Emamectin benzoate emulsion is a macrocyclic lactone insecticide that is not classified as an organophosphate or carbamate. We report the case of a man in his 80s with chronic kidney disease and cardiovascular comorbidities who ingested emamectin benzoate emulsion. On day 2, he presented with abdominal pain, diarrhea, and marked sialorrhea; his vital signs were stable; however, his serum cholinesterase (ChE) had markedly declined (18 U/L). The patient was discharged with supportive care. From day 3, watery diarrhea recurred and neurobehavioral symptoms progressed. On day 5, he presented with pinhole miosis and further ChE suppression (2 U/L). Therefore, atropine was administered, and the patient was transferred for close monitoring. After discharge (day 8), miosis and sialorrhea persisted, and ChE remained low for weeks. Findings suggestive of tubular injury were observed during follow-up. The patients' symptoms resolved gradually, with ChE partially recovering by days 75 - 95. This case underscores the need for serial reassessment and structured follow-up after pesticide exposure, even when the patient appears stable at the initial presentation.

Store-operated Calcium (Ca[2+]) entry (SOCE), mediated by stromal interaction molecule 1 (STIM1) and Orai1, is a central pathway controlling intracellular Ca[2+] homeostasis. Gain-of-function (GoF) mutations in STIM1 cause a spectrum of clinically overlapping disorders historically classified as Stormorken Syndrome (STK), tubular aggregate myopathy (TAM), and York Platelet Syndrome (YPS). However, increasing evidence indicates that these entities could represent a shared disease spectrum rather than distinct conditions. At the molecular level, STIM1 activation is governed by a series of autoinhibitory checkpoints that maintain the protein in a tightly controlled resting state. GoF mutations disrupt these regulatory constraints, leading to dysregulated SOCE activity that is frequently, but not uniformly, associated with constitutive channel activation depending on the specific mutation and cellular context. While many disease-associated variants localize to the EF hand, a highly conserved helix-loop-helix Ca[2+] binding motif, and the CC1 (coiled-coil 1) domain involved in molecular regulation of STIM1 activation, an increasing number of mutations in the C-terminal region further expands the mechanistic and clinical spectrum. In this review, we summarize current concepts of molecular STIM1 activation and discuss how distinct mutations perturb specific regulatory elements of the protein. By systematically integrating published case reports into a comprehensive overview, including a mutation-phenotype correlation table, we highlight the remarkable variability in and incomplete penetrance of clinical manifestations.

Raeder's paratrigeminal neuralgia is a rare clinical syndrome characterized by ipsilateral periorbital pain, partial Horner syndrome (ptosis and miosis without anhidrosis), and sensory disturbances in the ophthalmic division (V1) of the trigeminal nerve[1]. The syndrome results from involvement of sympathetic fibers traveling along the internal carotid artery (ICA), often in association with vascular or parasellar pathologies[2]. Among its etiologies, ICA dissection is particularly important, as it may present with unilateral headache and cranial autonomic features that closely mimic trigeminal autonomic cephalalgias (TACs)[2,3]. This overlap may lead to misdiagnosis and delay in the identification of potentially serious vascular conditions[4]. Recognition of distinguishing clinical features is therefore critical.

A 41-year-old male patient presented to the emergency department (ED) with left sided headache, radiating to the left ear while also complaining of dizziness. A non-contrast CT brain, performed during a previous presentation five days earlier, was normal. On his second presentation, the patient displayed clinical signs of carotid artery dissection including left sided partial Horner's syndrome.

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.