combined with ptosis repair.  9. Hering test: In patients with unilateral ptosis, the ptotic lid is gently elevated manually, and the contralateral eyelid observed. Due to Hering's law of equal innervation, the contralateral eyelid may drop (See-saw effect). It is important to demonstrate this to the patient preoperatively and warn them about the possibility of requiring ptosis surgery in the contralateral eye. In such cases, a planned under-correction may be the treatment.  10. Phenylephrine test: It is a useful test in patients with mild ptosis or ptosis due to Horner syndrome; instill 2.5% phenylephrine drops in the superior fornix. Ptosis measurements are repeated after 10 minutes. Patients in whom the ptotic lid elevates due to stimulation of Muller's muscle are ideal candidates for posterior approach ptosis correction (conjunctival – mullerectomy surgery).  11. Tests to rule out myasthenia gravis: Fatigue test: The patient maintains fixation in upgaze for 30 seconds. In patients with myasthenia, the eyelid gradually drops down due to muscle fatigue. Ice test: An ice pack is placed over the closed ptotic eyelid for 2 minutes. Ptotic measurements are repeated after 2 minutes. Improvement in PFH by 2mm or more is considered positive for myasthenia. This is because cooling improves neuromuscular transmission.  12. Hertel exophthalmometry: A Hertel reading helps rule out any proptosis or enophthalmos and thus excludes pseudoptosis.

Hidrocystomas are benign cystic tumors of sweat gland origin that may arise from eccrine or apocrine structures and frequently involve the periocular region. Their clinical resemblance to both benign and malignant adnexal lesions represents a diagnostic challenge. We report a case of multiple periocular eccrine hidrocystomas in a man in his 50s presenting with bilateral translucent cystic papules along the eyelid margins. Histopathologic evaluation revealed a well-circumscribed dermal cyst lined by a double layer of cuboidal epithelial cells without decapitation secretion, confirming eccrine differentiation. Given the potential for misdiagnosis as basal cell carcinoma or other adnexal neoplasms, accurate clinicopathologic correlation is essential to prevent unnecessary aggressive interventions. This case highlights distinguishing features, expands the differential diagnosis, and underscores the importance of histopathology in periocular cystic lesions.

The integration of artificial intelligence (AI) into ophthalmic subspecialties, encompassing oculoplastics, is rapidly evolving. AI has demonstrated significant promise in enhancing diagnostic accuracy, streamlining clinical workflows, and personalizing surgical decisionmaking. This review aims to summarize current applications of AI in oculoplastics, identify major challenges limiting its broader adoption, and explore future directions for research and clinical translation. We provide a narrative review of peer-reviewed studies and recent developments in AI-assisted diagnosis, image analysis, surgical planning, and patient monitoring within the domain of oculoplastics. Emerging AI applications include automated detection of eyelid tumors, facial analysis for ptosis and orbital disorders, preoperative planning, and postoperative outcome assessment. However, challenges such as limited data diversity, lack of interpretability, regulatory barriers, and ethical considerations persist. AI holds great promise in augmenting oculoplastic care. Moving forward, multidisciplinary collaboration, clinical validation, and advances in multimodal learning will be key to realizing the full potential of AI in this field.

Ocular rosacea (OR) is a chronic inflammatory disease of the ocular surface frequently associated with meibomian gland dysfunction (MGD), with limited therapeutic options and an underexplored pathophysiology. Here, we uncover the pivotal role of mineralocorticoid receptor (MR) pathway overactivation in driving MGD and OR. Analysis of eyelid tissues from OR patients revealed increased MR expression and altered local corticosteroid metabolism, associated with inflammation, fibrosis, and impaired meibocyte renewal. Using a transgenic rat model overexpressing human MR, we demonstrate that MR overactivation initiates subclinical MGD and, with aging or ultraviolet-B exposure, drives a full OR-like phenotype characterized by gland dropout, oxidative and mitochondrial stress, immune infiltration, epithelial barrier disruption, and secondary corneal damage. Cross-species transcriptomic integration of rat, human MGD, and rosacea datasets identified a conserved MR-dependent gene signature, highlighting S100A9 as a specific downstream target and biomarker of MR activation. Local pharmacological MR antagonism suppressed S100A9 expression. These findings establish MR overactivation as a unifying pathogenic driver of MGD and OR and identify MR blockade as a promising therapeutic strategy, with S100A9 as a candidate biomarker for patient stratification and treatment monitoring.