Electroencephalography (EEG) is a non-invasive technique for monitoring brain activity, but its signal quality is frequently degraded by artifacts from ocular movements, muscle activity, and environmental noise. ReHA-Net is a deep learning framework for robust EEG denoising, combining a U-Net-based encoder-decoder with three core modules. (1) Hybrid Attention integrates temporal, spatial, and frequency attention to emphasize neural patterns while suppressing structured noise. (2) The Multiscale Separable Convolution (MSC) block employs dilated and parallel depth-wise separable convolutions with varying kernel sizes to capture both short-term and long-term temporal dependencies. (3) Reversible Instance Normalization (ReVIN) enhances cross-subject generalization while retaining subject-specific features. The model trains on an enhanced EEGdenoiseNet dataset with a wider signal-to-noise ratio range, combined artifact conditions, and tailored normalization strategies. ReHA-Net achieved strong denoising performance, with a PSNR of 27.10 dB, an SNR of about 17.06 dB, and a correlation coefficient of 0.976 with clean signals and a relative root mean square error (RRMSE) of 0.165. These outcomes demonstrate effective artifact reduction while maintaining neural activity, highlighting its suitability as a preprocessing step for tasks such as seizure detection, imagined speech decoding, and cognitive state monitoring.

From structure to function: Biomechanical markers of symptomatic flatfoot during running and a single leg drop and hop.

Accurate assessment of extraocular muscle mechanics is crucial for diagnosing and treating ocular motility disorders, yet current methods, such as the forced duction test, rely on subjective tactile sensation and gross visual observation. To overcome the limitations of subjectivity and the impracticality of previous quantitative devices, we developed a novel biosensing system capable of simultaneously and objectively measuring passive ocular tension and rotation angle during forced duction. The system integrates custom-engineered surgical forceps equipped with dual strain gauges and an infrared video camera that precisely tracks pupil displacement to calculate real-time rotation angle. We clinically validated this system in a prospective study involving 10 patients (20 eyes) with intermittent exotropia, with measurements performed under general anesthesia. Reliable tension–angle curves were successfully obtained in all cases without complications. Passive tension increased progressively with ocular rotation, following a linear-parabolic trajectory up to 40°. The mean duction force of the medial and lateral rectus muscles showed comparable symmetry. This lightweight, practical, and objective biosensing system offers a reliable tool for quantifying ocular mechanics, with the potential to enhance diagnostic accuracy, enable individualized surgical planning, and support fundamental research in ocular motility disorders.

This study compared two rare diseases that present with enlarged lacrimal glands and analyzed their clinical features, among others, for identification. Setting - A single-center retrospective study. Patients treated at our center from 2013 to 2023 with pathologically diagnosed IgG4-ROD (n = 31, 42 eyes) and CD (n = 5, 5 eyes). No interventions administered. The analysis included patient demographics, laboratory tests, histopathological tests, imaging studies, treatment, and outcomes. Data collection involved visualizing medical records. The lacrimal glands/eyelid soft tissues and extraocular muscles of the IgG4-ROD group were affected. Histopathological examination showed lymphoid proliferation in both groups had lymphocyte hyperplasia, and the pathological IgG4+/IgG+ ratio in the IgG4-ROD group was higher than that in the CD group (P = 0.0057), which was more than 40%. IgG4-ROD exhibited significantly higher MASSON positivity than CD (78.1% vs. 33.3%, P = 0.0466). CD lesions exhibited a 50% reduction in Ki-67 proliferative activity relative to IgG4-ROD (P = 0.0349). Bone destruction was identified in 20% of CD versus none in IgG4-ROD (P = 0.024). Conversely, fibrotic imaging features demonstrated a significantly higher prevalence in IgG4-ROD (40%) compared to CD (P = 0.0103). Significant differences in pathology and imaging exist between IgG4-ROD and CD. IgG4-ROD is characterized by an IgG4+/IgG+ plasma cell ratio exceeding 40% and extensive fibrosis. Imaging predominantly reveals nondestructive fibrotic foci, reflecting the chronic inflammatory fibroproliferative nature of the disease. Conversely, CD exhibits higher local invasiveness and lower cellular proliferative activity.

Abstract Extraocular polymyositis (EOM) is a rare immune‐mediated condition in dogs, which affects all the extraocular muscles and has been exclusively described to manifest bilaterally. This case report describes a 1‐year‐old, male, entire miniature dachshund that presented with a sudden onset, moderate right‐sided exophthalmos without protrusion of the nictitating membrane. Head computed tomography and ocular ultrasound demonstrated findings that were reminiscent of EOM. The dog was treated with an anti‐inflammatory dose of oral corticosteroids and amoxicillin/clavulanic acid. Rapid clinical improvement was observed, prompting an increase to an immunosuppressive dose of oral corticosteroids, which were tapered over 24 weeks. The patient showed complete recovery with no relapse at the 376‐day follow‐up. To the authors’ knowledge, this is the first documented case of presumed unilateral EOM in a dog.

SUMMARYIn active vision, the brain receives and encodes discontinuous streams of visual information gated by saccadic eye movements. Saccadic modulation of neural activity is hypothesized to evolve to support perception and memory; however, it remains unclear whether this mechanism exist in humans, and potential functional roles have not been determined. We used eye tracking and intracranial local field potentials recorded from invasively monitored epilepsy patients when they performed visual encoding tasks, and observed consistent evoked potentials following saccades (saccade-related evoked potentials, SREPs) across the cerebrum. These SREPs were not attributable to ocular muscle activity or retinal input. Their magnitudes were not explained by spatial proximity to eye muscles or saccade eccentricity, and their polarity bore no relationship to saccade direction. Instead, the phase of pre-saccadic oscillation aligned with saccade timing and dissociated SREPs with positive polarity from those with negative polarity. Spatiotemporal profiling revealed that SREPs emerged earliest and with the greatest magnitude in the temporal lobes. We developed a saccade-related neural dynamic (SRND) model that characterized pre-saccadic oscillatory activity and SREP at each electrode contact location using finite features. Random forest models trained with these features achieved 62.6% balanced accuracy for predicting next-day recognition (long-term memory). Using the Shapley value, a framework for explaining machine learning models, we identified an SREP profile, characterized by earlier latency and larger magnitude, which was associated with successful visual encoding. In contrast, predicting saccade direction using the same SRND model performed at chance level, indicating that the observed SREP is less likely a corollary discharge signaling saccadic motor copy. These findings demonstrate SREPs as a neural mechanism of saccadic modulation with a role in human visual encoding.HighlightsWidespread, consistent evoked potentials follow saccades (Saccade-related evoked potentials, SREPs) in human subjects with intracranial electrodesSREPs are not oculomuscular artifacts and carry no discernible information about saccade directionSREPs in the temporal lobes have earlier latencies and higher amplitudes than in other anatomical regionsEarlier and high-amplitude SREPs across the cerebrum are associated with successful visual encodingGraphical abstract

Chronic progressive external ophthalmoplegia (CPEO), a genetic syndrome characterized by slowly progressive paresis of extraocular muscles, is often due to single large-scale deletions of the mitochondrial genome (mtDNA). Owing to heteroplasmy, mtDNA variants are often not uniformly expressed across tissues. This genetic variability affects clinical presentation and diagnostic testing. We report a case of a 34-year-old woman who presented with symptoms suspicious for a genetic myopathy: chronic asymmetric ptosis, slowly progressive asymmetric weakness, and external ophthalmoplegia. After initial nondiagnostic peripheral genetic testing, whole-exome and mitochondrial genome sequencing of muscle revealed a single large-scale mtDNA deletion, consistent with a diagnosis of mtDNA deletion-associated CPEO. Of interest, electrophysiologic studies showed myotonia in select muscles, a rarely reported finding. We discuss the clinical presentation and diagnostic approach in suspected CPEO, with an emphasis on common pitfalls in genetic testing for mitochondrial myopathies and the need for appropriate tissue and genetic testing modality selection.

Introduction: To report a rare presentation of an alveolar orbital rhabdomyosarcoma and the corresponding findings on computed tomography (CT), magnetic resonance imaging (MRI), and surgical outcome. Case Report: A 14-year-old Saudi boy, who presented with a progressively enlarging left upper eyelid mass. Associated with proptosis and limitation of extra-ocular muscles. He underwent imaging including CT scan and MRI which both modalities showed a large left intraconal mass with extraconal extension. The patient underwent a subtotal excision of the mass. Biopsy was sent for histopathology revealed a diagnosis of alveolar rhabdomyosarcoma, solid variant. Histogenetics, including fluorescence in situ hybridization (FISH) analysis for the FOXO1 gene, showed a negative gene rearrangement. The patient was referred to the oncology center in Dammam for confirmation of the diagnosis and to initiate appropriate management based on the disease stage. Conclusion: This case report highlights a rare instance of orbital alveolar rhabdomyosarcoma (RMS) in a 14-year-old boy from the Eastern Province of Saudi Arabia. Despite being a highly malignant tumor with aggressive progression typically affecting younger children, our patient presented with a relatively slower progression and a 6-week history of enlarging swelling and non-axial proptosis.

We report a case of a phenotypic shift of thyroid eye disease following treatment with teprotumumab. A 35-year-old female nonsmoker with Graves disease developed mild type I thyroid eye disease featuring unilateral lid retraction and was treated with teprotumumab. Following completion of treatment, a reactivation was associated with progression to severe type II phenotype, with marked extraocular muscle enlargement, bilateral proptosis, and nonsteroid-responsive compressive optic neuropathy requiring orbital decompression. This case raises important questions regarding the potential influence of Insulin-like growth factor 1 (IGF-1) suppression on the phenotype of thyroid eye disease.

Significance of T2 hyperintensity in extraocular muscle hypertrophy.

Background Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction that causes fluctuating weakness, often involving ocular and bulbar muscles. In older adults, these symptoms may closely mimic acute ischemic stroke, particularly when dysphagia is present. In acute care, this overlap poses a diagnostic challenge, as decisions about reperfusion therapies are time‐sensitive. When neuroimaging is negative for acute ischemia, alternative diagnoses such as MG should be considered to prevent misdiagnosis and avoid harmful interventions. Case Presentation An 82‐year‐old woman with atrial fibrillation and sick sinus syndrome with pacemaker placement (on rivaroxaban), hypertension, hyperlipidemia, and prior cerebrovascular accident presented with acute dysphagia. She reported progressive left eyelid drooping for two weeks and worsening neck weakness for one month. On the day of admission, she was unable to swallow her medications and was referred for suspected stroke. Neuro‐imaging revealed chronic infarction on CT head, no large‐vessel occlusion but 60% left internal carotid artery stenosis on CTA, and no acute changes on MRI brain. Examination showed marked left ptosis that improved with the ice‐pack test, diplopia on left gaze, a positive Cogan's lid twitch, fatigability with sustained upgaze, and weakness of the neck extensors. These findings, combined with negative imaging, strongly suggested MG. She was started on pyridostigmine 60 mg four times daily with improvement of ocular and bulbar symptoms. CT chest was negative for thymoma. Antibody testing later revealed elevated anti‐MuSK levels (10.7), and she was transitioned to immunomodulatory and steroid therapy. Discussion and Conclusion This case emphasizes the importance of recognizing MG as a stroke mimic in elderly patients with bulbar symptoms. Bedside tests such as the ice‐pack test, Cogan's lid twitch, and fatigability assessment are rapid, non‐invasive, and highly informative. Early recognition of MG prevents unnecessary thrombolysis/thrombectomy in anticoagulated patients and ensures timely initiation of appropriate therapy. image image

Abstract Introduction The co-existence of dermatomyositis and myasthenia gravis is an uncommon clinical scenario that presents many diagnostic and therapeutic challenges. Such cases are sparsely documented in the literature. While both are autoimmune conditions that can present with muscle weakness, they differ significantly in their underlying pathophysiology and management strategies. We present the case of a 17-year-old male who developed a combination of rash, myalgia, progressive muscle weakness, and dysphagia. He was diagnosed with dermatomyositis and myasthenia gravis, requiring treatment with a combination of corticosteroids, immunosuppressive agents, intravenous immunoglobulin (IVIG) and pyridostigmine. Case description A 17-year-old male presented with a three month history of progressive muscle weakness, fatigue, weight loss, rash, and a three week history of dysphagia. The muscle weakness began after a flu-like illness and affected his ability to walk, lift his arms, and grip objects. He developed an erythematous rash over the metacarpophalangeal joints, elbows, back, chest, thighs, and knees. Examination revealed proximal muscle weakness (power 2/5), a low MMT8 score (79/150), and signs suggestive of myasthenia gravis, including ptosis, eye muscle fatigability, and a positive ice pack test. Skin findings included heliotrope rash, Gottron’s papules, and shawl sign. Investigations revealed creatine kinase (CK) of 618, negative antinuclear antibodies (ANA), negative myositis specific and associated antibodies, and negative 3-hydroxy-3-methylglutaryl-coA reductase (HMGCR) antibodies. Interestingly, acetylcholine receptor antibodies (AChR) were found to be positive. MRI imaging showed extensive inflammatory myopathy affecting the shoulder girdle, chest, abdominal, pelvic and thigh musculature. Nerve conduction studies were consistent with inflammatory myopathy. Muscle biopsy was suggestive of dermatomyositis with features of perifascicular atrophy, perivascular inflammatory infiltrate and occasional regenerative fibres. Barium swallow and oesophageal manometry identified cricopharyngeal spasm and a hypercontractile oesophagus. He was commenced on intravenous methylprednisolone and subsequently on oral corticosteroids. Due to progressive dysphagia, nasogastric tube insertion was warranted. Two cycles of intravenous immunoglobulins (IVIG) 2g/kg were administered 4 weeks apart and subcutaneous methotrexate and oral ciclosporin were introduced as steroid-sparing agents. Oral pyridostigmine was also commenced following input from the neurology team as there was suspected overlap with myasthenia gravis and this brought on some improvement in his symptoms. After six weeks of treatment there was clinical improvement with MMT8 score 129/150, normal CK, with resolution of the rash. Subsequently, his dysphagia also improved, allowing removal of his nasogastric tube. Discussion The overlap between dermatomyositis and myasthenia gravis is a rare clinical entity. While both are autoimmune conditions characterised by muscle weakness, their distinct pathophysiology and management strategies differ. This case highlights the rare co-existence between these two conditions. The characteristic cutaneous findings in this patient along with elevated creatine kinase levels, MRI evidence of myositis, and confirmatory muscle biopsy findings supported a diagnosis of dermatomyositis. However, the presence of mild ptosis, muscle fatigability, and a positive acetylcholine receptor antibody test indicated concurrent myasthenia gravis. The diagnosis of this overlap was critical, especially as his dysphagia persisted despite optimal immunosuppressive therapy for dermatomyositis. Management of this overlap condition poses therapeutic challenges. Dermatomyositis typically requires high-dose glucocorticoids and long-term immunosuppression, whereas treatment for myasthenia gravis includes anticholinesterases and cautious use of steroids. Notably, high-dose corticosteroids may exacerbate symptoms of myasthenia gravis in up to one-third of patients, necessitating a gradual dose escalation under close monitoring. Initial treatment for this patient included high-dose corticosteroids, IVIG, and immunosuppressive agents (methotrexate and ciclosporin), leading to partial improvement in his muscle weakness and skin rashes. However, his dysphagia remained prominent and pyridostigmine was introduced, resulting in further clinical improvement. Both idiopathic inflammatory myositis and myasthenia gravis present with muscle weakness; however, muscle fatigability, ocular muscle involvement and bulbar symptoms, such as dysphagia and dysphonia, are more common in myasthenia gravis. Nevertheless, dysphagia has been reported in one out of three patients with idiopathic inflammatory myositis, and this can occur as an initial or sole symptom and is caused by inflammatory involvement of the swallowing muscles, albeit the variation in severity of clinical manifestations and response to treatment. If dysphagia is persistent or progressive despite immunosuppressive therapy, this should prompt consideration of other underlying neuromuscular conditions. Key learning points 1. The co-occurrence of idiopathic inflammatory myopathies and myasthenia gravis is rare but should be considered in patients with atypical or refractory myositis presentations. 2. Progressive dysphagia in myositis patients, despite immunosuppressive medications, should prompt consideration of other possible neuromuscular disorders and early involvement of the relevant specialties. 3. Management of dermatomyositis/myasthenia gravis overlap should include careful use of steroids along with a trial of pyridostigmine, in addition to immune-suppressive and immune-modulatory agents. 4. Seronegative myositis does not exclude the diagnosis; muscle biopsy remains critical in confirming inflammatory myopathies. 5. IVIG has shown efficacy in treating dysphagia in both dermatomyositis alone and dermatomyositis overlap. Early, aggressive, and individualised therapy, including immunosuppression, IVIG, and treatment for myasthenia gravis, can lead to significant functional recovery.

HighlightsWhat are the main findings?The Six1/Eya1 complex regulates the composition of type IIA, IIX/IIB and IIB myofibers in thyroid eye disease.FGFR1 and TGFβ signaling modulate the differentiation between myofibroblasts and fibroblasts in thyroid eye disease.What are the implications of the main findings?Targeting Six1/Eya1 signaling may provide a novel therapeutic strategy to control muscle hypertrophy and adipogenesis in thyroid eye disease.Human mesenchymal stem cell therapy has the potential to reverse pathological fibrosis and restore extracellular matrix composition in thyroid eye disease.Thyroid eye disease (TED) is an autoinflammatory condition characterized by fibrosis in orbital fat and extraocular muscles, primarily driven by TSH receptor antibodies and inflammatory cytokines. While research has predominantly focused on the involvement of fat tissue, the understanding of myopathy in TED remains limited. This study developed a TED mouse model and isolated myoblasts from both control individuals and TED patients for analysis. Single-cell RNA sequencing was used to investigate myofiber type changes in TED and their alterations following treatment with human-derived mesenchymal stem cells. Key regulatory genes involved in myofiber differentiation and fibrosis in myofibroblasts were identified, and their expression balance was validated in myoblasts derived from both normal individuals and TED patients. Our analysis revealed a disease-associated shift in myofiber types and identified Six1 and Eya1 as central regulators of myofiber differentiation and fibrosis suppression. These regulatory effects were validated in primary myoblasts isolated from both control and TED patients. Collectively, our findings uncover a novel role for the Six1/Eya1 axis in modulating muscle remodeling and fibrosis in TED and provide a foundation for the development of targeted therapies for TED-associated myopathy.

Background and Clinical Significance: Immune checkpoint inhibitors (ICIs), a revolutionary class of oncology therapeutics that enhance T cell-mediated antitumor immunity, are associated with various immune-related adverse events (IRAEs). While destructive thyroiditis and hypothyroidism are common, ICI-induced Graves’ disease (GD) is exceedingly rare, and the occurrence of concomitant Graves’ ophthalmopathy (GO) is even rarer. Case Presentation: A 57-year-old man with bladder cancer developed GO after receiving the first dose of the programmed death 1 (PD-1) inhibitor pembrolizumab. He presented with severe proptosis, extraocular muscle enlargement, hyperthyroidism, and significantly increased thyroid-stimulating hormone receptor autoantibodies (TRAb). Following the treatment with glucocorticoids and immunosuppressive therapy, his symptoms improved markedly but relapsed upon dosage reduction. To date, we have not identified any previous reports of GO with confirmed positive thyroid-related antibodies induced by pembrolizumab. Conclusions: This case offers valuable insights into the potential IRAEs, underscoring the importance of thorough clinical evaluation and early recognition to improve patient outcomes and quality of life. A literature review of ICI-induced GO was also performed, with further discussion of the potential pathogenic mechanisms, risk factors, and management strategies.

Background/AimsTo evaluate the prevalence of ptosis, strabismus and the combination of both after glaucoma surgery and determine which kind of surgery is most likely to be linked to these complications.MethodsA total of 705 clinical records of patients who underwent glaucoma surgery at the University Eye Clinic of IRCCS Ospedale Policlinico San Martino, Genoa, from January 1, 2010, to December 31, 2020, were retrospectively evaluated. Surgery procedures were divided in three groups: “Ab interno”, “Ab externo” and “Muscle isolation”.ResultsOut of all patients 26 developed ptosis alone (3.7%), two developed bilateral ptosis, with a mean of 2.2 ± 1.08 procedures per patient. Highest incidence of ptosis was noticed in patients who underwent muscle isolation surgery (5.7%). Twelve patients developed strabismus alone (1,7%), four underwent unilateral surgery and eight bilateral surgery, with an average of 3.3 ± 1.78 procedures per patient. Strabismus was more frequent following extraocular muscle manipulation surgery (7.5%), showing a statistically significant difference (OR: 6.57; 95% CI: 1.71–21.65; p = 0.003) Seven patients developed both strabismus and ptosis (1.0%), one patient with bilateral ptosis. Four underwent bilateral surgery and three underwent unilateral surgery. The mean number of surgeries was 2.9 ± 1.07, showing a statistically significant difference compared to the uncomplicated glaucoma group (OR: 1.58; 95% CI: 1.01–2.25; p = 0.02). The prevalence of both ptosis and strabismus was higher after muscle isolation surgery (1.9%).ConclusionPtosis, strabismus and the combination of both are rare complications after glaucoma surgery, mostly linked to surgery with muscle isolation.

Traditional treatments for ocular motility disorders and eye prosthetics face significant limitations in restoring natural, coordinated eye movements. Conditions such as strabismus or eye paralysis alter the delicate balance between the agonist and antagonist eye muscles, resulting in misalignment, poor focus, and restricted movement. Current interventions, including surgeries or static eye prostheses, often fail to replicate the full range of motion or provide the feedback necessary for dynamic visual function. Therefore, the development of Brain-Computer Interfaces for eye movement rehabilitation was developed with the aim to better the experience of eye motion, as well as to be able to enable precisely coordinated eye control for the amputees. This paper conducted a literature review on interface design, signal image conversions, age-related data differences, and the principles of P300 Speller BCI (a system used to show target characters on a computer screen). The question researched is, How do spellers and motor imagery function and in what scenarios are their applications suitable. After examining numerous papers, the conclusion is that BCI technology has the potential to restore eye performance for the unsighted, including clear visual feedback and the ability for precise eye coordination.

Orbital floor fractures are primarily caused by blunt trauma to the area around the eyes. These injuries most commonly affect the orbital floor and medial wall due to the fragility of these structures. The mechanism typically involves transmission of force through the orbital rim or an acute increase in intraorbital pressure caused by globe displacement. Blowout fractures often occur alongside additional maxillofacial fractures and periorbital soft tissue injuries. The reported causes mirror those of general maxillofacial trauma and include motor vehicle collisions, interpersonal violence, falls, sports-related injuries, incidents involving firearms, and occupational accidents. Here, we present the case of a 56-year-old male patient who sustained an exceptionally rare injury pattern characterized by a complete orbital floor fracture with globe dislocation into the maxillary sinus. Such extensive fractures are associated with significant functional impairments, including diplopia, enophthalmos, and restricted extraocular muscle movement, as well as marked aesthetic deformity. Comprehensive diagnostic imaging, comprising coronal, sagittal, and three-dimensional CT reconstructions, was crucial for accurately assessing the extent of bony disruption and soft tissue involvement. Particular emphasis should be placed on imaging that clearly delineates the extraocular muscles and the optic nerve, as precise evaluation of these structures is essential for surgical planning and prognosis. Surgical management involved repositioning of the globe and the orbital contents, followed by reconstruction of the orbital floor using a titanium mesh anchored to the infraorbital rim. This case highlights the technical challenges of total orbital floor reconstruction, emphasizing the importance of meticulous anatomical restoration for achieving optimal functional and aesthetic outcomes.

Pediatric orbital trapdoor and linear fractures may involve entrapment of the extraocular muscles (EOM), potentially causing irreversible ocular motility impairment if surgical intervention is delayed. The optimal timing for surgery in cases with EOM strangulation remains uncertain. We retrospectively reviewed 103 pediatric cases from our medical records of 389 patients with orbital fracture. A systematic review was conducted following PRISMA 2020 guidelines. Data from 10 previous studies and our institutional cohort were combined, including 101 patients under 20 years old with radiologically confirmed EOM entrapment. Patients were stratified by time to surgery: within 24 hours, 24-72 hours, and beyond 72 hours. Surgical intervention within 24 hours was significantly associated with better postoperative ocular motility outcomes compared to delayed surgery (p < 0.05). In our cohort, cases treated within 8 hours achieved excellent recovery, with Hess Area Ratio (HAR%) exceeding 85% and no residual diplopia. Patients without EOM entrapment improved with an average of 7 weeks of conservative management. This study supports urgent surgical repair within 24 hours for pediatric orbital fractures with EOM entrapment to maximize functional outcomes. In cases of soft tissue entrapment without sustained oculocardiac reflex, non-operative management with close follow-up may be appropriate. Prompt diagnosis and timely referral remain critical to avoid permanent sequelae.

The growing use of injectable cosmetic fillers has been accompanied by an increase in reports of acute vision loss, typically caused by inadvertent intravascular injection and subsequent embolization of the ophthalmic artery, resulting in ocular ischemia. Effective management of this complication remains challenging, as clear clinical guidelines for retrobulbar hyaluronidase injection are lacking. This ultrasound-based observational anatomical guideline provides practical recommendations for retrobulbar administration of hyaluronidase. Real-time ultrasonography allows for direct visualisation of orbital anatomy, enabling the injector to identify the optic nerve sheath complex and surrounding vascular structures. The central retinal artery's entry point into the optic canal is a key anatomical landmark for directing treatment. Based on ultrasound observations, the inferolateral quadrant of the orbit is identified as the safest and most accessible entry site, reducing the risk of damage to extraocular muscles, cranial nerves, and major vessels. The use of ultrasonography enhances both precision and safety, supporting timely and effective management of filler-related ocular complications. Ultrasound observation further confirms that the inferolateral orbital approach offers the most reliable and safe access for retrobulbar hyaluronidase injection. The superior orbital rim and close proximity of the globe restrict needle trajectory from above, increasing the risk of ocular injury. In contrast, the inferior approach provides a wider anatomical corridor, reduces the likelihood of direct contact with the eyeball, and allows safer navigation around critical neurovascular structures. Incorporating real-time ultrasound enhances precision, making the inferior approach the preferred route for managing filler-related ocular complications.

The aim of this paper is to report “Globe Intussusception” as an extreme form of globe dislocation outside the orbital pyramid, and provide a literature review. A single-center, retrospective, interventional case series of three patients is presented. A review of the English-language literature from the years 1971 to 2024 was performed using the search terms “traumatic globe dislocation”, “maxillary sinus” and “ethmoid sinus”. Three cases of globe intussusception are reported. Computed tomography imaging revealed orbital fracture, and globe prolapse into the maxillary sinus with or without involvement of ethmoid sinus. This was associated with complete intussusception of the globe through the conjunctiva, giving an “empty socket” appearance. In all three cases, fracture repair along with retrieval of the eyeball from the sinus was carried out surgically. Reduction of the intussusception, and bringing the eyeball out of the conjunctival pouch was a special additional challenge in these cases. The review of 35 cases reported in world literature till date is presented. We suggest retrieval of the intussuscepted eyeball via a 360° peritomy and suture tagging of extraocular muscles to ensure safe repositioning of globe with intact extraocular muscles.