To describe a sutureless technique for iris fixation of a 3-piece intraocular lens (3P-IOL) in the anterior chamber in eyes without capsular support, and to evaluate its outcomes. Twelve patients (10 aphakic, 2 with 3P-IOL subluxation post-Yamane technique) underwent detailed ophthalmologic evaluation. In required cases, anterior vitrectomy and 0.01% carbachol (Miostat, Alcon Laboratories, Fort Worth, TX, USA) were used to achieve miosis. Two mid-peripheral iridectomies were created with a vitrectomy probe. After viscoelastic injection, a 3P-IOL (SENSAR, Johnson and Johnson Vision, USA) was inserted into the anterior chamber using a cartridge. Haptics were positioned behind the iris through the iridectomy sites using microforceps. In subluxated intraocular lens (IOL) cases, the lens was repositioned similarly. Best corrected visual acuity (BCVA), intraocular pressure (IOP), central macular thickness (CMT), and corneal endothelial density (CED) were recorded preoperatively, at 1 month, and at the final visit. The cohort included eight males and four females (mean age: 71.08 ± 4.07 years). Postoperative BCVA improved significantly (P < 0.001). No significant differences were found in IOP, CMT, or CED (P > 0.05). One case of transient IOP elevation was managed medically. Over a mean follow-up of 20.9 ± 4.8 months, no complications such as pigment dispersion, uveitis, hemorrhage, IOL decentration, macular edema, or corneal decompensation occurred. Iris fixation of a 3-piece IOL without sutures is a fast and effective technique that has demonstrated favorable short-term safety in patients without capsular support, provided that adequate anterior chamber depth and endothelial health are present.

Presbyopia is a progressive, irreversible age-related decline in ocular accommodation caused by reduced lens elasticity, resulting in impaired near vision and a significant impact on daily activities and quality of life. Globally, presbyopia affects approximately 1.8 billion individuals, with projections rising to 2.1 billion by 2030. Current management options include spectacles, contact lenses, pharmacologic agents such as pilocarpine, and surgical interventions; however, each approach carries limitations related to convenience, adaptability, or visual compromise. Yuvezzi™ (carbachol 2.75% and brimonidine tartrate 0.1%) is a recently U.S. Food and Drug Administration (FDA)-approved dual-agent ophthalmic solution designed to improve near vision through pharmacologically induced miosis. Carbachol, a parasympathomimetic agent, stimulates muscarinic receptors to produce sustained pupillary constriction, while brimonidine, an α2-adrenergic agonist, inhibits iris dilator activity and prolongs the miotic effect, enhancing tolerability. Its approval was based on two Phase 3 randomized controlled trials, BRIO-I and BRIO-II, which demonstrated significant improvement in binocular uncorrected near visual acuity without compromising distance vision. Common adverse effects included ocular discomfort, irritation, visual disturbances, and headache. Yuvezzi™ offers a noninvasive, reversible alternative for presbyopia management; however, long-term safety and sustained efficacy require further evaluation.

We describe a unique case of combined baclofen and tizanidine overdose followed by dual withdrawal syndromes, highlighting overlapping and contrasting clinical features that may complicate diagnosis and management. A 26-year-old man with paraplegia from cervical spinal cord injury, prescribed baclofen and tizanidine for spasticity, was found unresponsive at home next to partially empty medication bottles. Clinical evaluation included laboratory testing, neuroimaging, continuous monitoring, and serial neurologic and cardiopulmonary assessments. On admission, the patient exhibited CNS depression, hypotension, bradycardia, hypothermia, and subsequent episodes of severe psychomotor agitation. Supportive care with fluids, vasopressors, and sedation was required, including 2 subsequent intubations for airway protection. Within 24 hours, fever, tachycardia, and worsening agitation developed, consistent with withdrawal. Reintroduction of home baclofen and tizanidine alongside benzodiazepines and dexmedetomidine led to gradual resolution of symptoms, and the patient was discharged at neurologic baseline with psychiatric follow-up. This case underscores the diagnostic and therapeutic challenges of overlapping baclofen and tizanidine toxicity and withdrawal. Recognizing key bedside features-such as hypotonia vs tremor and mydriasis vs miosis-is essential. Sedation and bradycardia may be more severe in combined overdose than in overdose of either agent alone. Clinicians should anticipate withdrawal even in the setting of persistent toxicity. Early recognition and tailored supportive care are the cornerstone of management.

A genetic mutation in stromal interaction molecule 1 (STIM1) at I115 (I115F) causes tubular aggregate myopathy (TAM) and Stormorken syndrome (STRMK), which are multisystemic disorders characterized by miosis, thrombocytopenia, asplenia, and congenital skeletal muscle weakness. The main cause of this skeletal muscle weakness is excess store-operated Ca[2+] entry (SOCE) resulting from the constitutively active I115F STIM1 mutant. This study investigated the detailed mechanisms underlying I115F-induced pathological defects and the possible mechanisms by which these defects can be restored at the cellular level. I115F was overexpressed in mouse primary skeletal myotubes, which were subsequently examined using live single-cell Ca[2+] imaging, transmission electron microscopy, and biochemical approaches. In addition, the restoration of I115F-induced pathological defects was examined using I115F-overexpressing myotubes codifferentiated with normal immature myotubes on day 2 of differentiation. Constitutively active I115F induced cytosolic Ca[2+] overload in I115F-overexpressing myotubes by increasing SOCE and the expression of canonical transient receptor potential cation channel 6 (TRPC6), resulting in an imbalanced Ca[2+] distribution between the cytosol and sarcoplasmic reticulum, abnormal mitochondria, low ATP production, and aberrant Ca[2+] release for skeletal muscle contraction. Codifferentiation reversed the I115F-induced defects, normalizing cytosolic Ca[2+] levels by increasing myogenin expression and myotube width and decreasing ORAI1 expression while maintaining TRPC6 expression. Moreover, codifferentiation reset the intracellular Ca[2+] distribution by increasing SERCA1a expression and providing sufficient ATP production. Therefore, this study suggests that I115F-induced cellular Ca[2+] dysregulation, which may contribute to skeletal muscle weakness in TAM and STRMK, may be attenuated by modulating myogenin, TRPC6, ORAI1, or SERCA1a expression or activity.NEW & NOTEWORTHY Using a mouse myotube model, this study characterizes cellular defects caused by the STIM1 I115F mutation and proposes a hypothetical recovery mechanism via codifferentiation with normal myotubes. Our findings suggest that this restoration could be mediated by modulating myogenin, SERCA1a, ORAI1, and TRPC6 expression, providing mechanistic insights into cellular pathways for restoring skeletal muscle function in patients with TAM and STRMK carrying the STIM1 I115F mutation.

Organophosphate compounds such as dichlorvos, a widely used pesticide, account for a substantial proportion of acute poisonings globally. These agents irreversibly inhibit acetylcholinesterase, leading to cholinergic overstimulation. A subgroup of these compounds, alkyl phosphates-originally developed as nerve agents such as tabun, sarin and soman-has been increasingly implicated in intentional ingestions. Diagnosis can be challenging, particularly in the absence of classic cholinergic features such as bradycardia, bronchorrhea and miosis. We present a case of a male patient in his early 20s who was admitted to the intensive care unit with impaired consciousness, respiratory failure, tachycardia and severe metabolic acidosis following ingestion of unidentified substances. Imaging revealed chemical gastritis and aspiration pneumonia. A profoundly reduced serum cholinesterase level prompted empiric initiation of obidoxime therapy. Admission toxicology was positive for amphetamines, plausibly explaining the patient's atypical tachycardia and attenuation of classical cholinergic signs. The patient recovered following intensive supportive care and later confirmed ingestion of dichlorvos in a suicide attempt. This review discusses the clinical presentation, diagnostic challenges and current evidence-based management of alkyl phosphate intoxication. Particular emphasis is placed on the utility of serum cholinesterase measurement, the role of oximes such as obidoxime, and adjunctive interventions including seizure control, and ventilatory support. Clinicians should be aware that severe organophosphate poisoning may occur even in the absence of classical cholinergic signs, requiring a high index of suspicion and timely antidotal therapy.

Neuroblastoma (NBL) constitutes the most common extracranial solid tumor in children that arises from the sympathetic ganglia. Its manifestations depend on the localization of the tumor and metastases. This research aimed to assess the incidence of ophthalmological symptoms and their correlations with different prognostic factors. We collected and analyzed retrospectively the data of 776 children with a clinical diagnosis of peripheral neuroblastic tumors reported between 2004 and 2022 from 14 Polish pediatric oncology centers. Ophthalmological symptoms occurred in 17.10% of the patients, and in 12.70% they were diagnosed at the time of the first presentation. The reported manifestations comprised opsoclonus-myoclonus syndrome (OMS), Horner syndrome (HS), exophthalmos, periorbital hemorrhages, with the highest incidence of OMS (4.74% of all the patients). Moreover, we described the cases with neurological manifestations of NBL like paraparesis and facial nerve paresis. The age correlated with the form of symptoms, and HS was observed in the youngest patients. Similarly, the time from the symptoms onset to NBL diagnosis differed significantly among the patients, therefore the diagnosis of HS was associated with the longest period. In conclusion, the ophthalmological manifestations of NBL represent an essential group of symptoms. Therefore, clinicians should consider them as possible signs of tumors, particularly HS, which may be most challenging in the diagnostic process.

Tubular aggregate myopathy (TAM) is a rare inherited muscle disorder characterized by the abnormal accumulation of tubular aggregates (TAs) within skeletal muscle fibers. These aggregates, composed of compacted sarcoplasmic reticulum (SR) tubules, are strongly linked to disturbances in calcium (Ca2+) homeostasis. Clinically, TAM manifests with slowly progressive proximal muscle weakness, exercise intolerance, cramps, and myalgia, frequently beginning in childhood and often present with elevated serum creatine kinase levels. These symptoms can also be associated with some additional disorders, such as thrombocytopathy, miosis, hypocalcemia, hyposplenism, and ichthyosis, thereby resulting in a clinical picture that overlaps with symptoms of Stormorken (STRMK) syndrome. Considerable heterogeneity exists in age of onset, severity, and extra-muscular involvement, suggesting that TAM and STRMK represent a continuum rather than distinct entities. Histopathological hallmarks include TAs staining positive for SR proteins and displaying a honeycomb-like ultrastructure, consistent with aberrant SR remodeling. Mutations in genes encoding key regulators of store-operated calcium entry (SOCE), including STIM1 and ORAI1 have been identified as major contributors to TAM and its broader clinical spectrum, which encompasses STRMK syndrome, whereas mutations in CASQ1 and RYR1, have been described in only a minority of patients. Despite advances in delineating the genetic and molecular basis of TAM, key questions remain regarding the mechanisms that drive TAs formation and translate Ca2+ dysregulation into muscle dysfunction and multisystem disease. Understanding the molecular mechanisms underlying TAM and STRMK syndrome is crucial for developing targeted therapies. Moreover, further research is needed to elucidate additional pathways involved in disease progression and to refine genotype-phenotype correlations. This review summarizes current knowledge on the genetics, pathophysiology, clinical features, and diagnostic hallmarks of TAM, with particular emphasis on the role of Ca2+ homeostasis.

Human coronavirus NL63 (HCoV-NL63) is typically associated with mild upper-respiratory infections, but rare neurological manifestations have been reported. These presentations may closely mimic acute vascular or epileptic events in children. We describe an 8-year-old previously healthy girl who developed vomiting followed by ocular deviation, limb tremors, and brief altered consciousness. On arrival, she was afebrile and hemodynamically stable, with right gaze deviation, miosis, and suspected right hemiparesis. Brain computed tomography (CT) and angiography revealed marked left-hemispheric hypoperfusion consistent with a postictal state. A multiplex respiratory viral panel was positive for HCoV-NL63, while cerebrospinal fluid, microbiological, and toxicological studies were unremarkable. Magnetic resonance imaging (MRI) performed 48 hours later demonstrated complete normalization of perfusion. The patient recovered fully without further seizures. This case highlights a temporal association between HCoV-NL63 infection and transient postictal hemispheric hypoperfusion, underscoring the importance of integrating clinical, radiologic, and virologic data to avoid misdiagnosis of stroke in pediatric patients.

A Pancoast tumor is a neoplasm arising in the superior sulcus (apex) of the lung that invades adjacent structures of the thoracic inlet. The superior sulcus is an anatomic pleuropulmonary groove formed by the subclavian artery as it curves anterior to the pleura and courses upward and laterally beneath the lung apex. Because of this location, Pancoast tumors frequently extend into the chest wall, brachial plexus, and sympathetic nerves, producing a characteristic pattern of local invasion and symptoms not typically seen with other lung cancers. The natural history of Pancoast tumors often involves a prolonged asymptomatic period, with symptoms typically arising only when the tumor becomes large enough to invade nearby structures. Common symptoms include shoulder pain, Horner syndrome, and weakness or atrophy of the hand muscles, also referred to as Pancoast-Tobias syndrome. Local invasion of the tumor into the brachial plexus and sympathetic chain produces these manifestations. Sympathetic nervous system involvement leads to the classic signs of Horner syndrome (ptosis, miosis, and anhidrosis on the affected side). Although initially localized, Pancoast tumors can be biologically aggressive and may metastasize to regional lymph nodes and distant organs, contributing to substantial morbidity and, if untreated, a poor prognosis. Pancoast tumors represent a distinct subset of lung cancer defined by their apical location, neurovascular involvement, and unique symptom complex. Early recognition and timely, interdisciplinary evaluation, including thoracic surgery, medical oncology, and radiation oncology, are essential to optimize staging, enable curative multimodality therapy, and improve patient outcomes.

As an optical system, the eyes function in line with the basic principles of refraction. Visual clarity depends on the ability to bring incident light rays to a point focus at the fovea centralis. Schematically, the cornea and crystalline lens provide the requisite total dioptric power (about +60 diopters; the cornea makes up about + 40 to + 48 diopters). Accommodation is the adaptative faculty that enables clear vision with subjective variation in the linear distance of visual targets. This is accomplished by the autonomic adjustment of crystalline lens dioptric powers to provide focus on the presented stimuli. The main stimulus is 'blur.' The focusing powers of the crystalline lens are directly proportional to the increase or decrease in lens convexity. At the near point of accommodation, the ciliary muscles contract and relax zonular tension, thus enabling increased convexity and focusing power. For the far point of accommodation, the ciliary muscles relax and exert greater tension on the zonules (of Zinn), thus reducing lenticular convexity.  Under typical conditions, the healthy eye responds to near-point (linear) stimuli by activating the near triad, which includes accommodation, convergence, and miosis. These mechanisms are synergistically engaged to enable single, clear binocular vision. Inhibition in one of these reflexes can most likely lead to dysfunction of accommodative response. Concerning the near reflexes, accommodation and convergence are most closely intertwined. This interrelationship can be reported as the 'accommodative convergence to accommodation (AC/A)  ratio. Depending on the underlying accommodative dysfunction, the ac/a ratio may be either low, normal, or high. The accommodative mechanisms can be subject to functional anomalies in maintaining visual clarity. Based on the Duke-Elder classification, these include: Accommodative insufficiency (AI). Accommodative spasm. Accommodative inertia. Ill-sustained accommodation. Accommodative infacility. AI is a functional vision anomaly characterized by the inability to sustain focus at near. With this condition, the accommodative response is often suboptimal compared to expected normal ranges.

This study quantified the effects of topical brimonidine 0.2% on anterior segment anatomy using swept-source optical coherence tomography (SS-OCT) in a prospective, interventional design. Seventy eyes were evaluated with the Anterion system. Baseline measurements were taken, followed by the instillation of one drop of brimonidine tartrate 0.2%. A second scan was performed 60 min later. Key outcomes included pupillary diameter (PD), angle opening distance at 500 μm (AOD500), iris thickness (IT), anterior chamber depth (ACD), lens vault (LV), lens thickness (LT), and white-to-white distance (WTW). Results showed a statistically significant reduction in PD and an increase in AOD500 and ACD after brimonidine, while IT decreased. No significant changes occurred in LV, LT, or WTW. Baseline gender differences were noted, with females exhibiting a larger PD and smaller AOD500 and ACD than males, as previously reported. The study also contributes normative biometric data for a Hispanic population, highlighting these relevant anatomical variations. Results show that brimonidine induces significant miosis and angle widening without altering lens parameters, supporting its potential use in managing postoperative photic phenomena. This study provides objective SS-OCT quantification of brimonidine's multiple acute effects.