Neck pain is a common cause of disability worldwide, but its basic pathology and pathophysiology are still unclear.Cervical spine has a very delicate proprioceptive system that plays a crucial role in controlling posture and balance.One of the main problems of patients with neck pain is that the alteration of cervical proprioception leads to the disturbance of cervical sensorimotor control.To date, eight neck sensorimotor control tests have been reported to evaluate patients with chronic neck pain, with the most commonly used test being the JPE test.Studies support the effectiveness of exercises targeting different aspects of sensorimotor function, in particular retraining aimed at improving cervical proprioception and muscle coordination. DIGITAL FEATURESThis article is published with digital features, including a summary slide, to facilitate understanding of the article. To view digital features for this article go to https://doi.org/10.6084/ m9.figshare.13379681.

Central neuroinflammation is important in the pathophysiological processes of neuropathic pain following peripheral nerve injury. Recently, interleukin-17 (IL-17) has been detected in different inflammatory conditions of the central nervous system and contributes to neuropathic pain associated with multiple sclerosis, experimental autoimmune encephalomyelitis. The present study, based on the rat model of spinal nerve ligation, analyzed the infiltration of cluster of differentiation (CD)4+ T cells and the expression of IL-17 in the spinal cord during the maintenance phase of neuropathic pain, and investigated central inflammatory reaction and astrocyte activation. The results demonstrated that the infiltrated CD4+ T cells in the spinal cord increased in the rat model of spinal nerve ligation, and immunofluorescence staining demonstrated that the CD4+/IL-17+ cells were located at superficial laminae of spinal dorsal horn. This was accompanied by significant upregulation of IL-17. Furthermore, the mRNA expression levels of IL-1β and IL-6 were also significantly enhanced in model rats compared with the sham and control groups in the spinal dorsal horn. In vitro, the proliferation ability and secretion of proinflammatory cytokines notably increased in the IL-17-stimulated astrocytes. Results from the present study indicate that IL-17 may contribute to neuropathic pain by promoting the proliferation of astrocytes and secretion of proinflammatory cytokines in spinal nerve ligation-induced neuropathic pain.

BackgroundIn moderate acute respiratory distress syndrome (ARDS) several studies support the usage of assisted spontaneous breathing modes. Only limited data, however, focus on the application in systemic sepsis and developing lung injury. The present study examines the effects of immediate initiation of pressure support ventilation (PSV) in a model of sepsis-induced ARDS.Methods18 anesthetized pigs received a two-staged continuous lipopolysaccharide infusion to induce lung injury. The animals were randomly assigned to PSV or volume controlled (VCV) lung protective ventilation (tidal volume each 6 ml kg-1, n = 2x9) over six hours. Gas exchange parameters, hemodynamics, systemic inflammation, and ventilation distribution by multiple inert gas elimination and electrical impedance tomography were assessed. The post mortem analysis included histopathological scoring, wet to dry ratio, and alveolar protein content.ResultsWithin six hours both groups developed a mild to moderate ARDS with comparable systemic inflammatory response and without signs of improving gas exchange parameters during PSV. The PSV group showed signs of more homogenous ventilation distribution by electrical impedance tomography, but only slightly less hyperinflated lung compartments by multiple inert gas elimination. Post mortem and histopathological assessment yielded no significant intergroup differences.ConclusionsIn a porcine model of sepsis-induced mild ARDS immediate PSV was not superior to VCV. This contrasts with several experimental studies from non-septic mild to moderate ARDS. The present study therefore assumes that not only severity, but also etiology of lung injury considerably influences the response to early initiation of PSV.

Clinical studies have found that patients withcervical degenerative disease are usually accompanied by dizziness. Anterior cervical surgery can eliminate not only chronic neck pain, cervical radiculopathy or myelopathy, but also dizziness. Immunohistochemical studies show that a large number of mechanoreceptors, especially Ruffini corpuscles, are present in degenerated cervical discs. The available evidence suggests a key role of Ruffini corpuscles in the pathogenesis of dizziness caused by cervical degenerative disease ( i.e . cervical discogenic dizziness). Disc degeneration is characterized by an elevation of inflammatory cytokines, which stimulates the mechanoreceptors in degenerated discs and results in peripheral sensitization. Abnormal cervical proprioceptive inputs from the mechanoreceptors are transmitted to the central nervous system, resulting in sensory mismatches with vestibular and visual information and leads to dizziness. In addition, neck pain caused by cervical disc degeneration can play a key role in cervical discogenic dizziness by increasing the sensitivity of muscle spindles. Like cervical discogenic pain, the diagnosis of cervical discogenic dizziness can be challenging and can be made only after other potential causes of dizziness have been ruled out. Conservative treatment is effective for the majority of patients. Existing basic and clinical studies have shown that cervical intervertebral disc degeneration can lead to dizziness.

Background: The lectin-like domain of TNF-α can be mimicked by synthetic TIP peptides and represents an innovative pharmacologic option to treat edematous respiratory failure. TIP inhalation was shown to reduce pulmonary edema and improve gas exchange. In addition to its edema resolution effect, TIP peptides may exert some anti-inflammatory properties. The present study therefore investigates the influence of the inhaled TIP peptide AP318 on intrapulmonary inflammatory response in a porcine model of systemic sepsis. Methods: In a randomized-blinded setting lung injury was induced in 18 pigs by lipopolysaccharide-infusion and a second hit with a short period of ventilator-induced lung stress, followed by a six-hour observation period. The animals received either two inhalations with the peptide (AP318, 2×1 mg kg