Articles: chronic.
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While genetic influences on chronic pain have been repeatedly demonstrated, we do not know whether these effects are stable or dynamic over time. ⋯ The variability in chronic pain is mainly explained by new environmental factors influencing incidence, aggravation and/or chronic pain remission. Integration of these findings may provide a useful conceptual framework for the treatment and prevention of pain and pain chronification.
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Peripheral nerve injury causes maladaptive plasticity in the central nervous system and induces chronic pain. In addition to the injured limb, abnormal pain sensation can appear in the limb contralateral to the injury, called mirror image pain. Because synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in the induction of chronic pain, cortical reorganization in the S1 ipsilateral to the injured limb may also accompany mirror image pain. ⋯ When local inhibitory circuits were blocked, astrocyte-dependent spine plasticity and allodynia were revealed. Thus, we propose that cortical astrocytes prime the induction of spine plasticity and mirror image pain after peripheral nerve injury. Moreover, this result suggests that cortical synaptic rewiring could be sufficient to cause allodynia on the uninjured periphery.
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Persons with spinal cord injuries (SCIs) are frequent utilizers of emergency medical services but are a poorly understood and medically complex population. As the treatment of acute spinal cord injuries improves, there is a growing population of patients suffering from the chronic neurological deficits and altered homeostasis resulting from those injuries. ⋯ A SCI is a devastating but increasingly survivable event. The long-term care of persons with SCIs is challenging because of the unique pathologies encountered in this population and the disruption of normal and expected physiological responses to common ailments. This review will facilitate a better understanding of the emergency care needs of this unique patient population.
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One specific behavior can be synergistically modulated by different neural pathways. Medial septal (MS) cholinergic system innervates widespread cortical and subcortical regions and participates in pain modulation, but the underlying neural pathways are not fully understood. This study examined the contribution of MS cholinergic neurons and 2 neural pathways: MS-rostral anterior cingulate cortex (rACC) and MS-ventral hippocampal CA1 (vCA1), in modulating perceptual and affective pain behaviors in a mouse model of chronic inflammatory pain. ⋯ By contrast, chemogenetic activation of MS cholinergic neurons also produced analgesia, but by rescuing hypofunctional pyramidal neurons in vCA1. These results clearly demonstrate that the MS cholinergic system differentially modulates chronic inflammatory pain through MS-rACC or MS-vCA1 pathways. More significantly, our research provides evidence for a novel paradigm of neural circuit modulation: MS cholinergic inhibition and activation induce similar analgesia but through distinct neural pathways.