Background/Objectives: Compression syndromes of the stylohyoid complex (SHC) encompass neural, arterial, and venous presentations extending beyond classic Eagle syndrome. Symptomatic disease is increasingly recognised as a dynamic neurovascular conflict determined not by styloid process (SP) length alone, but by three-dimensional orientation, vessel and nerve proximity, and positional musculoskeletal interactions. This review synthesises that literature and proposes a phenotype-based framework integrating neural, arterial, venous, and mixed presentations. Methods: This is a narrative, pathophysiologically organised review rather than a systematic or scoping review. Landmark anatomical, clinical, and cohort studies were synthesised alongside systematic reviews, meta-analyses, osteological data, and selected case reports illustrating mechanisms not captured at cohort level. Evidence strength was interpreted by study design, distinguishing pooled estimates from retrospective series and proposed mechanisms. Results: The SHC and adjacent C1 transverse process form a narrow corridor containing the internal jugular vein, carotid arteries, and lower cranial nerves. SP elongation is common, but symptomatic compression depends more on orientation, SP-to-C1 distance, vessel proximity, and dynamic positional factors than on length. Three-dimensional CT angiography/venography is the anatomical cornerstone for defining morphology and vessel relationships, whereas catheter venography with manometry remains the haemodynamic reference standard in selected venous cases. Jugular narrowing is frequent in asymptomatic individuals and is not diagnostic without clinical and haemodynamic correlation. Surgical decompression appears favourable in selected patients, whereas primary endovascular stenting, evaluated only in single-centre observational series, carries a substantial complication profile and should generally be reserved for refractory or combined presentations. Conclusions: SHC compression syndromes are best understood as overlapping neural, arterial, venous, and mixed phenotypes within a dynamic neurovascular corridor. A phenotype-based classification and a cautious "styloidectomy-first" strategy for osseous venous compression are proposed as practical frameworks, but require prospective validation.

Chronic venous disease (CVD) is a prevalent peripheral vascular disorder characterized by vascular remodeling driven by hemodynamic overload, yet available animal models are limited by high surgical difficulty and unstable induction efficiency. Here, we developed a novel mouse venous high-load remodeling model by selectively ablating the unilateral cervical venous drainage system. After 4 weeks, compensatory contralateral jugular veins were assessed via ultrasonography, histology, Western blot, and bulk RNA sequencing. The model displayed marked luminal dilation, wall hypertrophy, and excessive collagen deposition, along with downregulated smooth muscle contractile markers (α-SMA, SM22α) and upregulated adhesion molecule ICAM-1. Transcriptomic profiling identified 252 differentially expressed genes, predominantly enriched in extracellular matrix organization, angiogenesis, and complement-coagulation cascades, suggesting potential pathways involved in the venous remodeling process. This model reliably recapitulates the pathological features associated with hemodynamic overload-induced venous remodeling, offering a valuable tool for investigating CVD pathogenesis and intervention targets.

BackgroundIntracranial venous hypertension (IVH) is an underrecognised cause of persistent craniofacial symptoms, often presenting with nonspecific features such as pressure-type headaches, pulsatile tinnitus, and visual disturbances. This case illustrates a complex diagnostic dilemma in which symptoms classically attributed to Eagle Syndrome masked another vascular cause of intracranial venous hypertension. The patient provided informed consent for treatment and for the use of his clinical information in this case report.Case SummaryA 59-year-old woman presented with refractory craniofacial symptoms initially attributed to bilateral Eagle Syndrome. Despite bilateral stylodectomy, internal jugular vein (IJV) decompression, C1 transverse process resection, and right occipital sinus stenting, her symptoms persisted. During right-sided intervention for Eagle Syndrome, the right IJV was found to have been previously ligated at the clavicle during venous thoracic outlet syndrome surgery. Venous manometry demonstrated elevated pressures within the right IJV (32 mmHg) and torcula (29 mmHg), supporting IVH secondary to impaired venous outflow. Definitive treatment consisted of a right IJV-subclavian vein (SCV) bypass using a triple-panel great saphenous vein (GSV) graft to achieve an adequate conduit diameter. The postoperative course was complicated by early graft thrombosis and neck hematoma, requiring urgent hybrid open and endovascular reintervention. This included suction thrombectomy, angioplasty, sequential stenting of the bypass using bare-metal, covered, and dedicated venous stents, and open repair of a graft tear with bovine pericardial patch angioplasty. Following reintervention, the bypass remained patent on follow-up imaging, with complete resolution of headaches, pulsatile tinnitus, and visual symptoms.ConclusionThis case highlights the importance of comprehensive venous evaluation in patients with persistent craniofacial symptoms, particularly following thoracic outlet interventions. It also demonstrates the feasibility of triple-panel GSV grafting for central venous reconstruction and the value of a hybrid surgical-endovascular approach in managing complex venous complications.

Obtaining sterile anticoagulated whole-blood units is a key prerequisite for downstream laboratory and clinical applications involving blood-derived products. In bovine medicine, however, published information on blood collection into bags is mainly embedded in transfusion-oriented references or broader downstream studies, while formal validation of donor-oriented collection methods remains limited. The aim of this study was to develop and field-validate a large-volume bag-based method for whole-blood collection in donor dairy cows under commercial farm conditions. Whole-blood collections were performed in clinically healthy donor dairy cows using a jugular venipuncture protocol that was progressively refined during field validation. A true sequential multi-bag setup, enabled by extension tubing and a perforable connection device, was introduced on 24 October 2022. Protocol validation was based primarily on procedural success, defined as a bacteriologically negative blood unit with a collected volume of at least 400 mL per bag. A total of 294 procedures were included. Overall, 228/294 procedures (77.6%) were classified as successful, 48/294 (16.3%) as suboptimal, and 18/294 (6.1%) as failed. The median collected volume per procedure was 410 mL (IQR 400-430; range 124.5-1,280 mL). Overall, 276/294 collections (93.9%) were bacteriologically negative. Within the single-bag phase, later collection dates were associated with a lower probability of bacteriological positivity, supporting a learning-curve effect on microbiological reliability. Later implementation of the sequential multi-bag setup was associated with a higher total volume per procedure, without an apparent loss of microbiological safety. In conclusion, this large-volume bag-based protocol proved feasible for whole-blood collection in donor dairy cows under field conditions and may provide a practical upstream basis for subsequent laboratory applications and downstream processing workflows.

Current understanding of the fascial structures within the human carotid sheath (CS) is largely based on static anatomical descriptions, with limited knowledge of their dynamic developmental process. This study aimed to characterise the developmental progression of the fascial architecture surrounding neurovascular components within the CS across four stages in the New Zealand White rabbit. Twenty New Zealand White rabbits were divided into four groups (n = 5 each): early foetal (Gestational Day 10), late foetal (Gestational Day 20), newborn (3 days postnatal) and adult (3-4 months). Whole transverse cervical sections were processed with H&E staining and α-SMA immunohistochemistry. In the rabbit, the common carotid artery, internal jugular vein and vagus nerve within the CS consistently exhibited a three-layered fascial organisation comprising an inner fascial layer, an intermediate zone and an outer fascial layer. The arterial inner fascia showed the earliest onset and most pronounced thickening, forming a dense multilayered fibrous structure, while the venous and neural inner fasciae remained comparatively thin. This differential thickening pattern corresponds to the varying levels of intrinsic pulsatile haemodynamic stress among the three structures. The outer fascial layers of adjacent structures showed potential fusion, likely reflecting extrinsic mechanical interactions from surrounding tissues. This study demonstrates a consistent three-layered fascial organisation within the CS across developmental stages, and these histomorphological findings are consistent with a possible role of dual mechanical influences in CS development.

Cerebral venous sinus thrombosis (CVST) is an uncommon cerebrovascular disorder with heterogeneous manifestations and may occasionally precede the diagnosis of an underlying malignancy. We report the case of a 24-year-old man who presented with recurrent fever, headache, pharyngodynia, and systemic inflammation initially attributed to a sinonasal or odontogenic infectious process. He subsequently developed binocular horizontal diplopia, left abducens nerve palsy, papilledema, severe headache, and nausea. Neuroimaging demonstrated extensive CVST involving the left internal jugular vein, bilateral transverse sinuses, and superior sagittal sinus, without ischemic, hemorrhagic, or tumoral brain parenchymal lesions. Thrombophilia testing identified heterozygous prothrombin G20210A as the only established inherited thrombophilic factor. Despite initial neurological stabilization, the patient developed a rapidly recurrent frontal calvarial, epicranial, and cranio-dural lesion extending toward the superior sagittal sinus, without brain parenchymal involvement or imaging evidence of leptomeningeal disease. Initial morphological assessment suggested Langerhans cell histiocytosis. However, comprehensive histopathological and immunohistochemical reassessment demonstrated diffuse strong CD30 expression, nuclear and cytoplasmic ALK positivity, CD43 expression, and focal epithelial membrane antigen and granzyme B positivity, while CD1a and S100 were negative. These findings established the diagnosis of systemic ALK-positive anaplastic large cell lymphoma with secondary extra-axial cranio-dural involvement. Systemic staging demonstrated disseminated nodal disease and a noncontiguous cranio-dural extranodal lesion, consistent with stage IV disease. Treatment with anticoagulation and six cycles of brentuximab vedotin combined with cyclophosphamide, doxorubicin, and prednisone resulted in a favorable neurological and oncological outcome, with no metabolically active or residual enhancing disease on follow-up imaging. This case emphasizes the importance of continued etiological investigation in young patients with extensive CVST and an atypical clinical course, even when plausible infectious and inherited thrombotic risk factors coexist.