Copyright EMAP Publishing 2015 This article is not for distribution Keywords: Pain/Analgesia/Nervous Nursing Practice system/ Stimulus Review ●This article has been double-blind Pain management peer reviewed The first of a three-part series on the management of pain describes how pain is detected in the body and the implications for clinical practice paRT 1 OF 3: PAIN MANAGEMENT Physiology – how the body detects pain stimuli In this article... 5 key An overview of the pain pathway points Pain (noxious) How pain receptors detect pain 1stimuli may be How agonists and antagonists are used to manage pain mechanical, thermal or chemical Author Amelia Swift is senior lecturer at neuropathy), or to a change in the way the The threshold the University of Birmingham, Institute of nervous system detects and manages sen- 2of activation of Clinical Science sory signals (as is the case in chronic low pain receptors Abstract Swift A (2015) Pain management back pain). varies throughout 1: how the body detects pain stimuli. Acute pain is best relieved by inter- the body, with the Nursing Times; 111: 39, 20-23. rupting pain signals as they travel cornea in the eye Pain is the body’s way of telling us between their source and the brain, or by being more something is wrong. It has a sensory and boosting the body’s own efforts to alle- sensitive than the emotional component. This three-part viate pain such as the production of neu- skin, for example series focuses on acute pain, describing roactive chemicals like endorphins. The frequency the physiology of a normal and well- Chronic pain can be more difficult to 3a nociceptor behaved pain pathway and how this manage because of differences in the sig- fires relates to the relates to commonly used pain- nalling process. Therefore the starting pain intensity; a management strategies. This first article point for being able to provide effective higher frequency introduces the pain system and how the pain management is an understanding of means a greater body detects a threatening (noxious) the “normal” pain pathway associated pain intensity stimulus. Part two describes how that pain with acute pain. A glossary of terms is Analgesics message is transmitted to the spinal cord provided in Box 1 (page 23). 4such as and the brain, and the response of the morphine act as brain to the stimulus. The third article An overview of the pain system agonists, binding discusses the assessment of pain. Acute pain is a sensation triggered by a to the pain threatening (noxious) stimulus to the skin receptor and so ain is defined as an unpleasant (cutaneous pain), the musculoskeletal preventing it from sensory and emotional experi- system, or the internal organs (visceral firing a pain signal ence associated with actual or pain), which is then signalled to the brain Painkillers such Ppotential tissue damage or so it becomes aware of the threat and can 5as capsaicin described in terms of such damage decide how to respond (fight or flight). cream work by (Merksy and Bogduk, 1994). As a physical The signal may trigger a reflex response overstimulating a sensation pain usually signals a danger to that causes us to move out of range of the particular receptor, the body from an internal or external stim- threat. The pain “system” comprises a which is then spent ulus such as an infection or a knife wound. number of elements that detect the and will not fire for This type of pain is called physiological noxious stimulus, convert it to an electrical some time pain or acute pain and normally resolves signal and transfer that signal rapidly to afterwards once the stimulus has been removed and the spine and then the brainstem and the damaged tissues have healed. Chronic finally the cortex. These are illustrated pain, on the other hand, continues indefi- in Fig 1. nitely and might be related to an ongoing The basic elements of the pain pathway disease process such as osteoarthritis, are different kinds of sensory nerves that damage or dysfunction of the nervous connect the tissues to the spinal cord and system (as is the case in painful diabetic run together in bundles between the two. 20 Nursing Times 23.09.15 / Vol 111 No 39 / www.nursingtimes.net Copyright EMAP Publishing 2015 This article is not for distribution For more articles on pain management, Nursing go to nursingtimes.net/pain Times.net FIG 1. BASIC ELEMENTS OF THE paIN pathWAY Cell body Cells in the tissues Axon of sensory nerve fibre Direction of signal Pre-synaptic Terminals of terminal of sensory sensory fibre nerve fibre Secondary neuron Brain Axon of secondary neuron Acute pain is caused by activating pain receptors throughout the body Each sensory nerve terminates in a multi- » Chemical: acids, alkalis, irritants, (or noxious stimuli) are found at the nerve tude of specialised receptors that are capsaicin (active ingredient of endings of primary afferent A-delta and C spread across the skin and organ tissues; chilli peppers); fibres (Table 1). Primary afferent A-beta these connect by a long axon to their cell » Thermal: heat (above 42°C), cold fibres respond to non-noxious stimuli, body (which lies just outside the spinal (below -15°C); such as touch. cord). The cell body has a second axon that » Mechanical: punctate (sharp) pressure, A mechanical stimulus, such as an terminates in the dorsal horn of the spinal rotation beyond normal functional over-stretch of a muscle fibre or over- cord. The sensory nerve responsible for range (for example joints), distension rotation of a joint, causes receptors on the detection of a threat is the first step in the (for example, bowel). surface of the nerve ending to stretch. pain pathway and is called the primary A noxious stimulus is detected by Noxious heat or cold near the nerve ending afferent fibre (PAF). Afferent means sig- receptors that are situated on the cell and noxious chemicals interact with nals travel along it towards the spinal cord. membrane of the sensory nerve ending. specific receptors. The receptor responds Once the primary afferent fibre termi- The receptors are proteins that are made in to the triggering event chemically in one of nates in the spinal cord, it makes chemical the cell body of the nerve and then trans- three ways: and physical connections with other cells ferred to the surface of the nerve ending. » Agonism/excitation: the electrical including secondary neurons. The signal The types of receptors on the sensory nerve potential of the cell is raised above the is passed from the primary afferent fibre ending determine the type of stimulus that activation threshold and an action to the secondary neuron, which carries the nerve cell can respond to, and there are potential is initiated; the signal to the brain. It is not until the many types. The receptors that detect pain » Sensitisation: makes it easier for the signal reaches the cortex that the brain becomes aware of the pain. TABLE 1. TYPES OF SENSORY AFFERENT FIBRE Detection of a noxious stimulus Pain can be detected (or sensed) in most of Fibre Size Relative Myelin Stimulus type Alternative the body’s tissues except in healthy carti- speed name lage and the brain itself. The key elements C Small Slowest None ● Mechanical CM involved in detection are: ● Mechanical and heat CMH » A threatening or harmful (noxious) ● Mechanical, heat and stimulus; chemical Polymodal » Units that can respond to different ● In inflammation only noxious stimuli (sensory nerve endings – mechanical, heat and Silent with receptors). chemical Noxious stimuli are traditionally A-delta Medium Medium Light ● Mechanical and heat AMH divided into three categories: chemical, ● Mechanical and cold thermal or mechanical. To initiate a pain ● High-threshold AMC signal, the stimulus has to be above a par- mechanical ticular intensity (threshold) that would be AHTM enough to cause damage to the tissues. A-beta Large Fastest Yes ● Low-threshold mechanical LTM Examples of these include: Lamb Peter Alamy, www.nursingtimes.net / Vol 111 No 39 / Nursing Times 23.09.15 21 Copyright EMAP Publishing 2015 This article is not for distribution FIG 2. relatively small quantity of positive ions; CREatION OF AN ACTION POTENTIAL this will not be enough to trigger an action potential. Oscilloscope Significant tissue damage causes lots of agonists, so the nerve cell will achieve its Sensory 2. Agonist nerve activates action potential threshold, and will do so a ending receptor number of times in quick succession. This means the nerve will fire frequently (for Intracellular fluid example 50 action potentials per second) – this creates high pain intensity. Less Electrode frequent firing (for example one action Extracellular 1. Tissue damage potential per second) will produce a lower fluid breaks cells intensity of pain if it leads to pain at all. The maximum number of action Tissue cells potentials that a sensory fibre can achieve is about 100 per second (Bear et al, 2001). The action potential is then rapidly transmitted along the axon until it reaches Ion Action the sensory nerve fibre terminal in the channel potential opens achieved dorsal horn. Once an action potential has been cre- ated the nerve cell actively pumps positive ions back out into the extracellular fluid in order to return to its resting potential. These excitable nerve cells can be com- pared to a bottle of cola: they sit quietly fizzing, and while they have the potential to do something an input of energy is needed. If a soft mint sweet is added to the bottle, action potential is reached and the fizz is no longer quiet but loud and has cell to achieve its threshold for action axons by the movement of electrically enough energy to carry cola out of the potential generation; charged ions.