Trix,
Do some web research on the allodynia. It has to do with the c-nociceptive and non-nociceptive primary afferent neurones, and A-beta low threshold mechanoreceptors...Dr. Togut's meeting explanations.....

Allodynia
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Allodynia, meaning "other pain", is an exaggerated response to otherwise non-noxious stimuli and can be either static or mechanical. Allodynia is not referred pain and can occur in other areas that are not stimulated; it is also dysesthetic.

For example, a person with Allodynia may perceive light pressure or the movement of clothes over the skin as painful, whereas a "normal" individual will not feel pain.

One explanation of the mechanism for Allodynia is that the associated nerve damage results in decreased firing thresholds of nociceptive fibres.

Alternatively, it has been postulated that peripheral nerve injury could induce collateral sprouting of non-nociceptive primary afferent neurones, such as A-beta low threshold mechanoreceptors, into the superficial (nociceptive) laminae in the dorsal horn of the spinal cord. These collateral branches could form functional contacts with nociceptive second order neurones, normally innervated by C-fibre nociceptive primary afferent neurones and transmit an innocous input as noxious.
There are different kinds of Allodynia:

Mechanical allodynia (also known as tactile allodynia) - Pain from light touch/pressure applied to the skin in the area of the damaged nerve.
Thermal allodynia - Pain from normally mild skin temperatures in the affected area.

PainFrom Wikipedia, the free encyclopedia
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Look up Pain in Wiktionary, the free dictionary.For other uses, see Pain (disambiguation).
Pain is an unpleasant feeling which may be associated with actual or potential tissue damage and which may have physical and emotional components. According to the International Association for the Study of Pain (IASP), one should distinguish between pain and nociception[1]. The word "pain" comes from the Latin: poena meaning punishment, a fine, a penalty.

The term "pain" is a subjective experience that typically accompanies nociception, but can also arise without any stimulus, and thus includes the emotional response. Nociception, on the other hand, is a neurophysiological term and denotes specific activity in nerve pathways. It is the transmission mechanism for physiological pain, and does not describe psychological pain. These pathways transmit the nominally "painful" signals, though they are not always perceived as painful. Although pain can be associated with tissue damage or inflammation, this is often not the case.

Despite its causing suffering, pain is a critical component of the body's defense system. It is part of a rapid warning relay instructing the motor neurons of the central nervous system to minimize detected physical harm. Lack of the ability to experience pain, as in the rare condition Congenital insensitivity to pain or Congenital Analgesia, can cause various health problems.

The two most common forms of pain reported in the U.S. are headache and back pain. Pain is also a term specifically used to denote a painful uterine contraction occurring in childbirth.


An example of touch allodynia is pain from the touch of clothing. Thermal allodynia occurs from a draft of warm or cold air on the skin. The March 17, 1997 issue of Newsweek describes a patient who dreaded the breeze from a ceiling fan because it felt like razors cutting his flesh.

A good example of location allodynia is pain in the right ulnar forearm from a rough scratch on the patient's palm from whiskers on the right side of the face. If a physician demonstrates or presumes physical relocation of the pain signal, it is also proper to use the term ephapse, so literature may refer to this as either location allodynia or as ephapse.

Clinicians report ephapse in perhaps one percent of patients with Central Pain. Diligent testing may demonstrate ephapse or location allodynia in many patients that are unaware they have it. The quickest way to test for ephapse is to rub the palm of the hand (glabrous skin) against something rough, such as whiskers or a piece of sandpaper. Demonstration of an ephapse often requires prior sensitization by heat, followed by vigorous prickly scratching, or having the patient rub a dysesthetic hand or limb against something rough-textured.

Thermally-sensitized skin more dramatically and more easily demonstrates ephaptic phenomenon. Many Central Pain patients tested carefully this way demonstrate an ephapse or location allodynia. Almost no patients volunteer it on their own. One patient with very marked and reproducible ephapse did not recognize its presence after five years with the disease. Because there is such poor localization of sensation distally, the patient tends not to pay much attention to such matters.

Anatomically, it is unclear to what extent Devor's work on the ability of injured sensory neurons to humorally induce firing in surrounding fibers encompasses the phenomenon of an ephapse. Devor discovered crossed afterdischarge; the capacity of injured sensory neurons to induce passive autonomous firing in uninjured neighbor neurons. In such injury the entire axon may gain the power to behave as if it were a nerve ending. This earthshaking discovery ran contrary to long held theories of neurotransmission. Researchers believe that crossed afterdischarge is a humoral phenomenon, while ephapse refers to postulated physical phenomena involving proximity or direct contact between nerve fibers. (Wall 1994, Devor 1995)

Allodynic pain is dysesthetic, whereas hyperpathic pain is not. Ochoa reported a cold allodynia due to pure A-delta dysfunction separate from Central Pain. Since Central Pain involves transmissions from many different types of fibers, it is not clear whether the mechanisms are similar. Patients with Central Pain of the trigeminal area feel burning in the pulp of their teeth, but not in the dentin, which lacks C-fibers but does have A-fibers.