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.
Common Errors in the Evaluation of Allodynia
It is important to bear in mind that allodynia can refer either to pain at a location other than the area where a nonpainful stimulus is applied, or more commonly, dysesthetic pain resulting from a nonpainful stimulus.
- Situation: Physician asks whether patient ever feels pain in an area other than the area being stimulated. Patient replies in the negative.
- Error: Patients with Central Pain have such poor localization they often are unaware of this kind of allodynia. The proper technique is to apply phasic stimulation (rub) various areas of the body against something rough and ask the patient to pay attention to nearby areas for any dysesthetic burning.
- Situation: Physician observes that patient looks normal and so does not ask about allodynia.
- Error: Patients put their best foot forward when dealing with the medical profession. They often wear shoes or dress with more clothing than usual, with consequent agony, to avoid offending the physician over a state of undress. The physician should ask the patient if the touch of clothing causes burning. The physician should also note whether the patient has left areas of the body uncovered with clothing.
- Situation: Physician tests for allodynia by touching the skin with a cotton ball.
- Error: Allodynia is dysesthetic, which means it displays “slow summation”. Time is required for its display. Slow summation occurs much more rapidly with occlusive touch. Air circulation under the cotton ball makes it unsuitable for testing allodynia. It is also too gross to test subclinical loss of touch (von Frey hairs should be used). The physician should lay a piece of newspaper on the patient’s body and wait for a minute or so before asking if the patient feels pain.
- Situation: Physician tests for allodynia with an open safety pin.
- Error: Allodynia is pain from nonpainful stimulus. Pin prick is normally (nociceptively) painful and cannot test allodynia. What is being tested with pin prick is hyperpathia or overresponse to a painful stimulus. In Central Pain, hyperpathia displays “delay with overshoot”, meaning there is a diminished response initially due to the sensory loss, but as soon as the pain threshold is reached the response curve is very, very steep, making pin prick testing a true torture. Patients should not be tortured. Less sharp objects, such as a slightly blunted pin, should be used to evaluate hyperpathia. Hyperpathia usually increase proximally, the opposite of dysesthesia.
- Situation: Physician tests temperature sensibility with a cold or hot test tube of water.
- Error: This type of testing is too gross for Central Pain. The patient has a greatly narrowed range of comfortable temperatures. It is temperaturechange which most effectively initiates allodynia. Proper testing involves determining how many degrees difference in two test tubes (such as 4 degree. C) are required before a difference is perceived by the patient, under circumstances of varied ambient temperature at various reference points (e.g. sixty degrees F, seventy-two degrees F, and ninety degrees F).With time, the much narrowed thermal comfort range becomes reality to the Central Pain patient, who no longer comments on their increased sensitivity to temperature change nor their susceptibility to feeling pain from a sudden temperature change which would not be painful to people without Central Pain. Cold allodynia can be tested grossly by spraying room temperature (68-74 degree F) water on the skin with a spray bottle and watching for an overreaction, or questioning the patient about whether the spray was perceived as shocking or painful. Alternatively, the clinician may ask the patient whether a cold draft from a car air conditioner causes burning pain on the exposed part of the body.