Neuroscience
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An accumulating body of evidence suggests that the hypothalamic neuropeptide oxytocin (OT) has a modulatory effect on pain processing. Particularly strong evidence comes from animal models. Here, we review recent advances in animal research on the analgesic effects of OT and discuss possible target sites of OT within descending and ascending pain pathways in the brain. ⋯ Moreover, we also address how OT might alleviate pain by influencing socio-emotional components in humans. We conclude that further investigating specific OT and OT-sensitive circuits, which modulate pain processing especially in primates, will improve our understanding of OT-analgesic effects. In human research, the increased use of neuroimaging and autonomic measures might help to bridge the gap to animal studies.
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The transmission of noxious stimuli from peripheral receptors to the cortex involves multiple central ascending pathways. While projections to areas in the brainstem and diencephalon are likely involved in mediating the immediate behavioral responses to pain, the assessment of the sensory and emotional/motivational components of pain are likely processed in parallel ascending pathways that relay in the thalamus on their way to the cerebral cortex. ⋯ In addition, we outline experimental animal and human evidence of functional, anatomical and biochemical alterations in thalamocortical circuits that may be responsible for altered thalamocortical rhythms and the persistent presence of pain following nervous system damage. Finally, we discuss advances in clinical and preclinical development of chronic pain treatments aimed at altering neural and glial function.
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In the understanding of chronic pain, hypotheses derived from psychological theories, together with insights from physiological assessments and brain imaging, highlight the importance of mechanistically driven approaches. Physical system changes, for example following injury, can result in alterations of psychological processes and are accompanied by changes in corticolimbic circuits, which have been shown to be essential in emotional learning and memory, as well as reward processing and related behavior. In the present review, we thus highlight the importance of motivational, reward/pain relief, and fear learning processes in the context of chronic pain and discuss the potential of a mechanistic understanding of chronic pain within a clinical perspective, for example for the development of therapeutic strategies. We argue that changes in these mechanisms are not only characteristic for chronic pain, reflecting consequences of the disorder, but are also critically involved in the transition from acute to chronic pain states.
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Cortical reorganization has been proposed as a major factor involved in phantom pain with prior nociceptive input to the deafferented region and input from the non-deafferented cortex creating neuronal activity that is perceived as phantom pain. There is substantial evidence that these processes play a role in neuropathic pain, although causal evidence is lacking. Recently it has been suggested that a maintenance of the cortical representation of the former hand area is related to phantom pain. ⋯ Although often introduced as contradictory, we suggest that cortical reorganization, preserved limb function and peripheral factors interact to create the various painful and nonpainful aspects of the phantom limb experience. In addition, the type of task (sensory versus motor), the interaction of injury- and use-dependent plasticity, the type of data analysis, contextual factors such as the body representation and psychological variables determine the outcome and need to be considered in models of phantom limb pain. Longitudinal studies are needed to determine the formation of the phantom pain experience.
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A 62-year-old diabetologist diagnosed himself to have diabetes type-2, with an HbA1c of 9.5. Five months after lifestyle intervention and a multi-drug approach, HbA1c was 6.3, systolic blood pressure was below 135mmHg and BMI reduced to 27. But he suffered from severe painful diabetic neuropathy. ⋯ Are there imaging techniques helpful for the diagnosis of this diabetic complication, starting in the distal nerve endings of the foot and slowly moving ahead? 5. Can you suggest any drug, specific and effective, for relieving painful diabetic neuropathy? This review will use the experts' answers to the questions of the diabetologist, not only to give a summary of the current knowledge, but even more to highlight areas of research needed for improving the fate of patients with painful diabetic neuropathy. Based on the unknowns, which exceed the knowns in diabetic neuropathy, a quest for more public support of research is made.