• Humans
• Musculoskeletal Pain
• Kinesiophobia
• Psychometrics/methods
• Reproducibility of Results
• Pain Measurement/methods
• Surveys and Questionnaires

• ageing
• cynomolgus monkey
• intervertebral disc degeneration
• motor behavior
• pain

• Fundamental Research Funds for the Central Universities
• National Natural Science Foundation of China
• Sanming Project of Medicine in Shenzhen

The effect of lumbar spinal stenosis (LSS) and peripheral vascular disease (PVD), which occurs with similar degenerative conditions, when seen together, has not been studied. The aim of this study is to examine and compare the relationship between pain, balance, disability, fear of falling, and kinesiophobia in LSS patients with intermittent vascular claudication (IVC).

Seventy-two patients diagnosed with LSS using magnetic resonance imaging participated in this study. Thirty-five patients with IVC symptoms and showing vascular lesions by lower extremity venous and arterial Doppler ultrasonography imaging were included in the IVC-LSS group. The pain, static balance, dynamic balance, disability, fear of falling, and kinesiophobia were evaluated using the numeric rating scale, single leg stance test, Time Up and Go (TUG), the Oswestry Disability Index (ODI), Fall Efficacy Scale-International (FES-I), and Tampa Scale for Kinesiophobia (TSK), respectively.

Age and female sex were found to be higher in the IVC-LSS group (P = 0.024; P = 0.012). The IVC-LSS group had a shorter single leg stance time and TUG test duration, pain intensity, ODI, FES-I, and TSK scores were higher than patients with LSS (P = 0.001). Pain, fear of falling, and kinesiophobia were moderately correlated with disability in the IVC-LSS group. No relationship was found between pain and dynamic balance. Also, the pain was not related to kinesiophobia.

The findings indicated that IVC causes loss of balance and an increase in pain, disability, fear of falling, and kinesophobia in patients with LSS.

• Accidental Falls
• Catastrophization
• Disability Evaluation
• Doppler.
• Fear
• Intermittent Claudication
• Low Back Pain
• Peripheral Vascular Diseases
• Postural Balance
• Spinal Stenosis
• Ultrasonography

• Aging
• Intervertebral disc degeneration
• Low back pain
• Molecular pain
• Mouse model

• Aging/physiology
• Animals
• Female
• Fluorescent Antibody Technique
• Humans
• Hyperalgesia/metabolism
• Hyperalgesia/pathology
• Hyperalgesia/physiopathology
• Intervertebral Disc
• Intervertebral Disc Degeneration/metabolism
• Intervertebral Disc Degeneration/pathology
• Intervertebral Disc Degeneration/physiopathology
• Low Back Pain/metabolism
• Low Back Pain/pathology
• Low Back Pain/physiopathology
• Male
• Mice
• Mice, Inbred C57BL
• Weight Gain/physiology
• Weight Loss/physiology

• R01 AR065530 NIAMS NIH HHS

[Purpose] The purpose of this study was to compare patients with low back and neck pain with respect to kinesiophobia, pain, and quality of life. [Subjects and Methods] Three-hundred patients with low back (mean age 43.2±11 years) and 300 with neck pain (mean age 42.8±10.2 years) were included in this study. Pain severity was evaluated by using the Short-Form McGill Pain Questionnaire, which includes a Visual Analogue Scale, quality of life by the Nottingham Health Profile, and kinesiophobia by the Tampa Scale for Kinesiophobia. [Results] Pain severity was similar in both groups, with a Visual Analogue Scale score of 6.7±2 in the low back pain and 6.8±2 in the neck pain group. Nottingham Health Profile pain [z=−4.132] and physical activity scores [z=−5.640] in the low back pain group were significantly higher. Kinesiophobia was also more severe in the low back pain group, with a mean 42.05±5.91 versus 39.7±6.0 Tampa Scale for Kinesiophobia score [z=−4.732]. [Conclusion] Patients with low back pain developed more severe kinesiophobia, regardless of the pain severity, and had greater pain perception and lower physical activity levels. Kinesiophobia adversely affects the quality of life and requires effective management of low back pain.

• Kinesiophobia
• Pain
• Quality of life

• kinesiophobia
• pain perception
• psychological factors
• rehabilitation

• anxiety
• neck pain
• phobic disorders

• Adaptation, Psychological
• Adult
• Aged
• Anxiety/diagnosis
• Chronic Pain/diagnosis
• Female
• Humans
• Magnetic Resonance Imaging
• Male
• Middle Aged
• Multivariate Analysis
• Neck Pain/diagnosis
• Pain
• Pain Measurement
• Preoperative Period
• Psychometrics
• Social Class
• Sports
• Surveys and Questionnaires
• Treatment Outcome
• X-Rays

Lumbar radiculopathy, a group of diseases in which the dorsal root ganglia (DRG) or dorsal roots are adversely affected by herniated discs or spinal stenosis, are clinically characterized by spontaneous and evoked types of pain. The pain is underpinned by various distinct pathophysiological mechanisms in the peripheral and central nervous systems. However, the diagnosis of lumbar radiculopathy is still unsatisfactory, because the association of the pain with the neurobiological basis of radiculopathy is largely unknown. Several animal models used to explore the underlying neurobiological basis of lumbar radiculopathy could be classified as mechanical, chemical, or both based on the component of injury. Mechanical injury elevates the intraneural pressure, reduces blood flow, and eventually establishes ischemia in the dorsal root and the DRG. Ischemia may induce ischemic pain and cause nerve damage or death, and the subsequent nerve damage or death may induce neuropathic pain. Chemical injury predominately induces inflammation surrounding the dorsal roots or DRG and consequent inflammatory mediators cause inflammatory pain. Furthermore, DRG neurons sensitized by inflammatory mediators are hypersensitive to innocuous mechanical force (stretch or compression) and responsible for mechanical allodynia in radiculopathy. As well, central sensitization in the spinal cord may play an important role in pain generation in lumbar radiculopathy. Increasing knowledge of pain-generating mechanisms and their translation into clinical symptoms and signs might allow for dissecting the mechanisms that operate in each patient. With precise clinical phenotypic characterization of lumbar radiculopathy and its connection to a specific underlying mechanism, we should be able to design optimal treatments for individuals. This review discusses the present knowledge of lumbar radiculopathy and proposes a novel mechanism-based classification.

• Low back pain
• Acid-sensing ion channel
• Dorsal root
• Dorsal root ganglia
• Disc herniation
• Lumbar spine

Tumor necrosis factor-α (TNFα) has received significant attention as a mediator of lumbar radiculopathy, with interest in TNF antagonism to treat radiculopathy. Prior studies have demonstrated that TNF antagonists can attenuate heightened nociception resulting from lumbar radiculopathy in the preclinical model. Less is known about the potential impact of TNF antagonism on gait compensations, despite being of clinical relevance. In this study, we expand on previous descriptions of gait compensations resulting from lumbar radiculopathy in the rat and describe the ability of local TNF antagonism to prevent the development of gait compensations, altered weight bearing, and heightened nociception.

Eighteen male Sprague-Dawley rats were investigated for mechanical sensitivity, weight-bearing, and gait pre- and post-operatively. For surgery, tail nucleus pulposus (NP) tissue was collected and the right L5 dorsal root ganglion (DRG) was exposed (Day 0). In sham animals, NP tissue was discarded (n = 6); for experimental animals, autologous NP was placed on the DRG with or without 20 μg of soluble TNF receptor type II (sTNFRII, n = 6 per group). Spatiotemporal gait characteristics (open arena) and mechanical sensitivity (von Frey filaments) were assessed on post-operative Day 5; gait dynamics (force plate arena) and weight-bearing (incapacitance meter) were assessed on post-operative Day 6.

High-speed gait characterization revealed animals with NP alone had a 5% decrease in stance time on their affected limbs on Day 5 (P ≤0.032). Ground reaction force analysis on Day 6 aligned with temporal changes observed on Day 5, with vertical impulse reduced in the affected limb of animals with NP alone (area under the vertical force-time curve, P <0.02). Concordant with gait, animals with NP alone also had some evidence of affected limb mechanical allodynia on Day 5 (P = 0.08) and reduced weight-bearing on the affected limb on Day 6 (P <0.05). Delivery of sTNFRII at the time of NP placement ameliorated signs of mechanical hypersensitivity, imbalanced weight distribution, and gait compensations (P <0.1).

Our data indicate gait characterization has value for describing early limb dysfunctions in pre-clinical models of lumbar radiculopathy. Furthermore, TNF antagonism prevented the development of gait compensations subsequent to lumbar radiculopathy in our model.