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Endogenous pain control mechanisms: Review and hypothesis

Sickle cell pain includes three types: acute recurrent painful crises, chronic pain syndromes and neuropathic pain. The acute painful crisis is the hallmark of the disease and the most common cause of hospitalization and treatment in the Emergency Department. It evolves through four phases: prodromal, initial, established and resolving. Each acute painful episode is associated with inflammation that worsens with recurrent episodes, often culminating in serious complications and organ damage such as acute chest syndrome, multi-organ failure and sudden death. Three pathophysiologic events operate in unison during the prodromal phase of the crisis: vaso-occlusion, inflammation and nociception. Aborting the acute painful episode at the prodromal phase could potentially prevent or minimize tissue damage. Our hypothesis is that managing these events with hydration, anti-inflammatory drugs, aggressive analgesia and possibly vasodilators could abort the crisis and prevent or minimize further damage. Chronic pain syndromes are associated with or accompany avascular necrosis and leg ulcers. Neuropathic pain is not well studied in patients with sickle cell disease but has been modeled in the transgenic sickle mouse. Management of sickle cell pain should be based on its own pathophysiologic mechanisms rather than borrowing guidelines from other non-sickle pain syndromes.

Endogenous pain control mechanisms: Review …

To our knowledge, this is the first study to uncover that differential Pavlovian (i.e. respondent) conditioning is able to activate endogenous ‘pain inhibits pain’-like mechanisms. Associative learning processes thus seem to have the capacity to sustain HNCS-induced hypoalgesia. Our results do indeed show that after repeatedly associating a tonic noxious stimulus (i.e. cold water bath, HNCS) with a differential acoustic stimulation, the paired auditory cue (CS+) was able to attenuate the electrically induced pain sensations in the test group. This decrease in pain sensitivity was accompanied by a reduction of corrugator supercilious muscle activity. This finding is reminiscent of a previous work by Flor and co-workers describing successful classical conditioning of stress-induced analgesia and inherent opioid release.

Glossary | Linus Pauling Institute | Oregon State University

Recent imaging studies have shown that in addition to classically described spinal cord-brainstem loops, brain areas like the ACC and the amygdala are also involved in pain modulation evoked by HNCS , . Consequently, the implication of these brain structures in both learning , , , and pain modulation processes corroborates the hypothesized relationship between the endogenous pain control systems and associative learning of cues from an individual’s environment. Traditionally, learning processes have been claimed to be involved in the development and maintenance of pain and of pain-related behavior (for review see ). In contrast, the present study is devoted to the potential impact of learning on pain inhibition and hence on the potential usefulness of conditioning procedures for the treatment of pain states. Whereas Flor and co-workers investigated the influence of learning on stress-induced analgesia, we focused on HNCS-activated inhibition of nociceptive processing which proved to be a handy tool to assess endogenous pain control systems in both experimental , , and clinical , settings. The strong learning effects that we identified point to a potential relevance for the development of novel psychological treatment strategies. Further support for this notion may be derived from persisting effects of stimulation procedures like acupuncture or TENS. The positive therapeutic effect of these techniques has been discussed to result from DNIC-like processes . But since DNIC generally last for periods of several minutes , associative learning effects probably partially mediate the repeatedly proven, long-lasting therapeutic efficacy of acupuncture and TENS , .

DNIC-related analgesia was originally studied in animals by focusing mainly on spino-bulbo-spinal pathways , . More recently, functional magnetic resonance imaging (fMRI) studies in humans have shown that cerebral structures like the anterior cingulate cortex and the amygdala contribute to HNCS-induced hypoalgesia , . Interestingly, these limbic regions have also been found to be involved in learning processes , . It is thus conceivable that endogenous pain control systems may be influenced by cues from the environment that have been acquired through associative conditioning. The finding that stress-induced analgesia can be successfully conditioned provides further support for the assumption that associative learning processes may influence pain processing mechanisms and hence possibly play a role in the development of chronic pain (for review see ).

Mechanisms of Hypoglycemia-Associated Autonomic …

Endogenous pain control systems include mechanisms like descending inhibition, stress-induced analgesia and diffuse noxious inhibitory controls (DNIC) . In humans, DNIC has also been referred to as counter-irritation analgesia or conditioned pain modulation . It relates to the fact that pain present in one region of the body may be attenuated by an additional pain stimulus applied to another body region. Classically, DNIC appears upon heterotopic noxious counter-stimulation (HNCS) and is increasingly used as a model to study human endogenous pain control mechanisms in both experimental , , and clinical studies , .

Since the nocifensive RIII flexion reflex has repeatedly been assessed in studies on the DNIC phenomenon , , , we included it as a second objective indicator of nociceptive processing. In line with the cited previous findings, we also found a reduction of RIII-related EMG activity upon HNCS. In response to the post-conditioning CS+ presentation however, attenuations of withdrawal reflex responses were observed both in the test group and in the control group. Furthermore, the CS– induced reductions in the RIII reflex activity of the test group were quite similar to those provoked by CS+ stimulations. We can thus conclude that, contrary to our initial hypothesis, respondent conditioning had no significant influence on the RIII flexion reflex. The successful conditioning of pain perception and corrugator muscle activation and the lack of conditioning effects on RIII reflex amplitudes observed in the present study may be related to differential neural circuitry involved in the respective reactions. The nocifensive RIII reflex is known to depend mainly on segmental spinal processing to ensure rapid and reliable withdrawal from noxious stimuli . Accordingly, it was found to be unchanged in paraplegic patients . Corrugator muscle activity and pain sensitivity are more significantly governed by higher order brain structures like prefrontal and cingulate cortical areas and the amygdala , , which are also heavily involved in learning processes and in emotional regulation. It thus seems plausible that these structures provided a more suitable substrate for Pavlovian conditioning.

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Nox Enzymes and New Thinking on Reactive Oxygen: A …

Heterotopic noxious counter-stimulation (HNCS) is commonly used to study endogenous pain control systems. The resulting pain inhibition is primarily based on spinal cord-brainstem loops. Recently, functional imaging studies have shown that limbic structures like the anterior cingulate cortex and amygdala are also implicated. Since these structures are involved in learning processes, it is possible that the HNCS-induced pain inhibition may depend on specific cues from the environment that have been associated with pain reduction through associative learning. We investigated the influence of Pavlovian conditioning on HNCS-induced pain inhibition in 32 healthy subjects by using a differential conditioning paradigm in which two different acoustic stimuli were either repeatedly paired or unpaired with HNCS. Series of noxious electrical pulse trains delivered to the non-dominant foot served as test stimuli. Diffuse noxious inhibitory control (DNIC)-like effects were induced by concurrent application of tonic HNCS (immersion of the contralateral hand in ice water). Subjective pain intensity and pain unpleasantness ratings and electromyographic recordings of the facial corrugator muscle and the nocifensive RIII flexion reflex were used to measure changes in pain sensitivity. HNCS induced significant pain and reflex inhibitions. In the post-conditioning phase, only the paired auditory cue was able to significantly reduce pain perceptions and corrugator muscle activity. No conditioned effect could be observed in RIII reflex responses. Our results indicate that the functional state of endogenous pain control systems may depend on associative learning processes that, like in the present study, may lead to an attenuation of pain perception. Similar albeit opposite conditioning of pain control mechanisms may significantly be involved in the exacerbation and chronification of pain states.

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