BoH+Pain+Lecture+copy.pdf

Pain Physiology Bachelor Oral Health  What is pain? “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” IASP  What is pain? “an unpleasant sensory and emotional experience associ...

Pain Physiology Bachelor Oral Health  What is pain? “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” IASP  What is pain? “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” IASP “more like hunger and thirst, than vision and audition” (Wall,P. “On the relation of injury to pain”)  What is pain? Acute versus Chronic Nociceptive (Inflammatory) versus Neuropathic versus Nociplastic Cutaneous, Deep Somatic, Visceral Cancer Pain versus Non Cancer Pain “Each belongs so exclusively to its sensorium that it is hard to use the unqualified term pain” Distinct classes of mechanoreceptors for somatosensation. Nociceptors are usually considered a sub-type of mechanoreceptor. Referred to/ described commonly as “free-nerve endings”. Distinct classes of nociceptors. Thermal; Mechanical; Polymodal; and Silent. Two types of nerve fibre: A-delta, and C-fibres Nociceptors located from superficial to deep tissues. Thermal and mechanical nociceptors found most superficially Polymodal nociceptors found throughout body Silent nociceptors found in muscle, joint and viscera Transmission times (conduction velocities) have perceptual correlates. A-delta fibre: “first pain” C-fibre: “second pain” Lewis’ Triple Response “retrograde activation” of C-fibres Ø rubor, turgor and calor (+ dolor) due to release of transmitter from sensory ending Tissue damage triggers local release of bradykinin, PGs and K+ activates nociceptor Retrograde activation of collaterals triggers release of Substance P – mast cells degranulate and release histamine increased swelling & sensitises nociceptor Retrograde activation of collaterals triggers release of Substance P – acts on vessels plasma extravasation which may sensitise nociceptor Sensitisation of the nociceptors on peripheral fibres results in primary hyperalgesia/ allodynia By example a burn results in a region of flare, and beyond that a region of enhanced sensitivity to mechanical stimuli. Previously innocuous stimuli are now perceived as painful: “allodynia” Noxious stimuli are perceived as more noxious: “hyperalgesia” A-delta and C-fibres from the body project into spinal cord. Spinal cord is a laminated structure. Lamina designated 1 to 10 Each lamina has a specific function. Neurons in laminae 1, 2, 5, and 10 each receive inputs from nociceptors from distinct body tissues. A-delta and C-fibres are carried in each spinal nerve. Each spinal segment processes noxious signals arising from each dermatome. The maps of noxious input are not highly accurate. A-delta fibres project primarily into lamina 1 and 5 C-fibres project primarily into lamina 2 (substantia gelatinosa) Nociceptors contain neurotransmitters Glutamate and Substance P Spinal cord cells can be “wound-up” We call this central sensitisation Once the NMDA receptor is “opened-up” secondary hyperalgesia may result. The NMDA receptor has loci of therapeutic possibility to prevent/reverse pain centralisation. Nociceptors contain a number of opioid, adrenergic, GABA and 5HT receptors via which nociception may be modulated. Spinal cord cells also contain a number of opioid, adrenergic, GABA and 5HT receptors via which nociception may be modulated. Prolonged activation of the spinal neurons by nociceptive input can trigger cell death in the spinal cord. There is some evidence that the cells most vulnerable are the inhibitory type, which may lead to overactivity of the spinal cord. Prolonged activation of the spinal neurons by nociceptive input can trigger long-term changes in their function, via genomic regulation. The plasticity of the spinal response may lead to irreversible changes which underlie the emergence of neuropathic pain. It is possible that subsequent prolonged activation of supra-spinal regions may also undergo long-term changes in their function, via similar genomic regulation.  Spinal cord mechanisms of referred pain Convergence of primary afferent fibres onto common pools of spinal neurons. Results in a perceptual “mistake”. Not all referral patterns utilise convergence Reflex activation of the sympathetic nervous system can lead to referral Reflex activation of the motor outflow can lead to referral Fibres from spinal lamina 1,2,5 and 10 cross the midline in the spinal cord and ascend towards higher brain regions. Fibres travel in anterolateral quadrant = anterolateral tract Some fibres ascend directly to the thalamus, these fibres form a tract: the spinothalamic tract Pain from the head is relayed through the trigeminal nerve: ventral trigemino-thalamic tract The ventroposterior lateral and medial nuclei send their information to primary somatosensory cortex (S1). The signals are represented in a somatotopic map and the signals reflect, onset, location, intensity and “descriptive” quality. These pathways are usually referred to as the sensory-discriminative pathways of the pain system There are other pathways within the anterolateral tract that carry pain signals, these integrate many of the affective and motivational state changes that characterise physiological and clinical pain Descending modulation: Pathways for analgesics State dependency of pain experience Placebo effector pathways