Literature DB >> 2838108

Neurophysiology of gastrointestinal pain.

F Cervero.   

Abstract

The only non-general sensation that can be evoked from the gastrointestinal (GI) tract is that of pain ranging from mild discomfort to intense pain. However, in certain regions of the gut, such as the rectum and gastro-oesophagus, the feeling of pain can be preceded by non-painful sensations of distension at lower stimulus intensities. GI pain is often dull, aching, ill-defined and badly localized. In some cases, GI pain is projected to areas of the body away from the originating viscus ('referred' pain). These properties indicate that the representation of internal organs within the central nervous system is very imprecise. Behavioural, neurophysiological and clinical evidence shows that most forms of GI pain are mediated by activity in visceral afferent fibres running in sympathetic nerves and that the afferent innervation of the gut mediated by parasympathetic nerves is not primarily concerned with the signalling and transmission of GI pain. As for the encoding mechanism of the peripheral sensory receptor in the gut, there is evidence for the existence of specific visceral nociceptors in some locations (e.g. the biliary system) and for the existence of non-specific 'intensity' type receptors in other locations (e.g. the colon). In any case, the actual number of nociceptive afferent fibres in the gut is very small and this explains why large areas of the GI tract appear to be insensitive or require considerable stimulation before giving rise to painful sensations. The few nociceptive afferents contained in sympathetic nerves can excite many second order neurones in the spinal cord which in turn generate extensive divergence within the spinal cord and brain stem, sometimes involving long supraspinal loops. Such a divergent input can activate many different systems, motor and autonomic as well as sensory, and thus trigger the general reactions that are characteristic of visceral nociception: a diffuse and ill-localized pain sometimes referred to somatic areas, and autonomic and somatic reflexes that result in prolonged motor activity.

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Year:  1988        PMID: 2838108     DOI: 10.1016/0950-3528(88)90027-9

Source DB:  PubMed          Journal:  Baillieres Clin Gastroenterol        ISSN: 0950-3528


  7 in total

Review 1.  [Abdominal pain].

Authors:  J M Gschossmann; G Holtmann; P Netzer; M Essig; B M Balsiger; U Scheurer
Journal:  Internist (Berl)       Date:  2005-10       Impact factor: 0.743

2.  Rectal sensory evoked potentials: an assessment of their clinical value.

Authors:  C T Speakman; M A Kamm; M Swash
Journal:  Int J Colorectal Dis       Date:  1993-03       Impact factor: 2.571

3.  Cystitis increases colorectal afferent sensitivity in the mouse.

Authors:  Pablo Rodolfo Brumovsky; Bin Feng; Linjing Xu; Carly Jane McCarthy; G F Gebhart
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2009-09-24       Impact factor: 4.052

4.  Monitoring salivary amylase activity is useful for providing timely analgesia under sedation.

Authors:  Masaya Uesato; Yoshihiro Nabeya; Takashi Akai; Masahito Inoue; Yoshiyuki Watanabe; Daisuke Horibe; Hiroshi Kawahira; Hideki Hayashi; Hisahiro Matsubara
Journal:  World J Gastrointest Endosc       Date:  2014-06-16

5.  Abnormal perception of visceral pain in response to gastric distension in chronic idiopathic dyspepsia. The irritable stomach syndrome.

Authors:  M Lémann; J P Dederding; B Flourié; C Franchisseur; J C Rambaud; R Jian
Journal:  Dig Dis Sci       Date:  1991-09       Impact factor: 3.199

Review 6.  Pain management: physiopathology, future research and endpoints.

Authors:  M Sosnowski
Journal:  Support Care Cancer       Date:  1993-03       Impact factor: 3.603

7.  Modulation of visceral nociception, inflammation and gastric mucosal injury by cinnarizine.

Authors:  Omar M E Abdel-Salam
Journal:  Drug Target Insights       Date:  2007-02-12
  7 in total

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