SaveYourself.ca

What works for stubborn aches, pains, and injuries? What doesn’t? Why? SaveYourself.ca reviews your treatment options: hundreds of detailed, free self-help articles and several e-books about common pain problems, constantly updated, and readable enough for anyone but heavily referenced for professionals. (There’s also a giant bibliography.) I serve up the science with some sass — I try to have fun taking this subject seriously. The salamander? More mascot than logo, he’s a symbol for regeneration and unsolved mysteries of biology. ~ Paul Ingraham, publisher

International Association for the Study of Pain

Vision Statement: Working together for pain relief throughout the world.

Mission: IASP brings together scientists, clinicians, health care providers, and policy makers to stimulate and support the study of pain and to translate that knowledge into improved pain relief worldwide.

IASP Taxonomy of pain

IASP has established a very useful list of definitions of all types of pain. Every health professional should be aware of this list.

Mind and its potential: the role of the brain in chronic pain

Mind & Its Potential is a vibrant and stimulating conference experience which will attract 1,000+ delegates! We are committed to bringing together the world's preeminent scientists, researchers, philosophers and creative thinkers in order to offer you an experience second to none.

Mind and its Potential Conference, 2011 at the Sydney Convention & Exhibition Centre.

CHANGE YOUR MIND: CHANGE YOUR BRAIN

Body in mind: the role of the brain in chronic pain

• What role does the brain play in chronic and complex pain?

• How does the brain change when pain persists?

• Can you influence the amount of pain you feel?

• Why does someone who has lost a limb still feel pain? Can the pain be treated?

• What are the broader implications of the research in developing better treatments for people in pain?

Professor Lorimer Moseley, Professor of Clinical Neurosciences & Chair in Physiotherapy, University of South Australia; Senior Research Fellow, Neuroscience Research Australia; Author: Explain Pain and Painful Yarns: metaphors & stories to help understand the biology of pain.

Visit our Website: www.mindanditspotential.com/au 

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Read our Blog: blogs.terrapinn.com/happiness

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Mechanisms of somatic pain

This article, by the University of Utah pain research center, is very interesting but a little bit too detailed. But is worths reading it once and keeping in mind the  summary points:

1. Somatic pain is normally triggered by the activation of nociceptors. Particular types of nociceptors have been well characterized in cutaneous, articular and muscle nerves.
2. The activation of cutaneous Ad nociceptors causes a sensation of pricking pain, whereas stimulation of C polymodal nociceptors elicits burning pain. Muscle nociceptors produce aching pain.
3. Unlike sensitive mechanoreceptors and thermoreceptors, nociceptors can be sensitized by damaging stimuli. Sensitization appears to be triggered by the release of chemical substances, such as prostaglandins, bradykinin, serotonin, and histamine, into the environment of peripheral nociceptor terminals. Some nociceptors are quite unresponsive until they are sensitized.
4. Nociceptors project to particular laminae in the spinal cord dorsal horn. Cutaneous Ad nociceptive fibers end in laminae I, II, and V, whereas cutaneous C polymodal nociceptors end chiefly in lamina II. Fiber, joint, and muscle afferents project to laminae I and V.
5. Fine afferent terminals, presumably of nociceptors, in the dorsal horn contain peptides, such as substance P and CGRP, and also excitatory amino acids. Both classes of substances are likely to be released during intense noxious stimulation.
6. Noxious stimuli trigger both excitatory and inhibitory events in the dorsal horn. Inhibition is likely to be mediated by such agents as inhibitory amino acids and inhibitory peptides. The circuits may be local or involve a supraspinal loop.
7. STT cells that project to the ventral posterior lateral thalamic nucleus in monkeys and rats have response properties that suit them for a role in the sensory-discriminative aspects of pain. Their input can be from cutaneous, articular, muscle and/or visceral receptors. Convergent inputs may account for pain referral.
8. The responses of STT cells are altered by pathological processes. These neurons become more responsive following damage of the skin by intense mechanical, thermal, or chemical stimuli. A similar change occurs during the development of experimental acute arthritis. It is proposed that sensitization of STT cells helps account for the development of primary and secondary hyperalgesia and allodynia following damage.
9. The mechanism of sensitization of STT cells is likely to involve excitatory amino acid and NK1 receptors.
10. Experimental models of painful neuropathy are being developed by several groups. The responses of STT cells in these models are altered in a fashion consistent with the development of spontaneous pain, allodynia, and hyperalgesia.

Mechanisms of inflammatory pain

British Journal of Anesthesia

By B. L. Kidd1 and L. A. Urban

One of the cardinal features of inflammatory states is that normally innocuous stimuli produce pain. Since the publication of the Melzack–Wall gate control theory in 1965,45 it has been widely appreciated that the nervous system exhibits a range of responses according to different conditions (‘neural plasticity’). Subsequent research has characterized the mechanisms by which these changes occur and highlighted the importance of environmental factors on perception of pain.

This review focuses on key peripheral mechanisms that result in the hypersensitivity state that accompanies inflammation. Recent studies are described which characterize a series of receptors, ion channels and transmitters involved in inflammatory pain. The mechanisms by which inflammatory mediators interact with neurones to produce hypersensitivity are also explored.

Read more.

Pain and the endogenous opioids

A stimulus that causes - or could potentially cause - tissue damage usually elicits a sensation of pain. Receptors for such stimuli are known as nociceptors. Yοu can read more on the structure and function of the somatosensory nervous system here (go on slides 13).

Nociceptors (being free nerve endings) respond to intense mechanical deformation, extremes of temperature, and many chemicals; such as hydrogen cations, neuropeptide transmitters, bradykinin, histamine, cytokines, and prostaglandins, several of which are released by damaged cells or the immune system cells that are transferred to the site of injury. These substances act as binding to specific ligand-gated ion channels on the nociceptor plasma membrane (more on the mechanism of ligand-gated channels can be found here - slide 27, 58 and on).

Image 1. Convergence of visceral and somatic afferent neurons onto ascenting pathways - referred pain

Image 2. Regions of the body surface where we typically perceive referred pain from visceral organs

When incoming nociceptive afferents activate interneurons, it may lead to the phenomenon of referred pain, in which the sensation of pain is experienced at a site other than the injured or diseased tissue. For example, during a heart attack, a person often experiences pain in the left arm, because both visceral afferents from the heart and somatic afferents from the skin (left arm) converge on the same neurons in the spinal cord (Image 1). Excitation of the somatic afferent fibers is the most usual source of the feeling of pain, so we "refer" (we "think") the location of the receptor activation to the somatic source. Image 2 presents the regions of the body surface where we typically perceive referred pain from visceral organs.

Pain differs significantly from the other somatosensory modalities, in the sense that a series of changes occurs in components of the pain pathway that alter the way these components respond to subsequent stimuli - both increased (hyperalgesia) and decreased (hypoalgesia) sensitivity to stimuli can occur. Besides, the pain can last hours and at different intensity after the original stimuli. Moreover, pain can be altered by past experiences, suggestion, emotions, and the simultaneous activation of other modalities.

Image 3. Endogenous opioids

Very interesting is also the fact that specific areas of the CNS can produce a profound reduction of pain by inhibiting pain pathways. In this case, descending pathways that originate in the brain selectively inhibit the transmission of information originating in nociceptors (they inhibit the synaptic transmission between the afferent nociceptor neurons and the secondary ascending inter-neuron). These descending neurons release morphinlike endogenous opioids. Endogenous opioids (like beta-endorphin, dynorphin and enkephalins) are neurotransmitters released by certain neurons in a synapse together with other types. This specific type of neurotransmitters can diffuse away from the synapse and affect other neurons at some distance, in which case they are referred as neuromodulators (Image 3).

This amazing ability of our body to "manage pain" through the endogenous opioids can be seen in the following experiment: when patients were treated with morphine-placebo drug, about 35% of them experienced pain relief. It seems likely that pathways descending from the cortex activate these same regions to exert the placebo effect and inhibiting the transmission of pain at the spinal cord level.

The endogenenous-opioid systems also mediate other phenomena known to relieve pain. In clinical studies, 55-85% of patients experienced pain relief when treated with acupuncture, an ancient Chinese therapy involving the insertion of needles into specific locations on the skin. This technique is thought to activate afferent neurons leading to spinal cord and midbrain centers that release endogenous opioids and other nerotranmitters implicated in pain relief.

Finally, the use of transcutaneous electrical nerve stimulation (TENS) stimulates the non-pain, low threshold afferent nerves leading from a painful site on the surface of the skin leading to the inhibition of neurons in the pain pathways. It is exactly the same phenomenon (but of lower-tech version) when we vigorously rub our scalp at the site of a painful bump on the head.

(Widmaier EP, Raff H, Strang KT. Vander's Human Physiology: the mechanisms of body function. 12 ed.New York: McGraw-Hill International Edition; 2011)

Anatomy and physiology of pain

18 September, 2008 | By Sharon Wood

www.nursingtimes.net

A comprehensive guide to the anatomy and physiology of pain management

Many nurses have a poor understanding of pain and its management, which can result in failure to treat pain effectively. An insight into the anatomy and physiology of pain is essential to increase nurses’ understanding of what it is and how interventions can help to manage it. This section outlines the basic anatomy and physiology of pain.

A. Acute pain

Acute pain is a physiological response that warns us of danger. The process of nociception describes the normal processing of pain and the responses to noxious stimuli that are damaging or potentially damaging to normal tissue. There are four basic processes involved in nociception (McCaffery and Pasero, 1999). These are:

1. transduction
2. transmission
3. perception
4. modulation

A.1. Transduction of pain

Transduction begins when the free nerve endings (nociceptors) of C fibres and A-delta fibres of primary afferent neurones respond to noxious stimuli. Nociceptors are exposed to noxious stimuli when tissue damage and inflammation occurs as a result of, for example, trauma, surgery, inflammation, infection, and ischemia.

The nociceptors are distributed in the:

• somatic structures (skin, muscles, connective tissue, bones, joints)
• visceral structures (visceral organs such as liver, gastro-intestinal tract)
• the C fibre and A-delta fibres are associated with different qualities of pain

Noxious stimuli and responses

There are three categories of noxious stimuli:

• mechanical (pressure, swelling, abscess, incision, tumour growth)
• thermal (burn, scald)
• chemical (excitatory neurotransmitter, toxic substance, ischaemia, infection)

The cause of stimulation may be internal, such as pressure exerted by a tumour or external, for example, a burn. This noxious stimulation causes a release of chemical mediators from the damaged cells including:

prostaglandin; bradykinin; serotonin; substance P; potassium; histamine.

These chemical mediators activate and/or sensitise the nociceptors to the noxious stimuli. In order for a pain impulse to be generated, an exchange of sodium and potassium ions (de-polarisation and re-polarisation) occurs at the cell membranes. This results in an action potential and generation of a pain impulse.

A.2. Transmission of pain

The transmission process occurs in three stages. The pain impulse is transmitted:

• from the site of transduction along the nociceptor fibres to the dorsal horn in the spinal cord
• from the spinal cord to the brain stem
• through connections between the thalamus, cortex and higher levels of the brain

The C fibre and A-delta fibres terminate in the dorsal horn of the spinal cord. There is a synaptic cleft between the terminal ends of the C fibre and A-delta fibres and the nociceptive dorsal horn neurones (NDHN). In order for the pain impulses to be transmitted across the synaptic cleft to the NDHN, excitatory neurotransmitters are released, which bind to specific receptors in the NDHN. These neurotransmitters are:

adenosine triphosphate; glutamate; calcitonin gene-related peptide; bradykinin; nitrous oxide; substance P.

The pain impulse is then transmitted from the spinal cord to the brain stem and thalamus via two main nociceptive ascending pathways. These are the spinothalamic pathway and the spinoparabrachial pathway.

The brain does not have a discrete pain centre, so when impulses arrive in the thalamus they are directed to multiple areas in the brain where they are processed.

A.3. Perception of pain

Perception of pain is the end result of the neuronal activity of pain transmission and where pain becomes a conscious multidimensional experience. The multidimensional experience of pain has affective-motivational, sensory-discriminative, emotional and behavioural components. When the painful stimuli are transmitted to the brain stem and thalamus, multiple cortical areas are activated and responses are elicited.

These areas are:

The reticular system: This is responsible for the autonomic and motor response to pain and for warning the individual to do something, for example, automatically removing a hand when it touches a hot saucepan. It also has a role in the affective-motivational response to pain such as looking at and assessing the injury to the hand once it has been removed form the hot saucepan.

Somatosensory cortex: This is involved with the perception and interpretation of sensations. It identifies the intensity, type and location of the pain sensation and relates the sensation to past experiences, memory and cognitive activities. It identifies the nature of the stimulus before it triggers a response, for example, where the pain is, how strong it is and what it feels like.

Limbic system: This is responsible for the emotional and behavioural responses to pain for example, attention, mood, and motivation, and also with processing pain and past experiences of pain.

A.4. Modulation of pain

The modulation of pain involves changing or inhibiting transmission of pain impulses in the spinal cord. The multiple, complex pathways involved in the modulation of pain are referred to as the descending modulatory pain pathways (DMPP) and these can lead to either an increase in the transmission of pain impulses (excitatory) or a decrease in transmission (inhibition).

Descending inhibition involves the release of inhibitory neurotransmitters that block or partially block the transmission of pain impulses, and therefore produce analgesia. Inhibitory neurotransmitters involved with the modulation of pain include:

endogenous opioids (enkephalins and endorphins); serotonin (5-HT); norepinephirine (noradrenalin); gamma-aminobutyric acid (GABA); neurotensin; acetylcholine; oxytocin.

Endogenous pain modulation helps to explain the wide variations in the perception of pain in different people as individuals produce different amounts of inhibitory neurotransmitters. Endogenous opioids are found throughout the central nervous system (CNS) and prevent the release of some excitatory neurotransmitters, for example, substance P, therefore, inhibiting the transmission of pain impulses.

B. Chronic pain

Chronic pain can be a major problem for some people and affect their quality of life. It can be caused by alterations in nociception, injury or disease and may result from current or past damage to the peripheral nervous system (PNS), CNS, or may have no organic cause (Calvino and Grilo, 2006).

Pathophysiology of chronic pain

The exact mechanisms involved in the pathophysiology of chronic pain are complex and remain unclear. It is believed that following injury, rapid and long-term changes occur in parts of the CNS that are involved in the transmission and modulation of pain (nociceptive information) (Ko and Zhuo, 2004).

A central mechanism in the spinal cord, called ‘wind-up’, also referred to as hypersensitivity or hyperexcitability, may occur. Wind-up occurs when repeated, prolonged, noxious stimulation causes the dorsal horn neurones to transmit progressively increasing numbers of pain impulses.

The patient can feel intense pain in response to a stimulus that is not usually associated with pain, for example, touch. This is called allodynia.

This abnormal processing of pain within the PNS and CNS may become independent of the original painful event. In some cases, for example, amputation, the original injury may have occurred in the peripheral nerves, but the mechanisms that underlie the phantom pain are generated in both the PNS and the CNS.

C. Neuropathic pain

Neuropathic pain can be defined as pain initiated or caused by a primary lesion or dysfunction in the nervous system resulting from:

1. trauma, for example, complex regional pain syndrome, chronic post-surgical pain
2. infection, for example, post-herpetic neuralgia
3. ischaemia, for example, diabetic neuropathy
4. cancer
5. chemically induced, for example, as a result of chemotherapy (Farquhar-Smith, 2007)

Some types of neuropathic pain may develop when the PNS has become damaged, causing the pain fibres to transmit pain impulses repetitively and become increasingly sensitive to stimuli. Neuroplasticity may also develop and is characterised by abnormal neuronal sprouting in the PNS and within the dorsal horn of the spinal cord. This sprouting may result in additional generation of and increased transmission of pain impulses.

Characteristics of neuropathic pain

Neuropathic pain is distinctly different from nociceptive pain and is described as:

burning; dull; aching; tingling; like an electric shock; shooting.

Conclusion

This anatomy and physiology section has briefly illustrated the processes that are involved in generating the sensation of pain. This provided the basis for the assessment of pain and the selection of appropriate interventions for managing this pain effectively.

References:

• McCaffery, M., Pasero, C. (1999) Pain: A Clinical Manual. St Louis, MO: Mosby.
• Calvino, B., Grilo, R.M. (2006) Central pain control. Joint Bone Spine; 73: 1, 10-16.
• Farquhar-Smith, P. (2007) Anatomy, physiology and pharmacology of pain. Anaesthesia and Intensive CareMedicine; 9: 1, 3-7.
• Ko, S.M., Zhou, M. (2004) Central plasticity and persistent pain; Drug Discovery Today: Disease Models; Painand Anaesthesia; 1: 2, 101-106