Why do CP patients seek a cool ambient temperature, but avoid cold blasts? New work may have answers
Many patients with dysesthetic spinothalamic burning in CP find a narrow window for “comfort”. They seek a cooler than normal room temperature but dread a cold blast, such as that from a car air conditioner on the legs. This back and forth on cold can induce skepticism from the observer who demands to know, “Which is it? Hot or cold causing your pain?” Like many other questions, the CP sufferer cannot answer this challenge, until now.
Many neurotransmitters may be considered either excitatory or inhibitory. However, it is important to understand that the nature of the neurotransmitter is not nearly so important as the nature of the receptor, since one neurotransmitter may cause different results, depending on the receptor it reaches. In Central Pain, the receptor activating C fiber pain is thought to be the VR1 Ca2+ receptor, which is also known as the capsaicin receptor.
The capsaicin receptor, VR1, is known to release CGRP, an inflammatory peptide 37 amino acids in length, which causes pain. CP patients have long indicated that skin cooling helps the burning dysesthesia. Studies show that cooling of skin inhibits VR1 activity and inhibits CGRP release (excitatory to pain) until the temperature drops to where cold pain fibers kick in.
This process would be expected to be exaggerated in the hyperpathic state of CP. The window of comfortable temperature is narrowed. Not every CP patients is neuropathic to temperature, but many are.
In June Pain Petho et al attributed noxious heat transduction to the Capsaicin receptor (VR1), but also to the release of CGRP (calcitonin gene related peptide). However, blocking the VR1 receptor with capsazepine, an antagonist of capsaicin, did not stop noxious heat signaling.
The apparent unlinking of cold hypoalgesia and cold allodynia means it is likely that the mixed pattern of thermal hyperalgesia/thermal discrimination in humans, which is reported here, involves separate pathways. Thus, we can accept clinical histories comfortably in CP both from those WITH thermal hyperalgesia, as well as those WITHOUT thermal hyperalgesia.
As scientific notes, these studies may not seem earthshaking, but to CP patients constantly being challenged by others to justify the temperature accomodations to their illness, this study is most welcome. (See Pain, July 2004, Kuchko et al.)
F.A. Lenz has long been a distinguished researcher of nerve injury pain and we have cited him elsewhre. Thus, we credit the article by Greenspan, Lenz et al in Pain June 2004. Studying those with post-stroke central pain, Greenspan found that cold allodynia is MORE likely to occur in those who retain normal cold sensing ability. Thus, the pathway for cold signaling is not the same as the one responsible for cold allydnia. Greenspan’s work is consistent with the surveys in the Wall/McHenry database.
Although most with cold allodynia have NOT had testing for cold hypoalgesia, the information from those who have been tested gives no consistent indication that cold signalling has been altered. This is ocnsistent with Trigg’s finding that those with bright lesions on MRI tend to have no sensation, rather than central pain. CP is an INCOMPLETE injury.
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allodynia=pain from a stimulus which is not painful to normals
hypoalgesia=diminished perception of pain stimulus
CGRP=calcitonin gene related peptide, a pain neuropeptide released by the VR1 receptor
VR1 receptor=the receptors in C fibers which are associated with chronic pain
