Peripheral Sensitisation
- Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!
- If you would like to get involved in this project and earn accreditation for your contributions, please get in touch!
Tips for writing this page:
- Describe the physiological processes underlying peripheral sensitisation
- What is the purpose of peripheral sensitisation and how might it impact upon the pain experience?
Original Editor - Add a link to your Physiopedia profile here.
Top Contributors - Michelle Lee, Shaimaa Eldib, Melissa Coetsee, Admin, Jo Etherton, Bruno Serra, Khloud Shreif and Mathius Kassagga
Pathophysiology of Peripheral Sensitization[edit | edit source]
Following an injury or cell damage two main things can occur. Primary hyperalgesia and seconday hyperalgesia. Secondary hyperalgesia is indicitive of central sensitization.
Peripheral sensitization is an increased sensitivity to an afferent nerve stimuli. This occurs after there has been an injury or cell damage to the area, and produces a flare response due to nocioceptors producing lots of neuropeptides. This then results in an increased sensitivity to heat and touch stimuli which is referred to as primary hyperalgesia or primary allodynia if the stimulus was not a painful one prior to the injury. For example a gentle storke to the skin which before the injury is not painful but after is interpreted as pain.
There are 2 forms of peripheral sensitisation:
1. Upregulation of existing receptors:
This can occur as a result of imnflammation. Chemical mediators of imflammation such as histamine, bradykinn, acids and seratonin are released and can either stimulate them making them depolorize or sensitize them (brining the membrane potential closer to the depolorisation threshold). This infulence on the threshold is known as peripheral sensitization. This occurs when the chemical mediators stimulate the receptors on the nocioceptive terminals. This then influences the protein enzyme cascade which then upregulates the ion channels and sodium specific nocioceptive channels. This then results in them becoming more sensitive to the chemical mediators and causes an influx of ions. This influx of ions then cause the stimulation of action potentials which then in turn produces 'pain.'
2.
Sub Heading 2[edit | edit source]
Add text here...
Sub Heading 3
[edit | edit source]
Add text here...
References[edit | edit source]
References will automatically be added here, see adding references tutorial.
