Show Summary Details
Page of

The physiology of acute pain 

The physiology of acute pain
The physiology of acute pain

Lesley Bromley

Page of

PRINTED FROM OXFORD MEDICINE ONLINE ( © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 18 June 2021

Acute pain as a result of tissue damage is self-limiting.

Impulses are generated in primary sensory nerves by chemical mediators released from the damaged tissues.

The spinal cord receives these impulses in the dorsal horn.

At the level of the spinal cord, the impulses can be amplified or reduced in amplitude by descending inputs.

At the level of the spinal cord, the representation of the painful area and the sensitivity of other, surrounding areas can be modified.

At the level of the brainstem and thalamus, further modification can take place.

The final perception of the pain can be modified by other central phenomena such as anxiety and fear.

New imaging techniques have allowed a greater understanding of cortical representation of pain.

The role of the glia in maintaining painful states is evolving.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.