ABSTRACT
OBJECTIVE: This study compared adults with peripheral vestibular hypofunction (VH) to healthy controls and assessed the sensitivity and specificity of the Cervical Torsion Test (CTT) and the Head Neck Differentiation Test (HNDT). This study aimed to determine whether neck problems affected primary outcomes. METHODS: This cross-sectional study included adults from a specialist consultation for dizziness. VH had been diagnosed with the video Head Impulse Test. Exclusion criteria were conditions following head or neck trauma and diseases of the central nervous system. Sensitivity and specificity of the index tests were calculated, and regression analyses were performed to test for contributing factors. RESULTS: A total of 19 patients with VH and a historical cohort of 19 matched healthy controls were included. Most patients with VH (84.2%) experienced symptoms in at least 1 test component, compared to 5.2% of the control group. Of patients with VH, 78.9% had symptoms during the HNDT "en bloc" (en bloc = head and trunk rotated together) whereas only 26.3% reported symptoms during the CTT en bloc. Best discriminatory validity was found for the HNDT en bloc, with a sensitivity of 0.79 (95% CI = 0.54-0.94), a specificity of 0.86 (95% CI = 0.65-0.97), and a positive likelihood ratio of 5.79 (95% CI = 1.97-17.00). The number of symptoms of CTT "in torsion" (in torsion = trunk rotated actively with fixed head) was increased by a factor of 1.13 (95% CI = 1.01-1.27) for every additional point on the Neck Disability Index. CONCLUSIONS: The CTT and HNDT can serve as nonlaboratory tests in patients with dizziness. The HNDT en bloc has the best discriminatory validity, finding those with and those without VH. Symptom reproduction during torsion may help to identify when neck problems may contribute to dizziness. IMPACT: The HNDT en bloc may be useful for ruling VH in or out in patients with dizziness. Positive CTT and HNDT in torsion components may verify the likelihood of additional neck involvement.
ABSTRACT
The cartilaginous endplates (CEP) are key components of the intervertebral disc (IVD) necessary for sustaining the nutrition of the disc while distributing mechanical loads and preventing the disc from bulging into the adjacent vertebral body. The size, shape, and composition of the CEP are essential in maintaining its function, and degeneration of the CEP is considered a contributor to early IVD degeneration. In addition, the CEP is implicated in Modic changes, which are often associated with low back pain. This review aims to tackle the current knowledge of the CEP regarding its structure, composition, permeability, and mechanical role in a healthy disc, how they change with degeneration, and how they connect to IVD degeneration and low back pain. Additionally, the authors suggest a standardized naming convention regarding the CEP and bony endplate and suggest avoiding the term vertebral endplate. Currently, there is limited data on the CEP itself as reported data is often a combination of CEP and bony endplate, or the CEP is considered as articular cartilage. However, it is clear the CEP is a unique tissue type that differs from articular cartilage, bony endplate, and other IVD tissues. Thus, future research should investigate the CEP separately to fully understand its role in healthy and degenerated IVDs. Further, most IVD regeneration therapies in development failed to address, or even considered the CEP, despite its key role in nutrition and mechanical stability within the IVD. Thus, the CEP should be considered and potentially targeted for future sustainable treatments.
ABSTRACT
Low back pain is a highly prevalent, chronic, and costly medical condition predominantly triggered by intervertebral disc degeneration (IDD). IDD is often caused by structural and biochemical changes in intervertebral discs (IVD) that prompt a pathologic shift from an anabolic to catabolic state, affecting extracellular matrix (ECM) production, enzyme generation, cytokine and chemokine production, neurotrophic and angiogenic factor production. The IVD is an immune-privileged organ. However, during degeneration immune cells and inflammatory factors can infiltrate through defects in the cartilage endplate and annulus fibrosus fissures, further accelerating the catabolic environment. Remarkably, though, catabolic ECM disruption also occurs in the absence of immune cell infiltration, largely due to native disc cell production of catabolic enzymes and cytokines. An unbalanced metabolism could be induced by many different factors, including a harsh microenvironment, biomechanical cues, genetics, and infection. The complex, multifactorial nature of IDD brings the challenge of identifying key factors which initiate the degenerative cascade, eventually leading to back pain. These factors are often investigated through methods including animal models, 3D cell culture, bioreactors, and computational models. However, the crosstalk between the IVD, immune system, and shifted metabolism is frequently misconstrued, often with the assumption that the presence of cytokines and chemokines is synonymous to inflammation or an immune response, which is not true for the intact disc. Therefore, this review will tackle immunomodulatory and IVD cell roles in IDD, clarifying the differences between cellular involvements and implications for therapeutic development and assessing models used to explore inflammatory or catabolic IVD environments.
