Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Referred pain
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
==Mechanism== There are several proposed mechanisms for referred pain.<ref>{{cite journal | title = Referred Pain | date=December 2009 | volume = 3 | issue = 2 | doi=10.1590/S1678-77572009000600001 | pmid = 20027423| pmc = 4327510 | doi-access = free | last1 = Murray | first1 = G. M. | journal = Journal of Applied Oral Science| pages=i }}</ref> Currently there is no definitive consensus regarding which is correct. The cardiac general visceral sensory pain fibers follow the sympathetics back to the [[spinal cord]] and have their cell bodies located in thoracic dorsal root ganglia 1-4(5). As a general rule, in the thorax and abdomen, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers. The [[central nervous system]] (CNS) perceives pain from the heart as coming from the somatic portion of the body supplied by the thoracic spinal cord segments 1-4(5). Classically the pain associated with a myocardial infarction is located in the mid or left side of the chest where the heart is actually located. The pain can radiate to the left side of the jaw and into the left arm. Myocardial infarction can rarely present as referred pain and this usually occurs in people with<ref name=mcrh>{{cite web|url=http://www.mcrh.org/Myocardial-Infarction/Myocardial_infarction_comes_with_referred_pain_radiating_pain_2010828.htm |title=Myocardial infarction comes with referred pain or radiating pain? |date=January 2, 2011 |access-date=December 26, 2011 }}</ref> [[diabetes]] or older age. Also, the [[Dermatome (anatomy)|dermatomes]] of this region of the body wall and upper limb have their neuronal cell bodies in the same dorsal root ganglia (T1-5) and synapse in the same second order neurons in the spinal cord segments (T1-5) as the general visceral sensory fibers from the heart. The CNS does not clearly discern whether the pain is coming from the body wall or from the viscera, but it perceives the pain as coming from somewhere on the body wall, i.e. substernal pain, left arm/hand pain, jaw pain.{{citation needed|date=February 2021}} ===Convergent-projection=== This represents one of the earliest theories on the subject of referred pain. It is based on the work of W.A. Sturge and J. Ross from 1888 and later TC Ruch in 1961. Convergent projection proposes that afferent nerve fibers from tissues converge onto the same spinal neuron, and explains why referred pain is believed to be segmented in much the same way as the spinal cord. Additionally, experimental evidence shows that when local pain (pain at the site of stimulation) is intensified the referred pain is intensified as well.{{citation needed|date=February 2021}} Criticism of this model arises from its inability to explain why there is a delay between the onset of referred pain after local pain stimulation. Experimental evidence also shows that referred pain is often unidirectional. For example, stimulated local pain in the anterior tibial muscle causes referred pain in the ventral portion of the ankle; however referred pain moving in the opposite direction has not been shown experimentally. Lastly, the threshold for the local pain stimulation and the referred pain stimulation are different, but according to this model they should both be the same.<ref name=ArendtNeilsen/> ===Convergence-facilitation=== Convergence facilitation was conceived in 1893 by J MacKenzie based on the ideas of Sturge and Ross. He believed that the internal organs were insensitive to stimuli. Furthermore, he believed that non-nociceptive afferent inputs to the [[spinal cord]] created what he termed "an irritable focus". This focus caused some stimuli to be perceived as referred pain. However, his ideas did not gain widespread acceptance from critics due to its dismissal of visceral pain.{{citation needed|date=February 2021}} Recently this idea has regained some credibility under a new term, central [[sensitization]]. Central sensitization occurs when neurons in the spinal cord's dorsal horn or brainstem become more responsive after repeated stimulation by peripheral neurons, so that weaker signals can trigger them. The delay in appearance of referred pain shown in laboratory experiments can be explained due to the time required to create the central sensitization.<ref name=ArendtNeilsen/> ===Axon-reflex=== Axon reflex suggests that the afferent fiber is bifurcated before connecting to the [[posterior horn of spinal cord|dorsal horn]]. Bifurcated fibers do exist in muscle, skin, and intervertebral discs. Yet these particular neurons are rare and are not representative of the whole body. Axon-Reflex also does not explain the time delay before the appearance of referred pain, threshold differences for stimulating local and referred pain, and somatosensory sensibility changes in the area of referred pain.<ref name=ArendtNeilsen/> ===Hyperexcitability=== Hyperexcitability hypothesizes that referred pain has no central mechanism. However, it does say that there is one central characteristic that predominates. Experiments involving noxious stimuli and recordings from the dorsal horn of animals revealed that referred pain sensations began minutes after muscle stimulation. Pain was felt in a receptive field that was some distance away from the original receptive field. According to hyperexcitability, new receptive fields are created as a result of the opening of latent convergent afferent fibers in the dorsal horn. This signal could then be perceived as referred pain.{{citation needed|date=February 2021}} Several characteristics are in line with this mechanism of referred pain, such as dependency on stimulus and the time delay in the appearance of referred pain as compared to local pain. However, the appearance of new receptive fields, which is interpreted to be referred pain, conflicts with the majority of experimental evidence from studies including studies of healthy individuals. Furthermore, referred pain generally appears within seconds in humans as opposed to minutes in animal models. Some scientists attribute this to a mechanism or influence downstream in the supraspinal pathways. Neuroimaging techniques such as [[Positron emission tomography|PET]] scans or [[fMRI]] may visualize the underlying neural processing pathways responsible in future testing.<ref name=ArendtNeilsen/> ===Thalamic-convergence=== Thalamic convergence suggests that referred pain is perceived as such due to the summation of neural inputs in the brain, as opposed to the spinal cord, from the injured area and the referred area. Experimental evidence on thalamic convergence is lacking. However, pain studies performed on monkeys revealed convergence of several pathways upon separate cortical and subcortical neurons.{{citation needed|date=February 2021}}
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)