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Wednesday, 9 August 2017

The physiology of pain

The physiology of pain

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       Types of pain sensation:
      1- according to site of origin of pain
      2- according to quality of pain
       Pain pathway
      Fast pain pathway
      Slow pain pathway
      Function of cerebral cortex in perception of pain
      Arousal reaction of pain signal
      Pain threshold
      Types of pain sensation
      Cutaneous pain
      Neuropathic pain
      Visceral pain
      referred pain
      Control of pain
      Pain is unpleasant sensation for protection of the body. It occurs whenever there is physical or potential tissue damage
Pain receptors
       Pain receptors are free nerve endings attached to A delta & C fibers
       Pain receptors are the most widely distributed amongst receptors to other modalities
       They classified according to the mode of stimulation into:
       1- mechanical pain receptors: stimulated by injurious stimuli eg cuts & bruises
       2-thermal pain receptors: respond to extreme temperature
       3- chemical pain receptors: stimulated by chemical injurious elements or chemicals produced from tissue damage
       4- polymodal pain receptors: respond to all types of stimuli
       Distribution of pain receptors:
       1/ They are widely spread in superficial layers of the skin & some deep tissues like parietal surfaces (periosteum, pericardium, parital pleura), joint, arterial walls, wall of cranial sinuses
       11/ They are less distributed in other deep tissues
       111/ They are absent in liver parenchyma, lung alveoli & brain tissues (pain insensitive structures) but brain BVs & meninges, the liver capsule & bile ducts & the bronchi  & parietal pleura are sensitive to pain
       Adaptation: slowly or nonadaptive receptors
       Chemical mediators of pain:
       After nociceptors are stimulated the damaged tissues & the surrounding BVs release no of pain & inflammation producing chemical substances that are normally inside the cells à into ECF
       These substances include histamine, serotonin, K, ATP, substance P, bradykinins &PG
       Prostaglandins àlower pain threshold à further sensitize the nociceptors à producing hyperalgesia that often accompanies pain.
       Salicylates & other nonsteroidal anti-inflamatory analgesic reduce pain by inhibiting PG synthesis
       Types of pain sensation:
       1- according to site of origin of pain:
       Cutaneous pain: arising from skin & subcutaneous tis-
       Deep pain: arise from tissues deeper than skin eg muscles ,tendons, joints, ligaments & bones
       Visceral pain: arise from viscera
       Neuropathec pain
       2- according to quality of pain:
       Fast pain also called sharp, pricking or immediate 0.1s
       Slow pain, burning pain
       The two types (slow,fast)  of pain can be differentiated from other by:
       1- hypoxia (moderate compression of nerve trunk) will block Aδ fibers leaving C fibers à fast pricking pain is lost while the burning type remains
       2- low concentrations of local anesthetics block C fibers leaving Aδ fibersà slow burning pain is lost while the fast pricking type remain

  •        Fast pain
       Sharp, pricking, acute
       Immediate; felt within 0.1s after stimulation
       Short duration
       Well localized
       Mechanical & thermal pain receptors
       Arises from receptors in superficial tissues, serosal membranes & parietal surfaces
       A delta fibers
       Blocked by hypoxia & compression
       Neurotransmitter glutamate
       Pathway neospinothalamic
       PVN of thalamus
       Termination sensory cortex
       Perception in thalamus & sensory cortex

  •        Slow pain
       Dull, aching, burning, throbbing نابض, diffused
       Delayed: felt after 1sor more after stimulation
       Long duration & increase with time
       Poorly localized à diffuse
       All types of pain receptors
       Arises from receptors in superficial & deep tissues, viscera
       C fibers
       blocked by local aneathesia ( eg cocaine)

       Neur- substanceP
       Pathway paleospinothalamic
       Reticular formation then to intralaminar of the thalamus
       Termination Whole cortex
       Pain perception mainly in thalamus
       Pain pathway:
       Fast pain & slow pain utilize two separate pathways (within lateral spinothalamic tracts) for transmitting pain signals into CNS
       Fast nerve fiber ascend as neospinothalamic tract while slow pain fibers ascend as paleospinothalamic tract
       The path of the 3order neuron areas follow:
       First order neurons: on entering SC through lateral division of the dorsal root pain fibers ascend or descend few segments to end on posterior horn cells
       Type Aδ fibers (carrying fast pain) end in lamina 1 & V, while type C fiber (carrying slow pain) end in lamina 11 & 111
       Second order neurons:
       The pain fiber then cross the midline infront of the central canal & ascend in lateral spinothalamic canal in the opposite site of SC.
       Fast pain fibers ascend as neospinothalamic tract while slow pain fibers ascend as paleospinothalamic tract
       1/ neospinothalamic tract:
       Fast pain ascend upwards to end mainly in ventrobasal nuclei of the thalamus. Few fibers end in the reticular formation of brain stem
       Axons of the 3rd order neuron: arise from the thalamus & project to the somatic sensory cortex
       11/ paleospinothalamic tract:
       Slow pain fibers join neospinothalamic tracts in the SC till the brain stem where:
       1/10 of fibers pass to the thalamus then to cortex
       9/10 of fibers terminate widely in reticular formation of brain stem (also pretectal area, periaqueductal area)
       several interneurons then carry the input in these fibers mainly to the intralaminar (nonspecific) nuclei of the thalamus.
       Because reticular area of brain stem & intralaminar nuclei of thalamus form part of reticular activating system RAS à impulses arriving there have strong arousal effect of pain
       NB: through their way upwards the pain fiber give tributaries to:
       Anterior horn cells in the SC for accompanying motor reflexes: eg reflexes which remove part or all body from painful stimuli eg withdrawal reflex. Or may be in form of muscle rigidity (stiffness) à reflex contraction of somatic muscle in response to deep somatic & visceral pain à neck stiffnes in meningitis
       Reticular formation for cortical activation & arousal reactions
       Hypothalamus for accompanying autonomic reactions: vary with intensity & site of stimulation. Mild pain occurring in superficial tissues stimulate the posterior hypothalamic nuclei & result in sympathetic changes à tachycardia, rise in blood pressure, pupiludilatation etc. sever pain in superficial & deep tissues, & organ may stimulate anterior hypothalamus nuclei result in parasympathetic changes à bradycardia, decrease in blood pressure
       Limbic system for emotional  & behavioural reactions: unpleasant effect of pain eg anxiety, anguish, crying, depression. Emotional reaction vary widely among people although the threshold for pain is nearly the same
       Function of cerebral cortex in perception of pain:
       Cerebral cortex is not essential for perception (conscious awareness) of pain
       Pain perception can occurs subcortically in the thalamus
       Functions of sensory (parietal) cortex in pain perception:
       1- localization of pain: fast pain is v localized
       2- Discrimination of pain modality & intensity
       3- interpretation of its meaning
       The frontal lobe contributes to the accompanying emotional & behavioral effects of pain à frontal lobotomy for treatment of intractable pain patient still feel pain postoperatively but the emotional reactions is absent
       Arousal reaction of pain signal:
       The intraluminar (non specific) nuclei of the thalamus & reticular formation of the brain stem have strong arousal effect on nervous activities through reticular activating system (RAS) of the brain à this explain why person with sever pain is strongly aroused
       Threshold of the pain:
       Pain threshold is higher than that of other modalities ie painful stimuli must be strong & noxious. However pain remain specific sensation & can never be caused by overstimulation of other receptors
       Threshold  of pain is the same for all people but reaction to pain different from person to another  

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