The physiology of pain

The physiology of pain

•       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 3^rd 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