Tips for Incorporating Authentic Assessment into Health Profession Courses.

Student engagement with learning material is significantly affected by if, and how, students will be assessed. Despite the influence of assessment technique on student engagement, traditional methods like multiple-choice question examinations are most common despite known limitations. Authentic assessment, an alternative option, is a method that simulates a real-world scenario or problem encountered in practice where students must demonstrate a task or skill or create a product as a final outcome.

Sex-Related Pain Behavioral Differences following Unilateral NGF Injections in a Rat Model of Low Back Pain.

Low back pain (LBP) is a globally prevalent and costly societal problem with multifactorial etiologies and incompletely understood pathophysiological mechanisms. To address such shortcomings regarding the role of neurotrophins in the underlying mechanisms of pain, an LBP model was developed in rats involving two unilateral intramuscular injections of nerve growth factor (NGF) into deep trunk muscles. To date, behavioral investigations of this NGF-LBP model have been limited, especially as it pertains to female pain behaviors.

The Incomplete Tyranny of Dynamic Stimuli: Gaze Similarity Predicts Response Similarity in Screen-Captured Instructional Videos.

Although eye tracking has been used extensively to assess cognitions for static stimuli, recent research suggests that the link between gaze and cognition may be more tenuous for dynamic stimuli such as videos. Part of the difficulty in convincingly linking gaze with cognition is that in dynamic stimuli, gaze position is strongly influenced by exogenous cues such as object motion. However, tests of the gaze-cognition link in dynamic stimuli have been done on only a limited range of stimuli often characterized by highly organized motion.

Spinal Mobilization Prevents NGF-Induced Trunk Mechanical Hyperalgesia and Attenuates Expression of CGRP.

Introduction: Low back pain (LBP) is a complex and growing global health problem in need of more effective pain management strategies. Spinal mobilization (SM) is a non-pharmacological approach recommended by most clinical guidelines for LBP, but greater utilization and treatment optimization are hampered by a lack of mechanistic knowledge underlying its hypoalgesic clinical effects.

Methods: Groups of female Sprague-Dawley rats received unilateral trunk (L5 vertebral level) injections (50 μl) of either vehicle (phosphate-buffer solution, PBS; VEH) or nerve growth factor (NGF; 0.

Reliability of Human Lumbar Facet Joint Degeneration Severity Assessed by Magnetic Resonance Imaging.

Objective: The purpose of this study was to determine the reliability of the assessment of lumbar facet joint degeneration severity by analyzing degeneration subscales using magnetic resonance imaging (MRI) in human participants.

Methods: The reliability of articular cartilage degeneration, subchondral bone sclerosis, and osteophyte formation subscales of lumbar facet joint degeneration severity was assessed in MRI images from n = 10 human participants. Each scale was applied to n = 20 lumbar facet joints (L4/5 level).

Dysregulation of sphingolipid metabolism contributes to bortezomib-induced neuropathic pain.

The development of chemotherapy-induced painful peripheral neuropathy is a major dose-limiting side effect of many chemotherapeutics, including bortezomib, but the mechanisms remain poorly understood. We now report that bortezomib causes the dysregulation of de novo sphingolipid metabolism in the spinal cord dorsal horn to increase the levels of sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) ligands, S1P and dihydro-S1P. Accordingly, genetic and pharmacological disruption of S1PR1 with multiple S1PR1 antagonists, including FTY720, blocked and reversed neuropathic pain.

The Neurotoxin DSP-4 Induces Hyperalgesia in Rats that is Accompanied by Spinal Oxidative Stress and Cytokine Production.

Central neuropathic pain (CNP) a significant problem for many people, is not well-understood and difficult to manage. Dysfunction of the central noradrenergic system originating in the locus coeruleus (LC) may be a causative factor in the development of CNP. The LC is the major noradrenergic nucleus of the brain and plays a significant role in central modulation of nociceptive neurotransmission.

Chemotherapy-induced pain is promoted by enhanced spinal adenosine kinase levels through astrocyte-dependent mechanisms.

Development of chemotherapy-induced neuropathic pain (CINP) compromises the use of chemotherapy and greatly impacts thousands of lives. Unfortunately, there are no Food and Drug Administration-approved drugs to prevent or treat CINP. Neuropathological changes within CNS, including neuroinflammation and increased neuronal excitability, are driven by alterations in neuro-glia communication; but, the molecular signaling pathways remain largely unexplored.

Decreased spontaneous activity and altered evoked nociceptive response of rat thalamic submedius neurons to lumbar vertebra thrust.

The thalamus is a central structure important to modulating and processing all mechanoreceptor input destined for the cortex. A large number of diverse mechanoreceptor endings are stimulated when a high velocity low amplitude thrust is delivered to the lumbar spine during spinal manipulation. The objective of this study was to determine if a lumbar thrust alters spontaneous and/or evoked nociceptive activity in medial thalamic submedius (Sm) neurons.

Characteristics of Paraspinal Muscle Spindle Response to Mechanically Assisted Spinal Manipulation: A Preliminary Report.

Objectives: The purpose of this preliminary study is to determine muscle spindle response characteristics related to the use of 2 solenoid powered clinical mechanically assisted manipulation (MAM) devices.

Methods: L6 muscle spindle afferents with receptive fields in paraspinal muscles were isolated in 6 cats. Neural recordings were made during L7 MAM thrusts using the Activator V (Activator Methods Int.

Grading Osteoarthritic Changes of the Zygapophyseal Joints from Radiographs: A Reliability Study.

Objective: This study tested the reliability of a 5-point ordinal scale used to grade the severity of degenerative changes of zygapophyseal (Z) joints on standard radiographs.

Methods: Modifications were made to a Kellgren grading system to improve agreement for grading the severity of osteoarthritic changes in lumbar Z joints. These included adding 1 grade of no degeneration, multiple radiographic views, and structured examiner training.

Engagement of the GABA to KCC2 signaling pathway contributes to the analgesic effects of A3AR agonists in neuropathic pain.

More than 1.5 billion people worldwide suffer from chronic pain, yet current treatment strategies often lack efficacy or have deleterious side effects in patients. Adenosine is an inhibitory neuromodulator that was previously thought to mediate antinociception through the A1 and A2A receptor subtypes.

Endogenous adenosine A3 receptor activation selectively alleviates persistent pain states.

Chronic pain is a global burden that promotes disability and unnecessary suffering. To date, efficacious treatment of chronic pain has not been achieved. Thus, new therapeutic targets are needed.

Spinal neuroimmune activation is independent of T-cell infiltration and attenuated by A3 adenosine receptor agonists in a model of oxaliplatin-induced peripheral neuropathy.

Many commonly used chemotherapeutics including oxaliplatin are associated with the development of a painful chemotherapy-induced peripheral neuropathy (CIPN). This dose-limiting complication can appear long after the completion of therapy causing a significant reduction in quality-of-life and impeding cancer treatment. We recently reported that activation of the Gi/Gq-coupled A3 adenosine receptor (A3AR) with selective A3AR agonists (i.

The development and maintenance of paclitaxel-induced neuropathic pain require activation of the sphingosine 1-phosphate receptor subtype 1.

The ceramide-sphingosine 1-phosphate (S1P) rheostat is important in regulating cell fate. Several chemotherapeutic agents, including paclitaxel (Taxol), involve pro-apoptotic ceramide in their anticancer effects. The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.

Spinal mitochondrial-derived peroxynitrite enhances neuroimmune activation during morphine hyperalgesia and antinociceptive tolerance.

Treatment of severe pain by morphine, the gold-standard opioid and a potent drug in our arsenal of analgesic medications, is limited by the eventual development of hyperalgesia and analgesic tolerance. We recently reported that systemic administration of a peroxynitrite (PN) decomposition catalyst (PNDC) or superoxide dismutase mimetic attenuates morphine hyperalgesia and antinociceptive tolerance and reduces PN-mediated mitochondrial nitroxidative stress in the spinal cord. These results suggest the potential involvement of spinal PN signaling in this setting; which was examined in the present study.

Supraspinal peroxynitrite modulates pain signaling by suppressing the endogenous opioid pathway.

Peroxynitrite (PN, ONOO(-)) is a potent oxidant and nitrating agent that contributes to pain through peripheral and spinal mechanisms, but its supraspinal role is unknown. We present evidence here that PN in the rostral ventromedial medulla (RVM) is essential for descending nociceptive modulation in rats during inflammatory and neuropathic pain through PN-mediated suppression of opioid signaling. Carrageenan-induced thermal hyperalgesia was associated with increased 3-nitrotyrosine (NT), a PN biomarker, in the RVM.

Roles of reactive oxygen and nitrogen species in pain.

Peroxynitrite (PN; ONOO⁻) and its reactive oxygen precursor superoxide (SO; O₂•⁻) are critically important in the development of pain of several etiologies including pain associated with chronic use of opiates such as morphine (also known as opiate-induced hyperalgesia and antinociceptive tolerance). This is now an emerging field in which considerable progress has been made in terms of understanding the relative contributions of SO, PN, and nitroxidative stress in pain signaling at the molecular and biochemical levels. Aggressive research in this area is poised to provide the pharmacological basis for development of novel nonnarcotic analgesics that are based upon the unique ability to selectively eliminate SO and/or PN.

Zygapophyseal joint adhesions after induced hypomobility.

Objective: Adhesions (ADH) have been previously identified in many hypomobile joints, but not in the zygapophyseal (Z) joints of the spine. The objective of this study was to determine if connective tissue ADH developed in lumbar Z joints after induced intervertebral hypomobility (segmental fixation).

Methods: Using an established rat model, 3 contiguous segments (L4, L5, L6) were fixed with specially engineered, surgically implanted, vertebral fixation devices.

Reactive nitroxidative species and nociceptive processing: determining the roles for nitric oxide, superoxide, and peroxynitrite in pain.

Pain is a multidimensional perception and is modified at distinct regions of the neuroaxis. During enhanced pain, neuroplastic changes occur in the spinal and supraspinal nociceptive modulating centers and may result in a hypersensitive state termed central sensitization, which is thought to contribute to chronic pain states. Central sensitization culminates in hyperexcitability of dorsal horn nociceptive neurons resulting in increased nociceptive transmission and pain perception.