Characterization of health status and modifiable risk behavior among United States adults using chiropractic care as compared with general medical care.

Objective: The causes of death in the United States have moved from infectious to chronic diseases with modifiable behavioral risk factors. Simultaneously, there has been a paradigm shift in health care provisions with increased emphases on prevention and health promotion. Use of professional complementary and alternative medicine, such as chiropractic care, has increased.

Prevalence of musculoskeletal injuries sustained by students while attending a chiropractic college.

Objective: The purpose of this study was to assess the prevalence, distribution, severity, risk factors of, and response to musculoskeletal injuries to the low back, hand/wrist, and neck/shoulder among chiropractic students while receiving and/or administering adjustments/manipulation while attending a chiropractic college.

Methods: The study was an epidemiologic survey of chiropractic students at all levels of training (n = 890) at one chiropractic college. A self-administered anonymous 3-paged questionnaire was used.

Epidemiology of musculoskeletal injuries among students entering a chiropractic college.

Objective: The purpose of this study was to report the prevalence, distribution, and severity of injuries to students before entering chiropractic college and to explore the possible demographic risk factors to these injuries.

Methods: A cross-sectional survey was administered to first-year chiropractic students (n = 255) of one chiropractic college. Survey questions were adopted from the Standardized Nordic and Outcome Assessment Health Status Questionnaires.

Dissociation of dorsal root ganglion neurons induces hyperexcitability that is maintained by increased responsiveness to cAMP and cGMP.

Injury or inflammation affecting sensory neurons in dorsal root ganglia (DRG) causes hyperexcitability of DRG neurons that can lead to spontaneous firing and neuropathic pain. Recent results indicate that after chronic compression of DRG (CCD treatment), both hyperexcitability of neurons in intact DRG and behaviorally expressed hyperalgesia are maintained by concurrent activity in cAMP-protein kinase A (PKA) and cGMP-protein kinase G (PKG) signaling pathways. We report here that when tested under identical conditions, dissociation produces a pattern of hyperexcitability in small DRG neurons similar to that produced by CCD treatment, manifest as decreased action potential (AP) current threshold, increased AP duration, increased repetitive firing to depolarizing pulses, increased spontaneous firing and resting depolarization.

Spinal manipulation reduces pain and hyperalgesia after lumbar intervertebral foramen inflammation in the rat.

Objective: To document potential mediating effects of the Activator-assisted spinal manipulative therapy (ASMT) on pain and hyperalgesia after acute intervertebral foramen (IVF) inflammation.

Methods: The IVF inflammation was mimicked by in vivo delivery of inflammatory soup directly into the L5 IVF in adult male Sprague-Dawley rats. Thermal hyperalgesia and mechanical allodynia were determined by the shortened latency of foot withdrawal to radiant heat and von Frey filament stimulation to the hind paw, respectively.

cAMP and cGMP contribute to sensory neuron hyperexcitability and hyperalgesia in rats with dorsal root ganglia compression.

Numerous studies have implicated the cAMP-protein kinase A (PKA) pathway in producing hyperexcitability of dorsal root ganglia (DRG) sensory neurons under conditions associated with pain. Evidence is presented for roles of both the cAMP-PKA and cGMP-protein kinase G (PKG) pathways in maintaining neuronal hyperexcitability and behavioral hyperalgesia in a neuropathic pain model: chronic compression of the DRG (CCD treatment). Lumbar DRGs were compressed by a steel rod inserted into the intervertebral foramen.

Abeta-afferents activate neurokinin-1 receptor in dorsal horn neurons after nerve injury.

We provide new evidence demonstrating that peripheral nerve injury produces profound alterations in synaptic input to dorsal horn neurons mediated by non-nociceptive sensory neurons, and activation of neurokinin-1 receptor may be involved in the enhanced synaptic response and thus contribute to the tactile allodynia. Our results show that Abeta-fiber-evoked field potential significantly increased in the first postoperative week and decreased thereafter while maximal mechanical allodynia was exhibited. The neurokinin-1 receptor antagonist L703,606 significantly reduced Abeta-fiber-evoked field potential in nerve-injured but not in sham-operated animals.

Somata of nerve-injured sensory neurons exhibit enhanced responses to inflammatory mediators.

The effects of inflammatory mediators in modulating the activity of nerve-injured dorsal root ganglion (DRG) neurons were studied in rats in an in vitro nerve-DRG preparation 2-4 weeks after a loose ligation of the sciatic nerve (chronic constriction injury, CCI). An inflammatory soup (IS) of bradykinin, serotonin, prostaglandin E2 and histamine (each 10(-5) M, pH=7.4) was applied topically to the DRG.