Neuroscience letters
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Neuroscience letters · Jun 2012
ReviewCerebral interactions of pain and reward and their relevance for chronic pain.
Pain and reward are opponent, interacting processes. Such interactions are enabled by neuroanatomical and neurochemical overlaps of brain systems that process pain and reward. Cerebral processing of hedonic ('liking') and motivational ('wanting') aspects of reward can be separated: the orbitofrontal cortex and opioids play an important role for the hedonic experience, and the ventral striatum and dopamine predominantly process motivation for reward. ⋯ Further, reward, including pain relief, leads to operant learning, which can affect pain sensitivity. Indirect evidence points at brain mechanisms that might underlie pain relief as a reward and related operant learning but studies are scarce. Investigating the cerebral systems underlying pain-reward interactions as well as related operant learning holds the potential of better understanding mechanisms that contribute to the development and maintenance of chronic pain, as detailed in the last section of this review.
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We briefly summarize recent advances regarding brain functional representation of chronic pain, reorganization of resting state brain activity, and of brain anatomy with chronic pain. Based on these observations and recent theoretical advances regarding network architecture properties, we develop a general concept of the dynamic interplay between anatomy and function as the brain progresses into persistent pain, and outline the role of mesolimbic learning mechanisms that are likely involved in maintenance of chronic pain.
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Neuroscience letters · Jun 2012
ReviewInsights gained into pain processing from patients with focal brain lesions.
The recognition that dissociated sensory loss affecting selectively pain and temperature results from lesions of the operculo-insular cortex is due to Biemond in 1956. This contrasted with the prevailing view that the sensory aspects of pain did not imply regions above the thalamus. ⋯ Operculo-insular pain (parasylvian pain) is a distinct entity that can be clinically suspected and objectively diagnosed with combined radiological and electrophysiological methods, in particular evoked potentials to spinothalamic (laser) input. The region comprising the posterior insula and medial operculum may deserve being considered as a third somatosensory cortex (S3) contributing to the spinothalamic attributes of somatic perception.
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Human brain imaging has provided much information about pain processing and pain modulation, but brain imaging in rodents can provide information not attainable in human studies. First, the short lifespan of rats and mice, as well as the ability to have homogenous genetics and environments, allows for longitudinal studies of the effects of chronic pain on the brain. Second, brain imaging in animals allows for the testing of central actions of novel pharmacological and nonpharmacological analgesics before they can be tested in humans. ⋯ Pharmacological imaging in rodents shows overlapping activation patterns with pain and opiate analgesics, similar to what is found in humans. Despite the many structural imaging studies in human chronic pain patients, only one study has been performed in rodents, but that study confirmed human findings of decreased cortical thickness associated with chronic pain. Future directions in rodent pain imaging include miniaturized PET for the freely moving animal, as well as new MRI techniques that enable ongoing chronic pain imaging.
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Neuroscience letters · Jun 2012
Brainstem facilitations and descending serotonergic controls contribute to visceral nociception but not pregabalin analgesia in rats.
Pro-nociceptive ON-cells in the rostral ventromedial medulla (RVM) facilitate nociceptive processing and contribute to descending serotonergic controls. We use RVM injections of neurotoxic dermorphin-saporin (Derm-SAP) in rats to evaluate the role of putative ON-cells, or μ-opioid receptor-expressing (MOR) neurones, in visceral pain processing. Our immunohistochemistry shows that intra-RVM Derm-SAP locally ablates a substantial proportion of MOR and serotonergic cells. ⋯ We measure visceromotor responses in the colorectal distension (CRD) model in control and Derm-SAP rats, and using the 5-HT(3) receptor antagonist ondansetron, we demonstrate pro-nociceptive serotonergic modulation of visceral nociception and a facilitatory drive from RVM MOR cells. The α(2)δ calcium channel ligand pregabalin produces state-dependent analgesia in neuropathy and osteoarthritis models relating to injury-specific interactions with serotonergic facilitations from RVM MOR cells. Although RVM MOR cells mediate noxious mechanical visceral input, we show that their presence is not a permissive factor for pregabalin analgesia in acute visceral pain.