PURPOSE:To review contemporary evidence supporting selective laser trabeculoplasty (SLT) as an initial and longitudinal therapy for glaucoma and to examine its implications for clinical outcomes, functional disease control, and health system sustainability. RECENT FINDINGS:Randomized clinical trials and extension studies have demonstrated that SLT-first strategies provide intraocular pressure (IOP) control comparable to medication-first therapy while substantially reducing treatment burden. In the Laser in Glaucoma and Ocular Hypertension (LiGHT) Trial, ∼70% of patients initially treated with SLT remained free from topical therapy and incisional surgery at 6 years. Secondary analyses revealed lower rates of moderate or fast visual field progression among eyes treated with SLT-first pathways compared with medication-first pathways (∼17% vs. 26%). Repeat SLT has been shown to produce IOP reductions similar to initial treatment without increased adverse events. Baseline IOP influences treatment response, with greater absolute pressure reductions observed in eyes with higher pretreatment IOP. SLT-first strategies have also been associated with lower cumulative costs and fewer surgical interventions over long-term follow-up. SUMMARY:SLT has established itself as a cornerstone of early glaucoma management. By providing durable and repeatable IOP control, SLT-first strategies may reduce reliance on daily medications and improve functional disease stability. Ongoing studies will further elucidate the role and optimal timing of repeat SLT, refining its integration into long-term glaucoma care.
Advancements in home-based tonometry and perimetry have enabled glaucoma care to expand beyond the office into the home in recent years. By capturing data that would otherwise be missed during routine office visits, remote glaucoma monitoring provides a more comprehensive clinical picture and leads to more individualized and timely management decisions. In addition, shifting data collection to the home may facilitate patient engagement and reduce strain on office resources. Further validation of existing tools and the introduction of new technologies have the potential to revolutionize glaucoma care delivery in the future.
Glaucoma is a chronic and progressive optic neuropathy, necessitating lifelong monitoring for affected individuals. Traditional surveillance of the disease relies on evaluation of intraocular pressure (IOP), optic nerve anatomy, and visual function at the physician's office, which only provides limited snapshots of a disease characterized by dynamic physiological variation. Developments in portable ophthalmological technologies and digital health platforms have enabled home monitoring of glaucoma. This review synthesizes current evidence on the home monitoring of glaucoma, with a focus on self-tonometry and home-based visual field testing. Handheld tonometers such as iCare HOME and iCare HOME2 allow repeated, anesthesia-free self-measurement of IOP in a real-world setting. These devices have demonstrated good agreement with Goldmann applanation tonometry, the gold standard. Home tonometry captures diurnal variations of IOP, thus providing relevant insights for diagnosis and therapeutic decision-making. Home-based visual field testing (eg, tablet-based platforms, virtual reality-based testing) enables frequent, unsupervised functional assessment with repeatability and sensitivity comparable to standard automated perimetry. Increased testing frequency may facilitate earlier detection of rapid progression, particularly in the early stages of disease. Collectively, evidence suggests the feasibility and clinical relevance of these home monitoring modalities. However, patient compliance with testing schedules and cost-effectiveness remain as challenges.
Hypotony maculopathy, characterized by chorioretinal folds with potential for vision loss, can occur as a complication from overfiltration following trabeculectomy. Its rate has increased in the era of antifibrotics. The challenge in treatment involves raising intraocular pressure to treat hypotony maculopathy while maintaining a level low enough to control glaucoma progression. This review aims to cover the expanse of nonsurgical and surgical management options available. Since a gold standard for hypotony maculopathy treatment is not established, selecting and tailoring treatment options will depend on specific patient and bleb characteristics.
Phosphodiesterase type-5 (PDE5) inhibitors are widely prescribed for erectile dysfunction and exert their pharmacologic effects through augmentation of nitric oxide-cyclic guanosine monophosphate signaling, a pathway with important ocular vascular implications. Given the expression of PDE5 within ocular tissues, increasing attention has been directed toward the effects of these agents on intraocular pressure (IOP), ocular blood flow, and glaucoma-related outcomes. Most clinical and experimental studies evaluating PDE5 inhibitors demonstrate no clinically meaningful or sustained effect on IOP across a range of dosing regimens, exposure durations, and patient populations, including individuals with established open angle glaucoma. Although isolated studies have reported transient or modest IOP elevations, these changes were typically small, transient, and unlikely to be clinically significant. In contrast, substantial evidence indicates that PDE5 inhibition increases ocular blood flow, with effects that appear more pronounced in the choroidal circulation than in the retinal vasculature. Human and animal studies have consistently demonstrated increased choroidal perfusion and thickness after sildenafil administration, supporting a preferential choroidal vascular response. Regarding glaucoma, early concerns were largely based on isolated case reports and postmarketing observations. More recent large-scale observational analyses suggest that PDE5 inhibitor exposure is associated with a lower hazard of being diagnosed as a glaucoma suspect or with open angle glaucoma. Collectively, current evidence supports a neutral effect of PDE5 inhibitors on IOP, a consistent enhancement of choroidal blood flow, and a potential protective association with glaucoma, warranting further mechanistic and prospective investigation. In this review, we examine the available clinical and experimental evidence regarding the effects of PDE5 inhibitors on IOP, ocular perfusion, and glaucoma risk to clarify their ophthalmic safety profile and potential therapeutic implications.
Benzalkonium chloride (BAK) is the most widely used preservative in multidose glaucoma eye drops. Medical management of glaucoma often requires the chronic use of preserved eye drops, resulting in a high incidence of BAK‑associated ocular discomfort, ocular surface disease, accumulation within ocular structures, and inflammatory tissue changes. The use of BAK has also been associated with reduced surgical success in trabeculectomy. Although alternative preservatives exist, they have also been associated with some toxic effects. Switching from BAK‑containing formulations to preservative‑free (PF) formulations results in significantly fewer side effects, improved ocular surface disease, and enhanced patient comfort. However, barriers such as cost and ease of use have impeded the more widespread adoption of PF glaucoma drops.
PURPOSE:To report a case of cyclodialysis cleft closure following ab interno suprachoroidal spacer implantation (AlloFlo) resulting in a severe postoperative intraocular pressure (IOP) spike. OBSERVATIONS:An 80-year-old woman with uncontrolled open-angle glaucoma in the right eye and intolerance to multiple medications declined incisional glaucoma surgery due to scarring risk and eyelid anatomy limiting bleb management. She underwent ab interno cyclodialysis creation and placement of 2 suprachoroidal spacers composed of donor scleral tissue [AlloFlo, White Plains, NY]. On postoperative day 1, IOP decreased from 34 to 10 mm Hg with a quiet anterior segment and visible spacers on gonioscopy. The early postoperative course was unremarkable. At postoperative week 3, she presented with ocular pain and an IOP of 60 mm Hg despite anterior visualization of the spacers. Serial anterior chamber paracenteses and maximal medical therapy provided only transient pressure reduction. Ultrasound biomicroscopy ultimately demonstrated posterior closure of the cyclodialysis cleft without a posterior fluid lake. The patient subsequently underwent urgent tube shunt implantation. At 9 months postoperatively, vision was preserved, and IOP was controlled on 2 topical agents. CONCLUSIONS AND IMPORTANCE:Cyclodialysis cleft closure is a potential failure mechanism following suprachoroidal spacer implantation and may result in abrupt and marked IOP elevation. Careful patient selection, vigilant postoperative monitoring, and early imaging with ultrasound biomicroscopy are essential to guide timely management.
INTRODUCTION:Selective laser trabeculoplasty (SLT) is widely used to lower intraocular pressure (IOP) in glaucoma, including pseudoexfoliation glaucoma (PXG). While transient IOP elevations and mild inflammation are common, delayed keratitis with a secondary IOP spike remains rare. We present a case of inflammatory keratitis and delayed IOP elevation following repeat SLT in a patient with PXG and no prior history of herpes simplex virus (HSV) infection. CASE PRESENTATION:A 59-year-old man with PXG underwent repeat SLT in the left eye. He had a normal IOP reading 1 hour after the procedure. Five days later, he developed blurry vision, keratic precipitates (KPs), superficial punctate keratopathy, trace anterior chamber cells, and an IOP spike to 32 mm Hg. He denied any HSV history. Treatment with topical corticosteroids, IOP-lowering agents, and oral valacyclovir led to resolution of inflammation, though IOP remained elevated despite maximal medical therapy. CONCLUSION:Delayed corneal inflammation with IOP rise following SLT may reflect either viral reactivation or a noninfectious inflammatory response, particularly in eyes with pseudoexfoliation-related structural vulnerability. Awareness of this potential complication underscores the importance of discussing warning signs and symptoms with patients and consideration of empiric anti-inflammatory or antiviral therapy when KPs or corneal edema appear.
Canaloplasty is a minimally invasive glaucoma procedure that aims to restore aqueous outflow through the Schlemm canal. Despite its excellent safety profile, complications can occur, including hyphema, creation of a cyclodialysis cleft, and incorrect passage of the catheter into the suprachoroidal space. Descemet membrane detachment (DMD) is an infrequent complication of canaloplasty and can be associated with significant visual decompensation, particularly when involving the central visual axis. Herein, we describe a case of a patient who underwent canaloplasty through an iTrack microcatheter and whose course was complicated by a hemorrhagic DMD with viscoelastic trapped in the interface between the Descemet membrane and posterior corneal stroma. This case helps to highlight the importance of considering factors such as location, relationship to pupil, size, and contents when determining the management of DMDs.
BACKGROUND:The optic disc in a child with optic disc drusen (ODD) frequently mimics the optic disc in a child with papilledema, which may lead to unnecessary invasive investigations. Recent advances in imaging have transformed our understanding of pediatric ODD. METHODS:We reviewed the literature from 2018 to 2025, focusing on pediatric cohorts and novel imaging modalities, including optical coherence tomography (OCT) and OCT angiography (OCTA), and artificial intelligence (AI). RESULTS:Enhanced depth imaging OCT (EDI-OCT) has become the diagnostic reference standard with high sensitivity for detecting both superficial and deep ODD. A peripapillary hyper-reflective ovoid mass-like structure (PHOMS) is reported in up to 90% of children with ODD, in 8.9% of healthy children, and in over 80% of idiopathic intracranial hypertension (IIH) cohorts. A PHOMS primarily reflects optic nerve head crowding and displaced ganglion cell axons. Its high prevalence makes PHOMS a frequent confounder in the evaluation of pediatric optic disc elevation, emphasizing the importance of multimodal imaging. In addition, OCT-based deep-learning algorithms are emerging to enhance diagnostic accuracy, whereas fundus-photo-based algorithms have shown strong performance in differentiating buried ODD from mild papilledema. CONCLUSIONS:Recent imaging technologies and longitudinal data have reframed pediatric ODD as dynamic lesions with measurable progression. Integration of OCT, OCTA, and AI-with awareness of PHOMS as a frequent and confounding finding-supports accurate diagnosis, risk stratification, and structured follow-up while reducing unnecessary invasive testing.
Childhood nystagmus is a complex clinical presentation with diverse underlying mechanisms. While eye movement characterization aids description, it is often insufficient for establishing etiology. Accurate diagnosis relies on a structured evaluation that integrates careful clinical assessment with ancillary testing and genetic analysis. Recent advances in genetic testing have reshaped the diagnostic paradigm, allowing identification of molecular causes in an increasing proportion of children, refining prognostic counseling, and influencing clinical management. Ancillary studies-including electrophysiology, optical coherence tomography, and neuroimaging-remain essential in guiding and interpreting genetic results. This review outlines a practical neuro-ophthalmic framework for evaluating children with nystagmus, emphasizing the complementary role of genetic testing within a comprehensive, clinically driven diagnostic approach.
Cerebral/cortical visual impairment (CVI) occurs when there are abnormalities of visual function and functional vision due to neurological conditions that affect the post-geniculate visual pathways in the brain, while the ocular anatomy is normal or insufficient to explain the degree of visual dysfunction. CVI is a leading cause of pediatric visual impairment in low-, middle-, and high-resource countries, and its increasing incidence is commonly associated with increased survival of premature neonates. We present an overview of CVI definitions, etiologies, diagnostic strategies, methods to assess visual function and functional vision, and considerations for management in the context of a multidisciplinary team. We conclude with an update on current CVI research.
Thyroid eye disease (TED) produces chronic orbital inflammation that may result in restrictive extraocular myopathy and associated diplopia. TED-related strabismus can be challenging to address due to complex and often large-angle deviations, variable surgical results, high rates of reoperation, and profound impact on patients' function and quality of life. We address the evaluation and management of strabismus in TED, and discuss changes that the recent introduction of teprotumumab may have on timing and treatment options previously chosen.
Congenital optic nerve anomalies represent a group of structural malformations that impair vision, increase the risk of ophthalmic complications, and are frequently associated with systemic conditions. We provide a review of major congenital optic disc anomalies, including optic nerve hypoplasia, morning glory disc anomaly, optic disc coloboma, peripapillary staphyloma, persistent fetal vasculature, myelinated nerve fibers, tilted disc syndrome, optic disc pit, papillorenal syndrome, optic disc drusen, and congenital optic disc pigmentation. We will review the definition, epidemiology, pathophysiology, clinical presentation, diagnostic workup, and associated systemic findings. An emphasis is placed on screening and multidisciplinary management aimed at correcting and preserving vision and preventing complications, such as retinal detachment, maculopathy, strabismus, amblyopia, and endocrine disorders. Diagnosis tools, including optical coherence tomography (OCT), B-scan ultrasonography, magnetic resonance imaging (MRI), and computed tomography (CT), are highlighted for their role in screening for these conditions. Many congenital optic nerve anomalies lack a definitive cure, and some conditions are extremely rare and do not have well-defined treatment protocols. However, routine ophthalmic examination, correction of refractive errors, visual surveillance for systemic conditions, and surgical intervention can optimize patient outcomes. Furthermore, multidisciplinary collaboration between ophthalmologists and other physicians, including pediatricians, endocrinologists, neurologists, and geneticists is often needed to facilitate care.
Optic neuritis is a central demyelinating disease that can significantly affect vision. Favorable outcomes are contingent on prompt recognition, work-up, and treatment. Understanding key differentiations in the pediatric population compared with adults is necessary for accurate and timely diagnosis. Recent studies highlighting these distinctions have deepened insight into clinical variabilities in presentation, as well as neurological associations, treatments, and prognostic factors. Ongoing collaborative studies continue to shed light on the main considerations guiding research on this topic. This review provides a general overview of pediatric optic neuritis and spotlights the contributions that have significantly enhanced understanding in the field.
Congenital cranial dysinnervation disorders (CCDDs) are a group of rare, nonprogressive conditions characterized by abnormal development of the cranial motor nerves and variable ocular motility deficits, ptosis, incomitant strabismus, and facial palsy. Advances in genetics and neuroimaging have revealed that these disorders result from defects in neuronal differentiation or axon guidance of the cranial motor neurons. Duane retraction syndrome, the most common CCDD, results from the absence of the abducens nerve and innervation of the lateral rectus by oculomotor nerve axons; causative genes include CHN1, MAFB, HOXA1, SALL4, and EBF3, although most cases do not have a genetic diagnosis. Congenital fibrosis of the extraocular muscles (CFEOM), results from variants in KIF21A, PHOX2A, TUBB3, or other tubulin genes, and affects the oculomotor and trochlear nerves. Horizontal gaze palsy with progressive scoliosis (HGPPS), caused by ROBO3 loss of function, arises from failure of axonal midline crossing in the brainstem. Moebius syndrome, defined by abducens and facial nerve palsies, has no identified genetic cause and may result from non-Mendelian causes. Additional CCDDs with atypical or syndromic presentations are linked to COL25A1, ECEL1, and ACKR3, although many do not have a genetic explanation. The expanding list of CCDD-associated genes highlights shared developmental pathways, including neuronal differentiation, axon guidance, and microtubule dynamics. Improved genetic diagnosis informs prognosis and multidisciplinary management. This review synthesizes current understanding of CCDDs, emphasizing the shift from phenotypic classification to molecular subtyping, and underscores the importance of ongoing research to resolve genetically unsolved cases and refine diagnostic and therapeutic strategies.
Optical coherence tomography (OCT) has transformed adult neuro-ophthalmology, but pediatric adoption has lagged because of perceived technical, financial, and practical barriers. This chapter provides a pragmatic framework for integrating OCT into pediatric and pediatric neuro-ophthalmology clinics, emphasizing how to obtain reliable images in awake children and how to interpret them. We first review technical aspects of tabletop and handheld OCT in children, including positioning, fixation strategies, and when to prioritize single-line macular or optic nerve head B-scans over full segmented protocols. We then outline key clinical modalities: single-line foveal scans for "in vivo histology" and ganglion cell layer/inner nuclear layer (GCL/INL) ratio screening; single-line optic nerve head (ONH) scans to assess Bruch membrane contour and opening size; ONH cube maps for papilledema versus pseudopapilledema; macular cube maps with segmentation to detect retinotopic patterns of GCL loss; and strategies to correct RNFL interpretation for axial length. Using a structured table-based approach, we show how combined RNFL and GCL measurements narrow the differential diagnosis and guide urgency and systemic workup in children with decreased vision and normal, swollen, or atrophic optic nerves. Disease-focused sections illustrate OCT applications in papilledema, pseudopapilledema, optic neuritis, neuroretinitis, optic pathway glioma, optic atrophy (including INL microcysts), infantile nystagmus, and congenital optic nerve anomalies. Throughout, we highlight pitfalls such as pseudonormalization of the RNFL, segmentation errors in high-grade edema or anomalous discs, and misinterpretation in highly ametropic eyes. The chapter aims to make OCT a routine, child-friendly extension of the neuro-ophthalmic exam.
Pediatric idiopathic intracranial hypertension or pseudotumor cerebri is a condition characterized by elevated intracranial pressure (ICP) with the potential for irreversible, profound vision loss in the setting of bilateral swelling of the optic nerves or papilledema. Although there is an awareness of the impact of this condition on visual function, data on the risk factors for disease severity, the relevance of pubertal status on disease progression, and the optimal treatment approaches are lacking. Prospective, multicenter studies are needed to develop standardized guidelines for clinical management to maximize visual outcomes. The purpose of this review is to provide an update on the understanding of pediatric IIH, which will consider epidemiology, current diagnostic criteria, management options, and visual outcomes.
Pediatric myasthenia gravis encompasses a heterogenous group of disorders that cause impaired neuromuscular junction transmission. Patients exhibit a characteristic fatigable weakness that can be life-threatening if respiration is affected. In children, myasthenia gravis can be grouped into 3 subtypes: transient neonatal myasthenia (TNM) arising from transplacental antibody transfer, congenital myasthenic syndromes (CMS) related to genetic defects, and juvenile myasthenia gravis (JMG) caused by antibodies to synaptic components. Diagnostic evaluation combines clinical evaluation with serologic and electrophysiologic studies. The condition is managed medically with acetylcholinesterase inhibitors and immunosuppressive agents. Thymectomy is an important part of the treatment of JMG, and intravenous immunoglobulin (IVIG) and plasma exchange (PLEX) play a role in acute, severe exacerbations. Management of the ophthalmic complications, including strabismus and ptosis, is necessary to prevent permanent vision loss from amblyopia.
