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Anaesthesia & Exodontia

Anaesthesia & Exodontia
Third Year

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  • Hyperlink – reference McCance and Heuther chapter 14 p402. <br />
  • e.g. post therpetic neuralgia – after shingles, anaesthesia dolorosa can follow therapeuic transection of sensory nerves <br />
  • Central sensitization can develop from many chronic painful conditions. Continued stimulation by peripheral afferent nerves leads to distinct biochemical and physiologic changes. For example, nerve growth factor (NGF) begins to be produced in quantities sufficient to alter the nerve connections within the dorsal horn of the spinal cord. The number and types of receptors that respond to excitatory stimulation increase, resulting in heightened postsynaptic responsiveness to what would normally be perceived as mildly painful stimulus. <br />   <br />

Pain Pain Presentation Transcript

  • By Hesham Marei BDs, MSc, PhD, FDS RCS (Eng) Assistant Professor Oral and Maxillofacial Surgery,
  • Definition of Pain Types of Pain Pain Pathway Mechanism of Pain Control
  • An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
  •      Acute versus chronic Nociceptive versus Neuropathic Somatic versus visceral Referred versus non referred pain Somatogenic versus psychogenic
  • Acute pain Chronic pain •Sudden onset •Temporary (disappears once stimulus is removed) •Persistent – usually lasting more than six months •can be somatic, visceral, referred •Cause unknown – may be due to neural stimulation •Physiological responses to acute pain include increased RR, HR, BP and reduction in gastric motility – sympathetic response) •Physiological responses are less obvious especially with adaptation. •Psychological responses may include depression
  • Nociceptive pains result from activation of nociceptors (Pain receptors) Neuropathic pain result from direct injury to nerves in the peripheral nervous system. (Alcoholism, diabetic neuropathy, post-herpetic neuralgia, etc…)
  • Somatic pain  Superficial: stimulation of receptors in skin  Deep: stimulation of receptors in muscles, joints and tendons Visceral pain  Stimulation of receptors in internal organs, abdomen and skeleton  Often poorly localised as fewer receptors located in viscera  Visceral pain can be referred.
  • Pain experienced at a point distant to its point of origin Area of referred pain is supplied by same spinal segment as actual site of pain Brain misinterprets signals as coming from somatic regions Knowledge of different types of referred pain is important in clinical diagnosis because in many visceral ailments the only clinical signs is referred pain. Good section on referred pain can be found in Guyton and Hall (2006)
  • Somatogenic pain is a pain originating from an actual physical cause e.g. trauma, ischaemia etc Psychogenic pain is pain for which there is no physical cause. It is not however imaginary pain and can be as intense as somatic pain.
  • Pain threshold The pain threshold is the point at which a stimulus is perceived as pain. A patient who is hyper-reactive is considered to have a low pain threshold. On the other hand a patient with a high pain threshold can tolerate pain. The pain threshold is affected by: •Emotional status. •Fatigue. •Age. •Sex. •Fear and Apprehension.
  • Neuroanatomy of pain The portions of the nervous system responsible for the sensation and perception of pain may be divided into three areas: 1. afferent pathways 2. CNS 3. efferent pathways The afferent portion is composed of: a) nociceptors (pain receptors) b) afferent nerve fibres c) spinal cord network
  • The role of the afferent and efferent pathways in processing of pain information Nociceptors: Endings of small unmyelinated and lightly myelinated afferent neurons. Stimulators: Chemical, mechanical and thermal stimuli Mild stimulation → positive, pleasurable sensation (e.g. tickling) Strong stimulation → pain These differences are a result of the frequency and amplitude of the afferent signal transmitted from the nerve endings to the CNS. Location: In muscles, tendons, epidermis, subcutanous tissue, Visceral. - they are not evenly distributed in the body (in skin more then in internal structures)
  • Nociceptive pain: - mechanisms involved in development
  • Receptors respond to injury  Thermal –excessive heat or cold  Mechanical –tearing, crushing, stretching etc  Chemical Inflammatory mediators Lactic acid ischemia
  • There are four processes in the pain pathway 1. transduction  1. Transmission  1. Propagation of impulses along spinothalamic pathway. Modulation  1. Noxious stimuli translated into electrical activity at sensory nerve endings Transmission is modified Perception  Affective / motivational aspect Each of these processes present a potential target for analgesic therapy
  • Pain is detected by nociceptors (noci = harmful) Free nerve endings of sensory neurones Found in all tissues and organs (except brain) Can be classified as either:  Unimodal – respond to only one type of stimulus  Polymodal – respond to more than one type of stimuli.
  • When cellular damage occurs, tissues release chemicals that stimulate nociceptors  Bradykinin Histamine  Serotonin Acetylcholine  Potassium ions  Prostaglandins (PGE2, PGI2)  Substance P The activity and sensitivity of nociceptors is profoundly altered by such mediators (enhances receptor response to noxious stimuli). See article by Kelly et al ( 2001) for interesting information on this aspect
  • TRAUMA •Mechanical •Thermal •chemical Overall effect is increased nociceptor activation r epto c noci Mediators Bradykinin Histamine Serotonin Acetylcholine Potassium ions  Prostaglandins (PGE2, PGI2) Substance P 
  • Nociceptors respond to noxious stimuli and covert energy at the site of the stimulus into neural impulses Nociceptors are terminal endings of primary afferent fibres. These can be classed into two main types  Myelinated A-delta fibres  non-Myelinated C fibres When the threshold level of the stimulus is reached, then depolarization occurs along these fibres in the form of action potentials
  • A-Delta fibres C- fibres Myelinated Unmyelinated fast ( first) pain -conduct at 535m/sec Slow (second) pain – conduct at 0.5-2.0m/sec Associated with Sharp, brief, prinking pain Associated with dull,burning, aching, prolonged pain Well localised More diffuse Elicited by mechanical or thermal stimuli Elicited mainly by chemical stimuli or persisting mechanical or thermal stimuli
  • Primary (1o) Afferents ‘dull’ vague Aδ C
  •  Both A delta and C nociceptor fibres synapse in the dorsal horn of the spinal cord  Evidence suggests that neurotransmitters released at this point include substance P, glutamate, calcitonin generelated peptide (CGRP).
  • Secondary neurones cross the cord and ascend through the antero-lateral spinothalamic tract to the thalamus where they synapse with tertiary neurones These tertiary neurones ascend from the thalamus to somatosensory cortex.
  • cortex thalamus Tissue injury • histamine • bradykinin • etc. dorsal root ganglion primary afferent lateral spinothalamic tract Fig 3-25
  • Somatosensory cortex is involved in the localisation and identification of pain.
  •  • nociceptors → transmitted by small Adelta fibers and C- fibers to the spinal cord → form synapses with neurons in the dorsal horn(DH)  From DH → transmitted to higher parts of the spinal cord and to the rest of the CNS by spinothalamic tracts
  • Central Sensitization
  • Transduction, transmission, modulation interact to create subjective emotional experience of pain. The portion of CNS involved in the interpretation of the pain signals are the limbic system, reticular formation, thalamus, hypothalamus and cortex
  • The brain first perceives the sensation of pain • The thalamus, sensitive cortex : perceiving describing localising of pain • Parts of thalamus, brainstem and reticular formation: - identify dull longer-lasting, and diffuse pain • The reticular formation and limbic system: - control the emotional and affective response to pain Because the cortex, thalamus and brainstem are interconnected with the hypothalamus and autonomic nervous system, the perception of pain is associated with an autonomic response
  • Theory of pain production and modulation • Most rational explanation of pain production and modulation is based on gate control theory (created by Melzack and Wall) • According to this theory, nociceptive impulses are transmitted to the spinal cord through large A- delta and small C- fibers • These fibers create synapses in the SG • The cells in this structure function as a gate, regulating transmission of impulses to CNS
  • Stimulation of larger nerve fibers (A-alfa, A-beta) causes the cells in SG to "close the gate". A closed gate decreases stimulation of T-cells (the 2nd afferent neuron), which decreases transmission of impulses, and diminishes pain perception Stimulation of small fiber input inhibits cells in SG and "open the gate". An open gate increases the stimulation of T-cells → →↑ transmission of impulses → enhances pain perception • In addition to gate control through large and small fibers stimulation, the central nervous system, through efferent pathways, may close, partially close, or open gate. Cognitive functioning may thus modulate pain perception
  • Perception of pain is dependent upon:  Cellular damage  Receptor stimulation  Ascending neural pathways  Sensory cortex arousal  Conscious awareness of stimulation of pain
  • NSAIDs Aa COX PGs
  • Local Anesthetics (voltage-gated Na+ channels)
  • Opioids (µ, δ, κ)
  • NSAIDs: 1970’s opioids: 1970’s tramadol: 1980’s & 1990’s COX-2 inhibitors: 1990’s acetaminophen: unknown combinations adjuncts
  • Severe Moderate Mild Step 3 Strong opioids (e.g., morphine) with or without non-opioids Step 2 Weak opioids (e.g., codeine) with or without non-opioids Step 1 Non-opioids (e.g., NSAIDs, acetaminophen = paracetamol)