Pain 2020 PDF

PAIN NG SOOK LUAN, PhD Jabatan Diagnostik Kraniofasial & Biosains Fakulti Pergigian UKM 012-9305208 [email protected]  LEARNING OBJECTIVES 1. Explain the distribution and characteristics of different pain receptors. 2. Explain referred pain a...

PAIN NG SOOK LUAN, PhD Jabatan Diagnostik Kraniofasial & Biosains Fakulti Pergigian UKM 012-9305208 [email protected]  LEARNING OBJECTIVES 1. Explain the distribution and characteristics of different pain receptors. 2. Explain referred pain and its related theories 3. Discuss the role of thalamus & cerebral cortex in relation to perception of pain. 4. Explain the mechanism of pain modification.  PAIN IS A PROTECTIVE MECHANISM Definition of pain Pain is an unpleasant sensory & emotional experience associated with actual or potential tissue damage [The International Association for the Study of Pain (IASP)] Definition of nociception: Neural response related to potentially tissue damage stimuli Pain occurs when tissues are being damaged, and it causes the individual to react to remove the stimulus is a symptom is subjective, protective, and modified by developmental, behavioural, personality and cultural factors associated signs are crying, sweating, increased HR & BP, behavioural changes.  TYPES OF PAIN Fast pain Slow pain Also called sharp pain, pricking pain, acute pain Also called slow burning pain, aching pain, and electric pain throbbing pain, nauseous pain and chronic pain Felt within 0.1 sec after the stimulus is applied Felt only after 1 sec or more and then increases Well localised slowly over many seconds or even minutes Not felt in most deeper tissues of the body Poorly localised Usually associated with tissue destruction Can lead to prolonged, almost unbearable suffering Thin myelinated nerve (A delta fibre) Unmyelinated nerve fibres (C fibre) Somatic Visceral  PAIN RECEPTORS & THEIR STIMULATION Pain receptors are free nerve endings Widespread in the superficial layers of the skin, somatic tissues and certain internal tissues, except brain tissue and lung parenchyma E.g. periosteum, arterial walls, joint surface and etc. Types of stimuli: mechanical, thermal, chemical Fast pain is elicited by mechanical & thermal Slow pain by all three types Chemicals include bradykinin, serotonin, K+ ions, histamine, H+, lactic acids, ACh, proteolytic enzymes, leucotrienes, cytokines, capsaicin Prostaglandins and substance P do not directly stimulate nociceptors, increase the sensitivity of nociceptors for other stimuli (decrease threshold)  PAIN RECEPTORS & THEIR STIMULATION Non-adapting nature of pain receptors Adapt very little and sometimes not at all As the pain stimulus continues, esp. for slow, aching, nauseous pain, excitation of pain fibres becomes progressively greater – increase the sensitivity of pain receptor (hyperalgesia). Rate of tissue damage as a stimulus for pain Pain resulting from heat (>45°C) is closely correlated with the rate at which damage to the tissues is occurring and not with the total damage that has already occurred Intensity of pain is also closely correlated with the rate of tissue damage from causes other than heat (bacterial infection, tissue ischemia, tissue contusion)  CAUSE OF PAIN Tissue damage Bradykinin thought to be the agent most responsible for causing pain following tissue damage Intensity of pain felt correlates with local increase in K ion concentration or increase in proteolytic enzymes Tissue ischemia When blood flow is blocked, the tissue often becomes very painful and the greater the rate of metabolism, the more rapidly the pain occurs May be due to the large accumulation of lactic acid (anaerobic metabolism) as well as bradykinin and proteolytic enzymes (cell damage) Muscle spasm Results partially from the direct effects of muscle spasm in stimulating mechanosensitive pain receptors Also the indirect effects of muscle spasm to compress blood vessels and cause ischemia Spasm increases the rate of metabolism making the relative ischemia even greater – release of chemical pain-inducing substances  DUAL PAIN PATHWAYS: NEOSPINOTHALAMIC – FAST-ACUTE PAIN Neospinothalamic pathway Neospinothalamic tract is used for transmission of fast pain (Aδ fibre) Mechanical and acute thermal pain First order neuron (pain fibre) terminate lamina I (lamina marginalis) of the dorsal horns, then excite second order neuron of the neospinothalamic tract Glutamate is the primary neurotransmitter, secreted by Aδ fibre in the spinal cord Second order neuron decussates to the opposite side of the cord through the anterior commissure and then turn upward to the brain via the anterolateral columns - lateral spinothalamic tracts Most terminate in the thalamus (ventrobasal complex and posterior nuclear group), a few fibres terminate in the reticular Guyton & Hall (2020), 14th Edition, page 585 formation of brain stem, and then third order neuron transmits signals to the basal areas of brain and somatosensory cortex. Fast pain is localized more exactly  DUAL PAIN PATHWAYS: PALEOSPINOTHALAMIC – SLOW-CHRONIC PAIN Pain signals enter the spinal cored (first order neuron) First synapse is present in the dorsal horn of the spinal cord Afferent fibre (C fibre) enters the spinal cord Synapses at the laminae II & II of the dorsal horns (substantia gelatinosa) Neurotransmitter at the first synapse of the pain pathway is substance P (chronic pain) Cross over (decussate) through the anterior commissure to the opposite side The second order neuron travels through (ascends up) the lateral spinothalamic tracts Pain perception at the thalamus (10-25%), most terminate at reticular nuclei, tectal area & periaqueductal gray region The third order neuron sends impulses to the Substantia gelatinosa somatosensory cortex for the localisation of pain Localized only to a major part of the body  REFERRED PAIN Pain arising from viscera are not felt at the site of origin but referred to a distant site Sensations arriving at the segment of spinal cord can stimulate interneurons that are part of anterolateral pathway Activity in interneurons leads to stimulation of primary sensory cortex, so an individual feels pain in specific part of body surface Examples: Cardiac pain referred to left arm & chest pain Diaphragmatic pain referred to the shoulder Ureteric pain referred to the testes in male & inner thigh Sensory info from the heart and arm in female converge on the same nerve pathway in Gall bladder pain referred to epigastric region the spinal cord, Pain from the maxillary sinus referred to the nearby tooth  REFERRED PAIN - THEORIES Convergence theory Facilitatory theory The number of peripheral pain exceed the Somatic & visceral pain afferents connect number of lateral spinothalamic tract. So, with separate but adjoining spinothalamic both somatic & visceral afferents converge neurons and there may be some overlap of upon the same spinothalamic neurons at the neurons, visceral afferents have the spinal cord level. collaterals connecting to the spinothalamic neurons receiving somatic pain afferents. Hence when visceral pain impulses travel in the same pathway along which impulses This causes impulses to travel up the from the skin travels, the individual gets somatic spinothalamic pathway and the feeling that the pain originates in the causes the sensation of pain in the skin. skin itself.  PAIN PERCEPTION – AWARE OF PAIN Pain perception occurs at different levels Thalamus is an important centre of pain perception Lesion of thalamus produces severe type of pain known as “thalamic pain” Sensory cortex – necessary for the localisation and intensity of pain Other areas for pain perception – reticular formation, limbic areas, hypothalamus and other subcortical areas  PROCESS OF PAIN PHYSIOLOGY Transduction – Noxious stimuli is converted to electrical energy. This electrical energy is known as transduction. This stimulus sends an impulse across peripheral nerve fibre (nociceptor). Transmission – Transmission of pain impulse is carried by Aδ or C fibres and travels along the spinothalamic tract. Perception – aware of pain; nociceptive input reaches the cortex where perception occurs which immediately initiates a complex interaction in the neurons between higher centres of the brain Modulation – ability of CNS to control the pain transmitting neurons; inhibition of the pain impulse. Inhibitory neurotransmitters (endogenous opioids) work to hinder the pain transmission.  PAIN MODULATION / PAIN MODIFICATION Pain modulation means pain perception variability which is influenced by endogenous & exogenous mechanism, that can increase or decrease pain threshold Enhancement and inhibition all levels of the nervous system. Modulation at the peripheral nerve, spinal cord, brain sites influences pain perception.  PAIN MODULATION (PAIN SUPPRESSION) Pain suppression – analgesia system – block pain signals has 3 components: Periaqueductal gray and periventricular areas of mesencephalon and pons Raphe magnus nucleus in the pons and the nucleus reticularis in the medulla Pain inhibitory complex in the dorsal horns of the spinal cord Transmitters substances Enkephalin – causes both pre- and post-synaptic inhibition of incoming pain fibres (Aδ, C) Serotonin – released from the dorsal horn and causes the release of enkephalin Brain’s opiate system (endogenous opioid peptides) Endorphins (hypothalamus & pituitary) Enkephalins, dynorphin (brain stem)  OPIOID ACTIONS Endogenous opioid peptides: endorphin, enkephalin, dynorphin Exogenous opioid peptides: morphine, codeine, fentanyl, pethidine, opium (poppy plant), heroin Act presynaptically or postsynaptically Blocks Ca2+ channels and inhibits Ca2+ influx and thereby prevent pain neurotransmitter release (glutamate, substance P) from presynaptic membrane Open up K+ channels and causes K+ efflux and resulting in hyperpolarization of the membrane and prevents pain neurotransmitter activity Inhibits cAMP activity and alters pain neurotransmitter activity Activates descending pain modulatory (inhibitory) pathway Inhibit GABA-mediated inhibition of descending pathway activity  PAIN MODULATION (GATE CONTROL THEORY) Gate control theory – non-painful input closes the gates to painful input Proposed by Melzack & Wall (1965). Substantia gelatinosa (SG) in dorsal horn of the spinal cord acts as a “gate” – only allows one type of impulses to connect with the second order neuron If Aβ neurons are stimulated – SG is activated which closes the gate to Aδ & C neurons If Aδ & C neurons are stimulated – SG is blocked which closes the gate to Aβ neurons This theory provided basis for various methods of pain relief: Massaging a painful area Applying irritable substances to a painful area (counter irritation) Transcutaneous electrical nerve stimulation Acupuncture  GATE CONTROL THEORY When pain sensation is produced, other afferents particularly the touch fibres reaching the dorsal column of spinal cord are also activated. These dorsal column fibres (touch) send collaterals to the cells of SG in the dorsal grey horn. Thus impulses (touch) ascending via dorsal column fibres pass through the collaterals and reach SG. Here these impulses (touch) inhibit the release of substance P by the pain nerve endings. So E.g. inhibition of pain transmission by tactile sensory signals that, the pain sensation is suppressed. Rubbing the skin near painful areas and applying liniments often relives pain. This is due to the stimulation of Aβ sensory fibres from peripheral Thus, the gating of pain in dorsal grey horn tactile receptors depress transmission of pain signals. – Local lateral inhibition level is similar to presynaptic inhibition.  VARIETIES OF PAIN Phantom pain – no stimuli, but pain is felt Injured nerve endings able to fire abnormal action potentials E.g. amputated limb Psychogenic pain – individual feels pain but cause is emotional rather than physical Neuropathic pain – pain caused by a lesion or disease of the somatosensory nervous system (pain pathway) Damage to peripheral nerve (adrenaline released by sympathetic discharge) Repeated activation causes continuous pain. E.g. Diabetic neuropathy (injuries of small blood vessels that supply nerves) PAIN IN DENTISTRY  OROFACIAL PAIN PATHWAY Somatic inputs from the face and oral structures do not entre the spinal cord by way of spinal nerves Instead, sensory input from the face and mouth is carried by way of the CN V (trigeminal nerve)  DENTAL PAIN OF PULPAL ORIGIN Visceral in character and is of threshold type Responds to all types of noxious stimuli but to ordinary masticatory function Non-localize At basic clinical feature is that it does not remain the same indefinitely Generally, it resolves, becomes chronic or proceed to periodontal ligament (PDL) structures  DENTAL PAIN OF PDL ORIGIN Deep somatic pain of musculoskeletal type More localized than pulpal pain Intimately related to biomechanical function (masticatory) Receptors of PDL are capable of precise localization Characterized by discomfort during biting – under occlusal pressure – tooth feels sore or elongated