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AllodyniaClassification and external resources
DiseasesDB
30788
Allodynia, meaning "other pain", is a painful (noxious) response to a usually non-painful (innocuous) stimulus and can be either static or mechanical. Allodynia differs from referred pain, but can occur in areas other than the one stimulated. It is dysesthetic. Allodynia is different from hyperalgesia, an extreme reaction to a stimulus which is normally painful.
Contents
1 Types
2 Causes
3 Pathophysiology
3.1 Pathophysiology at the cellular level
3.2 Pathophysiology at the molecular level
4 Treatment
4.1 Endogenous body mechanisms for reducing pain
4.2 Drugs
5 References
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Types
There are different kinds or types of allodynia:
Mechanical allodynia (also known as tactile allodynia)
Static mechanical allodynia pain in response to light touch/pressure
Dynamic mechanical allodynia pain in response to brushing[1]
Thermal (hot or cold) allodynia pain from normally mild skin temperatures in the affected area
Causes
Allodynia is a clinical feature of many painful conditions, such as neuropathies, postherpetic neuralgia, fibromyalgia, and migraine. Allodynia may also be caused by some populations of stem cells used to treat nerve damage including spinal cord injury.[2]
Pathophysiology
Pathophysiology at the cellular level
The cell types involved in nociception and mechanical sensation are the cells responsible for allodynia. In healthy individuals, nociceptors sense information about cell stress or damage and temperature at the skin and transmit it to the spinal cord. The cell bodies of these neurons lie in dorsal root ganglia, important structures located on both sides of the spinal cord. The axons then pass through the dorsal horn to make connections with secondary neurons. The secondary neurons cross over to the other (contralateral) side of the spinal cord and reach nuclei of the thalamus. From there, the information is carried through one or more neurons to the somatosensory cortex of the brain. Mechanoreceptors follow the same general pathway. However, they do not cross over at the level of the spinal cord, but at the thalamus instead. In addition, they are grouped in tracts that are spatially distinct from the nociceptive tracts.
Despite this anatomical separation, mechanoreceptors can influence the output of nociceptors by making connections with the same interneurons, the activation of which can reduce or completely eliminate the sensation of pain. Another way to modulate the transmission of pain information is via descending fibers from the brain. These fibers act through different interneurons to block the transmission of information from the nociceptrors to secondary neurons.[3]
Both of these mechanisms for pain modulation have been implicated in the pathology of allodynia. Several studies suggest that injury to the spinal cord might lead to loss and re-organization of the nociceptrors, mechanoreceptors and interneurons, leading to the transmission of pain information by mechanoreceptors[4][5] A different study reports the appearance of descending fibers at the injury site.[6] All of these changes ultimately affect the circuitry inside the spinal cord, and the altered balance of signals probably leads to the intense sensation of pain associated with allodynia.
Different cell types have also been linked to allodynia. For example, there are reports that microglia in the thalamus might contribute to allodynia by changing the properties of the secondary nociceptors.[7] The same effect is achieved in the spinal cord by the recruitment of immune system cells such as monocytes/macrophages and T lymphocytes.[8]
Pathophysiology at the molecular level
There is a strong body of evidence that the so called sensitization of the central nervous system contributes to the appearance of allodynia. Sensitization refers to the increased response of neurons following repetitive stimulation. In addition to repeated activity, the increased levels of certain compounds lead to sensitization, as well. The work of many researchers has led to the elucidation of pathways that can result in neuronal sensitization both in the thalamus and dorsal horns. Both pathways depend on the production of chemokines and other molecules important in the inflammatory response.
A very important molecule in the thalamus appears to be cysteine-cysteine chemokine ligand 21 (CCL21). The concentration of this chemokine is increased in the ventral posterolateral nucleus of the thalamus where secondary nociceptive neurons make connections with other neurons. The source of CCL21 is not exactly known, but two possibilities exist. First, it might be made in primary nociceptive neurons and transported up to the thalamus. Most likely, neurons intrinsic to the ventral posterolateral...(and so on)