Background/Objectives: Persistent dizziness after the apparent resolution of an acute or episodic vestibular disorder remains a frequent and clinically challenging condition. In many patients, symptoms persist despite negative positional testing, absence of spontaneous nystagmus, and preserved high-frequency vestibular responses on video head impulse testing. This discrepancy suggests that persistent dizziness may not always be explained by incomplete recovery of a single peripheral vestibular lesion but may reflect a dissociation between transient/high-frequency vestibular responses and sustained/low-frequency or integrative vestibular processing. The aim of this study was to propose a hypothesis-generating, case-based clinical framework for interpreting this dissociation and its implications for targeted vestibular rehabilitation. Methods: This was a retrospective, hypothesis-generating, case-based clinical study derived from routine specialist neuro-otological practice. Four illustrative cases were selected because they represented distinct patterns of persistent dizziness in which preserved or near-preserved transient vestibular responses coexisted with abnormalities in sustained, otolithic, visual-vestibular, or velocity-storage-dependent processing. All patients underwent detailed clinical history assessment, bedside neuro-otological examination, and multidomain vestibular assessment according to clinical indication. The purpose of the study was not to estimate prevalence, validate diagnostic accuracy, or demonstrate treatment efficacy but to illustrate a physiology-based interpretive framework. Results: The four cases showed different patterns of time-domain dissociation. These included low-frequency integrative dysfunction without clear peripheral lateralization, incompletely compensated unilateral vestibular asymmetry, selective unilateral otolithic loss despite preserved semicircular canal high-frequency responses, and bilateral sustained vestibular hypofunction unmasked by an apparently resolved BPPV-like event. Across cases, persistent symptoms were better explained by the relationship between transient and sustained vestibular domains than by any single test result considered in isolation. Conclusions: Persistent dizziness may arise from different combinations of preserved transient vestibular responses and impaired sustained or integrative vestibular processing. The proposed framework does not introduce new vestibular tests and does not claim to validate a new diagnostic entity. Rather, it organizes established vestibular investigations within a time-domain model that may help identify clinically meaningful dissociations and guide individualized, domain-specific vestibular rehabilitation. Prospective studies with larger samples and external validation are required to determine the diagnostic and therapeutic value of this approach.

Myeloid sarcoma is an extramedullary tumor composed of myeloid blasts, most commonly involving the skin, lymph nodes, and soft tissues. We report a rare case of myeloid sarcoma of the central nervous system (CNS) causing neuropsychiatric symptoms in an elderly woman with a history of JAK2-positive polycythemia vera and acute myeloid leukemia (AML) in long-term remission. The patient presented with a one-month history of complex visual hallucinations, short-term memory loss, and personality changes. Magnetic resonance imaging revealed a 2.4-cm enhancing mass in the septum pellucidum extending between the frontal horns of the lateral ventricle. Cytological analysis of the cerebrospinal fluid showed pleocytosis, and flow cytometry identified a 50% population of CD34 + blasts, consistent with the immunophenotype of the patient's prior biopsy-proven AML. This case highlights an exceedingly unusual presentation of AML relapse and emphasizes the need for clinicians to consider CNS involvement in hematologic patients presenting with new-onset neuropsychiatric symptoms, regardless of remission status.

This case report presents the diagnostic complexity and longitudinal management of a 39-year-old woman with progressive headaches found to have idiopathic intracranial hypertension with an atypical presentation of recurrent unilateral subconjunctival hemorrhages and a reported association with IgA nephropathy. Her medical history included multiple miscarriages, partial colectomy, and a remote history of migraines resolved in adolescence. This report explores the diagnostic challenges posed by this presentation and discusses medical and surgical treatment considerations for idiopathic intracranial hypertension, emphasizing cautious interpretation of transverse sinus stenosis and individualized treatment selection based on visual risk and comorbidities.

Giant cell arteritis (GCA) is a medical emergency due to the high risk of permanent vision loss. It occurs most often in people of northern European ancestry, with a global prevalence of approximately 50-52 cases per 100 000 individuals aged 50 years and older. Distinguishing GCA from infectious processes can be challenging as both may produce constitutional symptoms and elevated acute-phase reactants. Septic emboli mimic GCA by causing transient or permanent visual disturbances and retinal lesions. This case report underscores the importance of ophthalmological evaluation to differentiate GCA from its mimics and ensure appropriate, safe management.

Usher syndrome type I (USH1) is characterized by congenital, bilateral, profound sensorineural hearing loss, vestibular areflexia, and adolescent-onset retinitis pigmentosa (RP). Unless fitted with a cochlear implant, individuals do not typically develop speech. RP, a progressive, bilateral, symmetric degeneration of rod and cone functions of the retina, develops in adolescence, resulting in progressively constricted visual fields and impaired visual acuity.

Complicated infections of the middle ear and paranasal sinuses remain a relevant clinical challenge. Although acute otitis media and acute sinusitis are generally self-limiting, a small but clinically significant proportion of cases progress to severe local, orbital, or intracranial complications. These include acute mastoiditis, labyrinthitis, facial nerve palsy, orbital complications, frontal bone osteomyelitis, intracranial abscess, meningitis, and cerebral venous sinus thrombosis, all of which are associated with considerable morbidity and potential mortality. The current review provides an overview of the classification, clinical presentation, red flags, diagnostic workup, and microbiological spectrum of complicated disease courses as well as therapeutic strategies. The literature review is based on a selective search of the PubMed database, with particular consideration given to the current Association of the Scientific Medical Societies in Germany (AWMF) guidelines (as of 2025). Early recognition of warning signs and prompt interdisciplinary diagnostic and therapeutic management are crucial to prevent irreversible sequelae such as hearing loss, visual impairment, and permanent neurological deficits.

Early hospital arrival is essential for timely reperfusion therapy in acute stroke. This study aimed to identify clinical, symptom-related, and prehospital factors associated with delayed hospital arrival among patients with first-ever acute stroke, with particular focus on the 4.5-hour therapeutic window. This prospective single-center observational study was conducted at a comprehensive stroke center in Istanbul, Türkiye, between December 2023 and October 2024. Among 362 patients screened for suspected acute cerebrovascular events, 205 adults with first-ever acute ischemic stroke, intracerebral hemorrhage, or transient ischemic attack managed through the acute stroke pathway were included. Data were collected using a structured clinical form and a questionnaire on barriers to accessing acute stroke treatment, administered through face-to-face interviews with patients' relatives. Prehospital delay was defined as the interval from last known well (LKW) to hospital arrival. Patients were analyzed according to arrival within 1 hour, 2 hours, 3 hours, and 4.5 hours, using appropriate comparative statistical tests. The mean LKW-to-arrival time was 338.66 ± 345.67 minutes, with a median (IQR) of 240 (90-720) minutes. Overall, 29.3% of patients arrived within 1 hour, 41.0% within 2 hours, 48.3% within 3 hours, and 58.5% within 4.5 hours. Facial droop was consistently associated with earlier hospital arrival across multiple time thresholds (p ≤ 0.004), and syncope was more frequent among early presenters (p = 0.001). Conversely, visual symptoms were associated with delayed presentation, including vision loss after 3 hours and diplopia beyond 4.5 hours (p = 0.042 for both). Diabetes mellitus was associated with delayed arrival at the 1-hour and 2-hour thresholds, while hypertension was more common among patients arriving after 4.5 hours. Prehospital delay remains a substantial barrier to timely acute stroke care. Recognizable symptoms such as facial droop may facilitate earlier presentation, whereas less typical symptoms, particularly visual disturbances, may contribute to delayed arrival. These findings support locally tailored public awareness strategies and optimized prehospital stroke pathways that emphasize both typical and atypical stroke symptoms.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune demyelinating disorder of the central nervous system in which optic neuritis is a frequent manifestation. Its presentation during pregnancy may pose a diagnostic challenge because bilateral optic disc edema and headache can mimic idiopathic intracranial hypertension or hypertensive disorders of pregnancy. We report a 39-year-old primigravid woman at 31 weeks of gestation with gestational diabetes and class III obesity who presented with progressive bifrontal headache followed by transient bilateral blurred vision, dyschromatopsia, and sudden severe visual loss in the right eye. Ophthalmologic examination showed bilateral papilledema, a relative afferent pupillary defect in the right eye, and reduced visual acuity. Ultrasound demonstrated an enlarged optic nerve sheath diameter, while brain and spine magnetic resonance imaging showed no major abnormalities. Visual evoked potentials revealed bilateral conduction delay, more severe in the right eye. Lumbar puncture showed a normal opening pressure (19.5 cmH2O) and normal cerebrospinal fluid cytochemistry, but cerebrospinal fluid-restricted oligoclonal bands were detected. Given the clinical suspicion of inflammatory optic neuropathy, serum testing for demyelinating disorders was performed and was positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies, whereas aquaporin-4 and systemic autoimmune antibodies were negative. The patient was treated with intravenous methylprednisolone followed by therapeutic plasma exchange because of limited initial response, with progressive visual recovery and no maternal or fetal complications. This case highlights that MOG-associated optic neuritis should be considered in pregnant patients with acute visual loss and bilateral optic disc edema. Intracranial hypertension was ruled out, and paraclinical studies concluded bilateral inflammatory optic neuritis. Early recognition, serologic confirmation, and timely immunotherapy are essential to improve visual outcomes. Careful postpartum follow-up is warranted because relapse risk may increase after delivery.

Optic neuritis is a severe blinding ocular disease, and identifying its etiology is crucial for selecting appropriate treatment strategies and evaluating patient prognosis. This paper reports the clinical data of a patient initially presenting with unilateral visual decline who was ultimately diagnosed with bilateral atypical optic neuritis. The patient was a 40-year-old male who presented with decreased vision in the left eye for 2 weeks. Fundus examination at admission revealed bilateral optic disc edema, leading to a diagnosis of bilateral atypical optic neuritis. Systemic examination showed a positive Treponema pallidum particle agglutination test. After a series of serological and cerebrospinal fluid examinations for syphilis, syphilitic optic neuritis was excluded. The patient showed a poor response to conventional treatment for optic neuritis. Further comprehensive brain and ocular examinations were performed. After excluding multiple possible causes of optic neuritis, mitochondrial gene testing ultimately confirmed the diagnosis of Leber hereditary optic neuropathy (LHON). For young male patients presenting with acute vision loss, bilateral involvement, and typical fundus findings, etiological investigation should be emphasized, particularly the application of genetic testing, to achieve early diagnosis and timely treatment.

Intraocular tuberculosis often evades diagnosis owing to its nonspecific clinical features and frequent absence of systemic signs. We describe a rare case of primary tubercular chorioretinitis in an immunocompetent woman in her early 20s who presented with acute vision loss, ocular pain, and redness in the left eye. Multimodal imaging demonstrated active inflammation arising within-not at the margin of-pre-existing focal chorioretinal atrophy, accompanied by retinal vasculitis and choroidal hypoperfusion. Systemic workup revealed no extrapulmonary involvement; however, interferon-gamma release assay was strongly positive. Following initiation of standard four-drug antitubercular therapy, adjunctive oral corticosteroids were administered, achieving complete resolution of intraocular inflammation and marked visual recovery, with no recurrence during long-term follow-up. This case highlights intralesional reactivation within chorioretinal atrophy as a distinctive imaging hallmark suggestive of tubercular etiology. Recognition of this pattern may facilitate earlier diagnosis of intraocular tuberculosis, particularly in endemic regions or in patients lacking overt systemic disease. Given the potential for irreversible vision loss, timely initiation of antitubercular therapy-guided by multimodal imaging and immunologic testing-is critical. Our findings underscore the need to consider ocular tuberculosis in the differential diagnosis of posterior uveitis, even in immunocompetent individuals with isolated ocular symptoms, and advocate for heightened awareness of this subtle yet pathognomonic feature to improve diagnostic precision and clinical outcomes.