Allodynia Research Paper

Everyone experiences physical pain at some time in their life, but it’s not treated all the same. Dr. Miles Day, the Medical Director of the Grace Health System Pain Management Center, says there are two separate kinds of pain. The first is called nociceptive pain, which is what you feel when you sprain your ankle, break a bone, or burn your finger. Cancer pain and arthritis pain are common types of chronic nociceptive pain. It responds well to pain medications, anti-inflammatory agents, or other drugs.

“Pain is much more than a physical sensation caused by a specific stimulus. An individual's perception of pain has important affective (emotional), cognitive, behavioral, and sensory components that are shaped by past experience, culture, and situational factors. The nature of the stimulus for pain can be physical, psychological, or a combination of both.” (Potter, Perry, Stockert, Hall, & Peterson, 2014 p. 141) As stated by Potter et al, the different natures of pain are dealt with differently depending on many factors. Knowing this, treating pain can be very difficult as there is no single or clear cut way of measuring it; “Even though the assessment and treatment of pain is a universally important health care issue,

Nociception is a neural process that senses and responds to harmful stimuli, for instance in this scenario Linda rolling her ankle. Nociceptive pain comes from an actual or potential mechanical or chemical stimuli that causes injury to non-neural tissue, this is due to the activation of nociceptors. (1)

Injury or inflammation of a bodily tissue can lead to profound changes in the internal chemical environment. Damaged cells discharge their intracellular components, releasing substances, notably ATP, potassium ions (K+) and acetyl chloine (ACh). Some of these contents act on nociceptors directly, triggering an action potential which will end up in the brain. Other components released from the cells can sensitize the terminals, making them hypersensitive to further stimuli. This allows a pain signal to be transmitted when a seemingly

Chronic and widespread pain is understandably the most distressing symptom of fibroyalgia and predominantly why patients seek medical help in the first place. Fibromyalgia is a pain disorder of the central nervous system that distorts not only the person’s perception of intensity of pain but also the person’s perception of what causes pain in the first place because of malfunctioning nociceptors (Clauw et al., 2011).

Capsaicin has been shown to reduce the amount of substance P associated with inflammation- however this is not believed to be its mechanism in pain relief. Capsaicin's mechanism of action is attributed to "defunctionalization" of nociceptor fibers by inducing a topical hypersensitivity reaction on the skin. This alteration in pain mechanisms is due to many of the following: temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fiber

Capsaicin is a natural product of capsicum peppers, that is an active ingredient in many hot foods. When nociceptors- neurons that transmit information regarding tissue damage to pain-processing centers in the spinal cord and brain- come in contact with capsaicin, the neuron gets excited, and there is a perception of pain, and the a local release of inflammatory mediators. These nociceptors get excited by increasing permeability of plasma membrane to cations, but the molecular mechanism explaining this phenomenon is unclear. Capsaicin is being used in an analgesic agent in the treatment of painful disorders, causing long-term loss of

Pain can be categorized as acute or chronic pain. Chronic pain is described as pain that is both long-term and continuous, or is pain that persists after the expected healing time following an injury (British Pain Society, n.d.) Acute pain can provide a warning signal that an illness or injury has occurred. It is defined as pain that lasts less than three months and lessens with healing (Briggs, 2010). Acute pain can then be described in more detail by the following categories; somatic, visceral and neuropathic pain. Somatic pain is a localized pain described as sharp, burning, dull, aching or cramping. It is seen with incisional pain and orthopedic injuries or procedures. Visceral pain refers to an injury to the organs and linings of the body cavities. It produces diffuse pain and can be described as splitting, sharp or stabbing. This is pain that be described from patients with appendicitis, pancreatitis or intestinal injuries and illnesses. Injuries to the nerve fibers, spinal cord and central nervous system cause neuropathic pain. This pain can be described as shooting, burning, fiery, sharp, and as a painful numbness. This can be seen after an

Generally, acute stress induces analgesia (found, e.g., among athletes injured in games and soldiers injured in battle), while the effects of chronic stress in nociception are less predictable [211]. Epidemiological studies have implicated stress (psychosocial and physical) as a trigger of first onset or exacerbation of many painful disorders such as irritable bowel syndrome [212] and low back pain [213]. An individual’s response to stress, either physical or emotional, includes activation of the hypothalamic-pituitary-adrenal (HPA) axis, which is accomplished by the secretion of corticotrophin-releasing hormone and arginine vasopressin from the paraventricular nucleus of the hypothalamus [214]. There is evidence that the HPA axis is involved in acute pain and chronic pain. However, it is unclear whether the observed HPA axis abnormalities in stress-related pain syndromes such as fibromyalgia, chronic headaches and temporomandibular disorder reflect preexisting vulnerability to these syndromes or whether chronic somatic symptoms alter HPA axis activity

Pain is defined as the patient’s described experience to actual or potential tissue damage (Yukari, Noriko, & Okamoto, 2010). It is an issue in the care of any patient, because pain adversely affects the health of the patient. Not only is pain uncomfortable, it causes the release of specific hormones, adrenaline, and other chemicals that make healing difficult, if not impossible. It decreases patient mobility, leading to complications of secondary pneumonia and pressure ulcers (Yukari, Noriko, & Okamoto, 2010). It can have such a severe effect on the body that it may cause a shock like syndrome that can cause death (Yukari, Noriko, & Okamoto, 2010). For all of these reasons, pain management is paramount to any patient care plan.

There are many different types of pain which can be categorised depending on how the pain is caused and how long the pain lasts. If pain results from tissue damage then it is called nociceptive pain and this includes pain from pressure applied outside of the body, like a cut or a burn, or from pressure inside the body such as a tumour. Another type of pain is neuropathic pain which is pain experienced when there is damage to

Eicosapentaenoyl serotonin is a hybrid molecule patterned after arachidonoyl serotonin. Arachidonoyl serotonin is an inhibitor of fatty acid amide hydrolase (FAAH) and also acts as an antagonist of transient receptor potential vanilloid-type 1 (TRPV1) channels. Arachidonoyl serotonin is analgesic, reducing both acute and chronic peripheral pain in rodents [1, 2]. The effects of replacement the arachidonoyl portion with eicosapentaenoic acid have not been investigated. Replacement of arachidonate with saturated 11- or 12-carbon fatty acids generated compounds that potently inhibited capsaicin-induced TRPV1 channel activation with an IC50 of 0.76 μM. This compound showed no effects on wblocking FAAH-mediated hydrolysis of arachidonoyl ethanolamide

Using rat models of neuropathic pain, Nav 1.7 selective blockers have been seen to be successful in inhibiting Nav 1.7 activity (4).

Pain is something that connects all of us. From birth to death we can identify with each other the idea and arguably the perception of it. We all know we experience it, but what is more important is how we all perceive it. It is known that there are people out there with a ‘high’ pain tolerance and there are also ones out there with a ‘low’ pain tolerance, but what is different between them? We also know that pain is an objective response to certain stimuli, there are neurons that sense and feel pain and there are nerve impulses that send these “painful” messages to the brain. What we don’t know is where the pain

These disorders include fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. However, there is still indecision as to whether exercise has a positive effect on the processes involved in central pain modulation (CPM) (Nijs, Kosek, Van Oosterwijck, & Meeus, 2012). There is an assumption that exercise-induced endogenous analgesia is the result of endogenous opioids being released and growth factors, along with the activation of (supra) spinal nociceptive inhibitory mechanisms coordinated by the brain (Nijs et al., 2012). An investigation into (CPM) as a potential mechanism of EIH revealed that this was not the case (Ellingson, Koltyn, Kim, & Cook, 2014). The testing for intensity and unpleasant rating to noxious heat stimuli, included painful exercise, non-painful exercise, and quiet rest. According to the findings pain sensitivity, significantly decreased during both types of exercise session but there was no significant change during quiet rest (Ellingson et al.,