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

Average pain is processed by nociceptors via two sets of neural pathways. The ascending neural pathway is activated by painful stimuli like extreme temperature, pressure, and impact. The ascending pathway sends nociceptive signals to send neurotransmitters

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

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

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.

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 subjective and identifying pain objectively is very complex. It can influence the patient’s behavior and can negatively affect the patient’s heart rate and blood pressure. When caring for these individuals and attempting to control their pain,

1. The difference between acute pain and chronic pain is based on their characteristics such as causes, function, and neuron structure. Acute pain travels along the spinothalamic tract to the sensory-motor cortex, as chronic pain is less localized in the anterolateral pathway to the brainstem. The fibers that are used in acute pain are myelinated fibers that carry signals rapidly, and when there is no stimulation the signal stops. Unlike chronic pain where the fibers are unmyelinated, carry signals slowly, and the signal does not stop when stimulation stops. In chronic pain, there is also continuing tissue damage, as the nociceptive pathway neurons become more sensitive. In acute pain, there are tissue damages, but it is not continuous as

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.,

Nociception is the sensation of pain which is normally a warning signal to brain in respond to a potential hazard. Generally noxious stimulations are detected by specialised high-threshold sensory neurons, which are refer to nociceptors. The signals are then transferred to an electrical potential and conducted to the brain via spinal cord. However sometimes abnormal nociception can lead to a moderate to severe pain although a noxious stimulus is missing. This kind of pain are usually trigger by nerve injury, while the pain sensation remains after the tissue had been healed. Although the prevalence of neuropathic pain is not significant, about 7% to 8% of the European population is affected, and about 5% are suffering severe pain (Torrance et al., 2006; Bouhassira et al., 2008). Normally the neuropathic pain is induced by injury of somatosensory nerves, and the pain remains after the tissue being healed. It can bring abnormal nociception while noxious stimuli are missing, which called dysesthesia. Beside, pain can be triggered by non-painful stimuli, which is called allodynia). Many research has linked the neuropathic pain to neuronal damages where endogenous ATP being released. Therefore purinergic receptors that can respond to ATP are involved. In this essay, after a brief introduction of P2X receptors, the role of microglial P2X4 and P2X7 in neuropathic pain will be discussed.

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

These pain relievers are small polypeptide chains made in the brain and are also responsible for the feelings of euphoria encountered when you eat spicy food or after exercise. Opioid drugs mimic the action of these peptide chains, however some enkephalins are a thousand times as effective as drugs such as morphine. Because of this, chemists are trying to synthesise new drugs based on the enkephalins but their duration of analgesic action is short as they can be easily hydrolysed in the body by the enzyme peptidase2.3,10.