We may have cancer and feel good, or be submitted to substantial disability and suffering without doctors finding any evidence of disease. Medicine gives no acceptable answers to the last situation and arbitrarily appeals to denying the reality of suffering, making the calvary of patients even more unbearable. This blog tries to contribute with the knowledge of the neuronal network, giving a little light to this confusing section of pathology.
Wednesday, March 16, 2011
Receptors of consummated or imminent necrosis
There are no pain receptors. Only perceptors, ie, suffering, receiving, addressee individuals of that hurting event that arises from the brain to catch your attention and behavioral involvement in a threat assessment. Danger! Pain!
What DO exist are the ones called NOCI-CEPTORS by Nobel Laureate Charles Sherrington: noxiousness detectors. That was back in 1906.
Nociceptors are neurons that specialize in the detection of states and agents with a violent destructive capacity: extreme temperatures, mechanical energy that’s higher than the physical strength of tissues, acids, lack of oxygen ... Danger-detecting neurons are distributed over the surface and inside of the body and on their terminals they have receptors or sensors of dangerous stimuli. The receptors are proteins embedded in the membrane that, when contacting with a noxious agent, suffer a transformation that leads to the opening of a channel through which ions enter, ie, an electrical current. This electrical signal is transmitted to various processing centers and contains information on risk in a particular point. The danger may be mechanical, thermal or chemical.
Under normal conditions, nociceptors are only stimulated with what violently destroys tissues. If there are no extreme temperatures, acids, low oxygen or destructive mechanical stimuli, no signal is generated. There are no alerts of damage projected to the brain. Usually, the projection of pain doesn’t arise from the brain. The alarm doesn’t go off.
When a noxious agent has destroyed tissue, the dead cells (necrosated) release molecules that induce a change in the sensitivity of nociceptors. They make them respond to innocuous stimuli. Touching a wound generates a signal in sensitized nociceptors. Information on activated nociceptors reaches the brain and the brain projects pain on that area. While proceeding to repair the injury, the area is sensitive, with the population of nociceptors adapted to the state of vulnerability.
As the injury is being repaired, nociceptors go back to their basal state and innocuous stimuli stop generating signals. The brain is no longer informed with news of danger. The brain doesn’t project pain, it warns. The individual resumes normal activity. End of the repair process. Tissues in condition to be used. Innocuous stimuli no longer activate the nociceptors.
Nociceptors respond to local, real, actual danger at that time and place. If there is necrosis (violent cell death) or if it’s about to happen if the conditions don’t change inmediately, (I quickly move my hand away of the burning pan) the danger and consummated necrosis sensors generate a signal and, predictably, this will be enough to activate the perception of pain from the brain.
Nociceptors also respond to the prediction of danger from the various processing centers. The indication of warning, vulnerability, can be generated from above, memory and prediction systems and induce sensitization. Innocuous stimuli will generate a signal of nociceptors even when nothing dangerous is happening.
The central alert states, activated by threat assessment in the absence of consummate or imminent harm, facilitate the traffic and generation of nociceptor signals. The pain is projected from the brain in advance with no need of prior injury notifications. There is only prediction. Enough to activate perceptive messages of pain.
The central alert ends up sensitizing all the layers of processing, from the nociceptors to the conscious individual (the receptor of pain). There are warning signals everywhere. From the individual (“it hurts me”) to the sensitized nociceptor that generates a damage signal without damage.
The pain only certifies an assessment of danger. It doesn’t certify damage and the danger assessment doesn’t have to be correct.
There is erroneous inflammation (allergy) and erroneous pain (migraine, fibromyalgia...). Nociceptors in erroneous pain are sensitized.
It doesn’t hurt because there are sensitized nociceptors in the erroneous pain. It’s not the nociceptors that are wrong and have been activated for no reason. It hurts because the nociceptive system as a whole has generated a condition assessed as threatening. This includes global sensitization.
Sometimes it’s all about the facts, the burn, infection, lack of oxygen, consummated or inminent necrosis. Other times it’s about memories, fears, uncertainty, misinformation, unjustified neuronal alarmism.
The professional must assess both factors: vulnerable tissues and/or sensitizing brains and try to deactivate alarms, giving back the normal condition to the tissues and a reasonable confidence to the assessment centers.
The goal is not analgesia at any price, but the recovery of the integrity and body management from a reasonable management of danger.
Maintaining the security of the building with a chronically turned on alarm makes no sense.
Neither does disabling the siren to generate the fiction that if it doesn’t sound, there are no thieves.
The nociceptor is not a pain receptor, whoever says so...
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