Allodynia means "other pain". It refers to:
- Pain from stimuli which are not normally painful
- Pain which occurs other than in the area stimulated.
It is not synonymous with referred pain.
Allodynia of location transfer is not referred pain in the sense that referred pain
transfers to areas which represent embryonic position of the nerves. Rather it occurs in a
body part close to the stimulated area, but in such a location as to indicate either an
ephapse signal, or a translocated signal occurring in cord or brain. Clinicians use terms
such as detour or sidetrack in conjunction with location allodynia.
Literature does not differentiate well between the different types of allodynia
present in Central Pain. Some authors refer to one type as location allodynia while others
seem to regard all such phenomena as ephaptic. Physicians refer to pain from motion as
motion allodynia, and pain at ambient temperatures not unpleasant to the average person as
cold allodynia.
These usage's give allodynia a functional definition, without declaring an anatomical
one. They do not strictly differentiate allodynia from an ephapse; an anatomical term
referring to a proposed jumping of the pain signal around an area of damage onto a
neighboring neuron or nerve tract.
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.
So-called temperature reversal occurs with ciguatera poisoning. The term really should
be "cold reversal", since the patient feels cold as hot, but not hot as cold.
Central Pain, with its simultaneous presence of hot and cold dysesthesias, teaches us that
it is incorrect to conceive of heat as the embodiment of stimulus and cold as its mere
lack. The experience of Central Pain patients shows that to the CNS cold is not merely
heat at a lower level. Recent discoveries confirm that there are separate fibers for hot
and cold.
Free nerve endings are capable of responding to both heat and cold. Central Pain may
enhance this process. Researchers thought for a time that the discovery that free nerve
endings are capable of responding to both heat and cold disproved the view that Krause's
corpuscles register cold and Ruffini's corpuscles register heat. Evidence that undedicated
neurons may participate in non-typical types of transmission has been mounting Central
Pain suggests that highly sensitized fibers may be chemically "recruited" to act
in ways they normally would not. Parts of the neuron which normally cannot generate a pain
action potential may do this in Central Pain.
The number of neuron types is proliferating as research progresses, with neuron types
being split into subtypes. Even physiologic sensitization may affect different free nerve
endings differently. For example, people who don't suffer from Central Pain usually feel
more discomfort when their hands are hit while they are cold, and hands that hot are more
likely to feel clammy. Central Pain needs this kind of research at the neuron level as
well.
With Central Pain, temperature extremes or rapid changes in temperature quickly
sensitize dysesthetic skin to many stimuli, yet the dysesthetic perception is always
thermal, and always hot. The Central Pain patient can usually differentiate cold burn from
heat burn, but that may merely reflect the rudimentary or fragmentary retention of slight
sensory discrimination when the stimulus is sufficiently strong. Another way of saying
this is that while the pain apparatus is dysesthetic, residual sensory or cognitive clues
may allow the patient to distinguish hot from cold, when the temperature extreme is
marked.
Similarly, the patient may not be able to differentiate texture from heat when the
stimulus is low-grade. For example, the patient may be able to distinguish a hot stove
from sandpaper, but the suede inside shoe tongues, a texture stimulus, may simply feel
like heat. In this case, the sensitization/stimulus is performed by rubbing, but the
touching of sueded leather against the skin is perceived as heat, not as texture.
As another example, the Central Pain patient exposed to a cold draft will feel the cold
as a definite burn, but by cognitive reasoning may decide to treat the "cold
burn" with a warm shower. However, if the same shower is taken on a hot day, the warm
shower will eventually lead to slow summation and consequent greater susceptibility to
dysesthetic burning after it has relieved the burning due to prior skin cooling.
This is a complicated situation and difficult for the patient to explain to the doctor.
For unknown reasons, warm water and warm air are slower to evoke dysesthetic burning than
cold air or cold water.
The one-dimensional reading of both cold and hot as burning is termed "read only
burning" or R. O. B. pain.