A Pathophysiological Hypothesis of Dorsocervical Fat Pad (Neck Hump), Investing Fascia, Carotid Sheath, and the Promotion of Vascular Patency and Prevention of Thrombosis

Background: Dorsocervical fat pad, commonly referred to as neck hump, is a common soft-tissue lesion at the cervicothoracic junction. Its systemic pathophysiological significance has long been underestimated. Hypothesis: This article proposes the investing fascia–carotid sheath mechanical coupling hypothesis. The hypothesis posits that the deep indurated tissue of the dorsocervical fat pad is not merely fat but rather a fascial–ligamentous–adipose complex. This complex is centered on fibrotic thickening of the superficial layer of the deep cervical fascia (investing fascia) and includes the ligamentum nuchae, supraspinous ligament, trapezius aponeurosis, and surrounding fibrofatty tissue. Once the investing fascia loses its viscoelastic buffering capacity, abnormal shear forces generated by routine micromovements of the head and neck can be transmitted through the deep cervical fascial network to the carotid sheath. Evidence: The carotid sheath is an anatomic hub in which multiple structures coexist within a single sheath. The structures within and adjacent to the sheath can be categorized into six functional domains: arterial perfusion, venous return, lymphatic immune clearance, glymphatic cerebrospinal fluid–interstitial fluid clearance, sympathetic output, and the vagal anti-inflammatory pathway. These six functional domains are not mutually exclusive; rather, they are spatially shared, functionally coupled anatomic–physiologic units. Among these, the arterial baroreflex, sympathetic output, and the vagal anti-inflammatory pathway are neurally related pathways that participate in central integration via the nucleus tractus solitarius (NTS) and related nuclei. Venous return, lymphatic immune clearance, and glymphatic cerebrospinal fluid–interstitial fluid clearance contribute more to amplification through pressure coupling, humoral immunity, and clearance functions. Humoral immunity and pressure-coupling pathways participate in amplifying the pathologic process through mechanisms such as Ang II/AT1R-YAP, GPR146-PIEZO1, and impaired lymphatic clearance. In this hypothesis, these steps constitute a hypothetical positive feedback loop: investing fascia fibrosis → carotid sheath compression → coordinated dysfunction of the six functional domains → elevated blood pressure → pathologic vascular remodeling → increased plaque instability. Elevated blood pressure may, in turn, aggravate investing fascia fibrosis. Increased neck circumference has been clearly associated epidemiologically with cardiovascular events and the progression of carotid atherosclerosis. The latter is one of the important upstream risk factors for cerebral infarction. However, direct population-based evidence linking the dorsocervical fat pad to increased neck circumference remains lacking. Most existing studies have used neck circumference or posterior cervical fat accumulation as surrogate markers; no population-based study has used the dorsocervical fat pad as an inclusion criterion. Implications: Within this framework, eliminating the dorsocervical fat pad—that is, relieving the sustained mechanical constraint of the investing fascia on the carotid sheath—has a pathophysiological rationale worthy of systematic investigation for the prevention of cardiovascular and cerebrovascular diseases, especially cerebral thrombosis. Nonetheless, this remains a hypothetical inference. Conclusion: This article systematically elaborates the anatomic basis, mechanical transmission mechanisms, pathophysiology of the six functional domains, derivation of the causal chain, relationship between promoting vascular patency and preventing thrombosis and dorsocervical fat pad, testable predictions, and interventional implications of this hypothesis. It also clarifies its evidentiary boundaries.