Upper cervical structural disease can alter vertebral artery biomechanics, although a mechanical contribution cannot be established by anatomical proximity alone. We describe an older woman with seronegative inflammatory arthritis and chronic atlantoaxial abnormality who developed abrupt vertigo, nausea, and inability to walk despite a National Institutes of Health Stroke Scale (NIHSS) score of 0. Computed tomography angiography (CTA) demonstrated left V3 vertebral artery dissection with pseudoaneurysmal dilation at the craniovertebral junction. Magnetic resonance imaging (MRI) showed a dominant acute left posterior inferior cerebellar artery (PICA)-territory infarction. Cervical imaging demonstrated atlantoaxial deformity, pannus-like peri-odontoid tissue, and a C1 arch abnormality adjacent to the affected V3 segment. Echocardiography and inpatient telemetry did not identify an embolic source. Anatomical colocalization of the C1-C2 abnormality and V3 lesion, together with the ipsilateral PICA infarction, suggests a possible mechanical contribution to the dissection, with subsequent artery-to-artery thromboembolism to the cerebellum. Dynamic compression was not demonstrated; spontaneous dissection, intracranial atherosclerosis, and occult embolism remain alternative or additional mechanisms. The patient received dual antiplatelet therapy followed by aspirin, statin therapy, and rehabilitation. This case emphasizes the limitations of the NIHSS in posterior circulation stroke and the importance of evaluating the craniovertebral junction when a V3 lesion occurs near upper cervical structural disease.

Cisplatin-induced ototoxicity is a significant clinical issue linked to ferroptosis and mitophagy dysfunction. This study investigated how mitophagy regulates ferroptosis in cisplatin-induced hearing loss using cultured primary rat cochlear marginal cells in vitro and a C57BL/6J mouse model of cisplatin-induced ototoxicity in vivo. Cisplatin suppressed the PTEN-induced putative kinase 1 (PINK1) pathway, impaired mitophagy, and triggered ferroptosis characterized by iron overload, lipid peroxidation, increased acyl-CoA synthetase long-chain family member 4 (ACSL4), and decreased glutathione peroxidase 4. Pharmacological activation of mitophagy or PINK1 overexpression alleviated ferroptosis in vitro, while deferoxamine treatment reduced cisplatin-induced hearing loss and blood-labyrinth barrier damage in vivo. Mechanistically, restoration of mitophagy was associated with increased mitochondrial targeting and reduced cytosolic accumulation of ACSL4, potentially through mitophagic clearance, thereby suppressing ferroptosis. These findings support a model in which impaired PINK1-associated mitophagy contributes to cytosolic ACSL4 accumulation and ferroptotic injury. Modulating mitophagy and ACSL4 subcellular distribution may represent a potential strategy for mitigating cisplatin-induced ototoxicity.

Benign paroxysmal positional vertigo (BPPV) is the most common cause of patient-reported vertigo. The accurate diagnosis of BPPV requires high-quality physician training and knowledge of the advantages and disadvantages of different diagnostic methods. Most studies focus on a limited number of diagnostic approaches; the purpose of this review is to consolidate and systematize the available information on the wide range of existing methods. This review includes comparative descriptions of the clinical utility of 12 different techniques used to diagnose BPPV. The diagnosis of BPPV relies primarily on a thorough analysis of clinical history and the professional application of positional tests (primarily the Dix-Hallpike and the Pagnini-McClure maneuvers). Several methods can be used to enhance the efficiency of positional testing: rotary chair, electronystagmography (ENG), videonystagmography (VNG), and potentially artificial neural networks for the analysis of VNG results. The VEMP (vestibular evoked myogenic potential) technique, vestibular caloric testing, the video head impulse test, computerized posturography, and CT and MRI of the head are all useful auxiliary methods for the differential diagnosis of BPPV in complex cases. When selecting diagnostic approaches, it is important to consider the balance between resource and time expenditure and diagnostic accuracy. This review enables a comprehensive and well-rounded understanding of a wide range of diagnostic methods, which is necessary for the development of optimal diagnostic and subsequent treatment and monitoring tactics.

Background/Objectives: Skull vibration-induced nystagmus (SVIN) is a reproducible marker of vestibular asymmetry, but its relationship with age in patients with normal conventional tests remains unclear. We evaluated whether age is associated with the presence of SVIN and with its slow-phase velocity (SVIN-SPV). Methods: In this retrospective cross-sectional analysis, 164 patients with dizziness or vertigo and normal video head impulse test (vHIT) and VEMPs were studied (107 SVIN-positive, 57 SVIN-negative). Logistic regression tested whether age predicted SVIN positivity; among the 107 positive patients, SVIN-SPV was analyzed by correlation and multivariable linear regression. Results: Age did not predict a positive SVIN (odds ratio 1.01 per year, p = 0.28), whereas male sex did (odds ratio 2.31, p = 0.02). Among positive patients, mean SVIN-SPV was 3.0°/s and correlated with age (r = 0.25, p = 0.009); age was the only significant covariate in multivariable regression (β = 0.035°/s per year, p = 0.010), and patients aged ≥60 years showed higher SVIN-SPV (p = 0.028). Conclusions: Thus, age was not associated with whether SVIN was present but with its intensity once present, compatible with possible age-related changes in vestibular asymmetry or central compensation, although the underlying mechanism was not directly assessed; these findings should not be generalized to physiological vestibular aging.

Persistent postural- perceptual dizziness (PPPD) is a functional disorder that is the most frequent cause of chronic dizziness. Diagnostic criteria for PPPD were published by Bárány Society in 2017 and were then included in the International Classification of Diseases, 11th revision (ICD-11). Core symptoms are dizziness, unsteadiness or non-spinning vertigo, lasting more than three months. Persistent symptoms occur without specific provocation, but are exacerbated by upright posture/walking, active or passive motion, and exposure to moving or complex visual stimuli. An acute or episodic vestibular disorder often precedes the onset of PPPD, but conventional vestibular function tests typically show normal results. Studies using resting-state functional MRI have revealed that functional connectivity between the vestibular cortex and visual areas were low, while that between the somatosensory and visual areas was high, suggesting sensory upweighting of visual and somatosensory information. Such central changes have been shown to associate with peripheral hyper-responsiveness as demonstrated by visual stimulus-loaded posturography and head-roll tilt subjective visual vertical testing, which detects visual and neck proprioceptive hypersensitivity, respectively. As a result, symptoms are exacerbated by visual stimulation or somatosensory input associated with body motion. After visual stimulation, gaze stability remains reduced, which would account for the prolonged dizziness induced by visual stimuli. Pharmacological treatments using serotonergic anti-depressants, vestibular rehabilitation, and cognitive behavioral therapy have been shown favorable effects; however, they are not always effective for all patients. There is an urgent need to establish novel treatments tailored to the pathophysiology of PPPD, i.e., sensory upweighting of visual/somatosensory inputs.

[This corrects the article DOI: 10.3389/fneur.2026.1910905.].