Mechanical allodynia (other pain) is a painful sensation caused by innocuous stimuli like light touch.
Unlike inflammatory hyperalgesia that has a protective role, allodynia has no obvious biological utility.
Allodynia is associated with nerve damage in conditions such as diabetes, and is likely to become an increasing clinical problem.
Unfortunately, the mechanistic basis of this enhanced sensitivity is incompletely understood.
From Wikipedia: Allodynia refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation.
Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.
Allodynia is different from hyperalgesia, an extreme, exaggerated reaction to a stimulus which is normally painful.
In this review, we describe evidence for the involvement of candidate mechanosensitive channels such as Piezo2 and their role in allodynia, as well as the peripheral and central nervous system mechanisms that have also been implicated in this form of pain.
Specific treatments that block allodynia could be very useful if the cell and molecular basis of the condition could be determined.
There are many potential mechanisms underlying this condition ranging from
- alterations in mechanotransduction and
- sensory neuron excitability to
- the actions of inflammatory mediators and
- wiring changes in the CNS.
- As with other pain conditions, it is likely that the range of redundant mechanisms that cause allodynia will make therapeutic intervention problematic.
The body of this article gives many details on this phenomenon, which you can peruse using these direct links to parts of the article:
Conclusions and future prospects
Strategies for dealing with allodynia fall into four broad categories.
- First, identifying and blocking the mediators that sensitise mechanosensory neurons within the peripheral and central nervous system has had some success. In particular, a number of mediators released from activated microglia such as BDNF, as well as various cytokines and NGF all play a role in regulating mechanosensitivity and are potential targets.
- Secondly,blocking the mechanotransducing channels themselves may be attractive when we finally have a complete list of the molecules involved. As yet, only Piezo2 has been shown to have a potential role in allodynia.
- Thirdly, attacking electrical excitability in the peripheral neurons that are implicated in allodynia may be useful. A number of pharmacological treatments have been described that diminish allodynia in animal models through sodium channel block, including conotoxin sodium channel-selective blockers that target Nav1.7 and Nav1.8 and limits mechanical hyperalgesia and allodynia .
- Finally, dismantling the aberrant circuitry that has been linked to allodynia is a potential, if exceptionally complex approach to the problem
It is clear that allodynia results from peripheral drive involving subsets of neurons that are not classical nociceptors, and the sympathetic nervous system plays an important role in some allodynic syndromes