BackgroundBow Hunter's Syndrome (BHS) is a rare condition in which dynamic vertebral artery (VA) compression during neck rotation induces transient symptoms, such as vertigo, whereas major arterial occlusion is extremely uncommon. There is no standardized treatment for BHS, and management includes conservative, surgical, and rarely endovascular approaches. We report a unique case of BHS with acute VA occlusion successfully treated by mechanical thrombectomy followed by elective stent placement.Case ReportAn 87-year-old woman presented with right gaze deviation, dysarthria, right hemiparesis, and sensory disturbance. Magnetic resonance imaging showed acute infarcts in the left pons and cerebellum, while magnetic resonance angiography showed poor visualization from the VA to the basilar artery. Emergency cerebral angiography showed VA occlusion, and subsequent thrombectomy was performed, which resulted in successful recanalization. Post-recanalization angiography showed residual stenosis at the V3 segment and an anomalous course of the VA running caudal to the posterior arch of the atlas. A dynamic ultrasonographic examination with neck rotation showed occlusion of the VA, which confirmed the diagnosis of BHS. Stent placement was planned because compression of the left VA was confirmed to be caused by soft tissue rather than by bony structures. Balloon angioplasty showed resistance to external compression. Subsequently, a balloon-expandable stent was successfully deployed using a distal access catheter and a stiff micro guidewire. Follow-up imaging confirmed VA patency with preserved flow during head rotation. The patient showed neurological improvement without recurrence during 6 months of follow-up.ConclusionWe report a rare case of BHS presenting with acute VA occlusion treated effectively with endovascular therapy. BHS should be considered as a potential cause of large-vessel occlusion in posterior circulation stroke when abnormal arterial courses are identified. In selected cases, stent placement may be a feasible therapeutic option depending on the compressive structure.

Chronic neck and upper thoracic pain are common and frequently classified as non-specific when no single structural lesion explains the presentation. Although forward-head posture, prolonged device use, sedentary behaviour, and occupational loading are often considered contributors, the association between static posture and chronic neck pain is inconsistent. This narrative review examines persistent cervicothoracic muscle mechanical stiffness as a potential time-dependent mechanism linking cumulative postural loading to chronic symptoms. The central construct is persistent or repeatedly elevated mechanical stiffness, particularly passive stiffness assessed under standardised resting conditions; active stiffness related to ongoing activation or guarding is considered distinct but potentially relevant. PubMed, Scopus, and Web of Science were searched for English-language articles published from January 1990 to June 2026 addressing cervicothoracic posture, loading, fatigue, muscle mechanical properties, and chronic neck or upper thoracic pain. Findings were synthesised narratively without meta-analysis. Static posture alone does not consistently predict chronic neck pain. Sustained or repeated cervicothoracic loading may nevertheless increase muscular demand and contribute to fatigue, altered recruitment, impaired relaxation, reduced movement variability, and mechanical stiffness when exposure exceeds tissue tolerance and recovery capacity. Persistent mechanical stiffness has been proposed as a possible contributor to pain through mechanical sensitivity, altered perfusion relative to demand, metabolic stress, nociceptive sensitisation, and pain-related guarding. However, direct cervicothoracic evidence in patients with chronic neck pain remains limited; much of the biological rationale is extrapolated from studies of general muscle pain, myofascial pain, trapezius myalgia, and experimental models. In the absence of an identified neurological or vascular cause, alterations in neural-interface mechanics have been hypothesised to contribute to nerve-like symptoms; however, any relationship with surrounding muscle mechanical stiffness remains theoretical and has not been directly established. This review proposes a testable conceptual model in which cumulative postural loading, recovery capacity, neuromuscular adaptation, cervicothoracic muscle mechanical stiffness, and pain-related mechanisms interact over time. Objective assessment may help determine whether cervicothoracic muscle mechanical stiffness precedes pain, contributes to the proposed pathway, or identifies a clinically relevant subgroup. Direct longitudinal evidence validating this proposed pathway remains limited.

Intracranial hypotension is a typically self-limiting or treatable condition characterized by orthostatic headache and neck stiffness. However, it may be severe and may be associated with neurological complications, particularly sixth cranial nerve palsy. We report two young women who presented to the emergency department with diplopia secondary to acute unilateral sixth cranial nerve paresis in the context of intracranial hypotension following anesthetic procedures. In both cases, clinical and radiological findings consistent with a cerebrospinal fluid (CSF) deficit were documented, including bilateral subdural collections in one case. One case required an epidural blood patch, which resulted in complete resolution, whereas the other resolved spontaneously. The clinical manifestations, radiological findings, and therapeutic options are reviewed. These cases underscore the importance of careful clinical and radiological assessment in patients with acute ophthalmoplegia, in whom orthostatic headache is a key diagnostic clue, as well as of treatment aimed at correcting the CSF deficit.

Non-aneurysmal subarachnoid hemorrhage (NASAH) is defined as bleeding into the subarachnoid space without an identifiable aneurysm. In patients with long-standing diabetes mellitus (DM), chronic microvascular damage may contribute to vascular fragility and hemorrhage. Emerging evidence suggests a possible association between NASAH and diabetes, particularly through microangiopathic mechanisms. We report the case of a 40-year-old female patient with a 14-year history of poorly controlled Type 1 DM (T1DM) who presented with sudden-onset severe occipital headache, neck stiffness, and vomiting. On examination, she was neurologically intact with a Glasgow Coma Scale score of 15/15, with mild nuchal rigidity. Non-contrast head CT revealed diffuse subarachnoid hemorrhage. CT angiography showed no aneurysm or vascular malformation, confirming NASAH. She was managed conservatively with nimodipine, analgesics, and supportive care, with good clinical recovery and no residual deficits. This case highlights NASAH as a potential microvascular complication of long-standing T1DM. Early recognition and appropriate imaging are essential for diagnosis, particularly in resource-limited settings, and can lead to favourable outcomes.

Whiplash injuries due to rear impact vehicle collisions remain a significant global concern, with females facing a disproportionately higher risk of permanent medical impairment compared to males. Current rear impact testing predominantly uses 50th percentile male dummies, such as the BioRID II, which are not representative of the female population. A 50th percentile male dummy roughly corresponds to a 90th-95th percentile female in stature and mass, which appear to render whiplash protection systems less effective for women. In preparation for future investigation of car models with known differences in whiplash injury risk between female and male occupants, the development of an upgraded average size female BioRID prototype, denoted P50F_V2, was initiated to further improve the first female BioRID prototype. The aim was to better represent female properties by reducing upper torso stiffness and improving spinal curvature, as well as simplifying the H-point position measurement and refining the external contours of the head, hands and feet. The dynamic response of the upgraded prototype was evaluated with regard to rear impact sled tests, comprising female volunteers close to the 50th percentile female size. Overall, the dynamic response of the upgraded prototype showed improvements, in particular, the T1 rearward angular displacement better matched the female volunteer response corridors. Although the biofidelity of the upgraded prototype leaves room for further improvement, it is deemed sufficient to provide an understanding of the differences in dynamic response between female and male occupants in rear impacts. Overall, the upgraded BioRID P50F, used as a complement to the BioRID II, is a significant step towards sex-inclusive crash testing.

Adult obstructive sleep apnoea (OSA) is an established cardiovascular risk factor, but paediatric OSA has been framed mainly around neurocognition and growth. We reviewed PubMed, Ovid-Embase and Web of Science (2000-2026), prioritising eligible paediatric studies with quantifiable outcomes (ambulatory/office blood pressure (BP), autonomic indices/heart-rate variability, endothelial function/arterial stiffness, carotid intima-media thickness (cIMT) and echocardiographic structure/function) and key interventional data. Across cohorts, 24-h ambulatory blood pressure monitoring (ABPM) most consistently demonstrates higher nocturnal BP and reduced dipping; emerging exposure metrics such as hypoxic burden (the integrated depth and duration of oxygen desaturation across sleep) may capture physiological stress better than the apnoea-hypopnoea index alone. Autonomic imbalance, including sympathetic predominance, altered sleep-stage autonomic modulation and reduced baroreflex gain, provides a plausible bridge between respiratory events and early vascular/cardiac remodelling, and often improves after adenotonsillectomy. Vascular data suggest early functional abnormalities (endothelial reactivity, wave reflection/central haemodynamics) with smaller and inconsistent differences in structural markers, such as cIMT, strongly modified by obesity and development. Cardiac studies most reproducibly show increased left-ventricular mass/geometry and impaired diastolic relaxation, while right-heart and pulmonary vascular signals appear most relevant in selected higher-risk groups. Treatment effects appear more readily detectable in autonomic/endothelial measures than in office BP over short follow-up, reinforcing ABPM as a preferred research and selected high-risk clinical end-point. Paediatric OSA should therefore be approached through an early-risk framework, including identifying higher-risk phenotypes, quantifying nocturnal haemodynamic burden when feasible and integrating OSA therapy with weight and guideline-directed BP management.