Page 330 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Pain
       Pain stimuli are received by nociceptors in the  jected to the innervation area of the nerve. A
       skin and the viscera which are excited by high-  special form of projected pain is phantom pain
       intensity, non-noxious stimuli (distension,  of an amputated limb or part thereof. In neu-
       temperature) as well as by tissue lesions  ralgia continued abnormal stimulation of a
                          +
       (→ A). Necrotic cells release K and intracellu- +  nerve or posterior root results in chronic pain
    Systems  lar proteins. An increase in extracellular K  in the area of innervation.
       concentration depolarizes the nociceptors,
                                        The impulses along the afferent nerves syn-
       while the proteins and, in some circumstances,
                                       apse in the spinal cord and pass via the ante-
                                       rolateral tracts to the thalamus and from there
       infiltrating microorganisms may cause an in-
    Neuromuscular and Sensory  ators are released (→ p. 294ff.). Leukotrienes,  the cingular gyrus, and the insular cortex
                                       to, among others, the somatosensory cortex,
       flammation. As a result, pain-producing medi-
                                       (→ C). Appropriate connections produce var-
       prostaglandin E 2 , and histamine sensitize the
                                       ious components of pain sensation: sensory
       nociceptors so that even otherwise subthresh-
                                       (e.g., perception of localization and intensity),
       old noxious and harmless stimuli can produce
       pain (hyperalgesia or allodynia). Tissue lesions
                                       affective (ailment), motor (protective reflex,
                                       muscle tone, mimicry), and autonomic (chang-
       also activate blood clotting and thus the re-
                                       es in blood pressure, tachycardia, pupillary di-
       lease of bradykinin and serotonin (→ p. 294). If
       and the resulting extracellular accumulation
                                       the thalamus and spinal cord are inhibited by
               +
          +
                                       the descending tracts from the cortex, mid-
       of K and H further activates the sensitized
    10  there is vascular occlusion, ischemia occurs  latation, sweating, nausea). The connections in
       nociceptors. The mediators histamine, bradyki-
                                       brain periaqueductal gray matter, and raphe
       nin, and prostaglandin E 2 have a vasodilator ef-  nucleus, these tracts employing norepineph-
       fect and increase vascular permeability. This  rine, serotonin, and especially endorphines. Le-
       results in local edemas; the tissue pressure ri-  sions of the thalamus, for example, can pro-
       ses and this also stimulates the nociceptors.  duce pain through an absence of these inhibi-
       Their stimulation releases the peptide sub-  tions (thalamus syndrome).
       stance P (SP) and the calcitonin gene-related  To counteract pain, the activation of pain
       peptide (CGRP), which promote the inflamma-  receptors can be inhibited, for example, by
       tory response and also produce vasodilatation  cooling of the damaged area and by prosta-
       and increase vascular permeability.  glandin synthesis inhibitors (→ C1). The trans-
         Vasoconstriction (by serotonin), followed by  mission of pain can be inhibited by cooling
                                             +
       vasodilatation, is probably also responsible for  and by Na channel blockers (local anesthet-
       migraine attacks (recurring severe headache,  ics; → C2). Transmission in the thalamus can
       often unilateral and associated with neurolo-  be inhibited by anesthesia and alcohol (→ C5).
       gical dysfunctions due, in part at least, to cere-  Attempts have now and again been made to in-
       bral vasomotor abnormalities).  terrupt pain transmission by means of surgical
         Afferents from organs and the surface of the  nerve transection (→ C6). Electroacupuncture
       skin are intertwined in parts of the spinal cord,  and transcutaneous nerve stimulation act via
       i.e., the afferent nerves converge upon the  activation of the descending, pain-inhibiting
       same neurons in the spinal cord (→ B). Excita-  tracts (→ C3). The endorphine receptors are
       tion of the nociceptors in an organ then trig-  activated by morphine and related drugs
       gers pain sensations in those areas of the skin  (→ C4). Endogenous pain-inhibiting mecha-
       whose afferents make connections in the same  nisms can be aided by psychological methods
       spinal cord segment (referred pain; → B1). In  of treatment.
       myocardial infarction, for example, pain radi-  An absence of pain brought about by phar-
       ates into the left shoulder and left arm (Head’s  macological means or the very rare congenital
       zones).                         condition of congenital analgesia interrupt
         Projected pain is produced by stimulation  these warning functions. If the cause of the
  320  of a nerve (e.g., of the ulnar nerve in the ulnar  pain is not removed, the consequences can be
       sulcus; → B2). The perception of pain is pro-  life-threatening.
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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