A pain response occurs even when the conscious feeling of pain is absent
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Peer-reviewed research shows that brain activity related to pain can increase without altering conscious pain perception, though sources do not fully establish that a pain response occurs when conscious feeling is absent altogether.
Pain is a complex and subjective experience often associated with noxious stimulation. However, in the past several decades it has become clear that the central nervous system can augment or even cause pain in the absence of noxious input. For some individuals, the most common cause of pain is related to altered central nervous system function and collectively referred to as chronic overlapping pain conditions (COPCs). Together, these conditions are characterized by diffuse hyperalgesia (an elevated response to painful stimuli) and allodynia (perception of pain for non-noxious stimuli), in addition to sleep disturbances, fatigue, and mood disorders. Moreover, many chronic pain patients also have increased sensitivity to multiple sensory stimuli, that include light suggesting a global dysfunction in sensory processing. This dissertation aims to examine intrinsic network alterations in the central nervous system in fibromyalgia (FM), a prototypical chronic pain condition, and determine how aberrant visual processing may be associated with sensory hypersensitivity in chronic pain conditions. Neuroimaging has enhanced our understanding of the neural correlates of pain. Pain processing in the CNS normally occurs via ascending and descending nociceptive pathways that integrate in several brain regions to include the insular cortex. Resting state functional MRI has shown aberrant intrinsic functional connectivity among chronic pain patients between the insula and the Default Mode Ne
Understanding how hydration status influences pain perception is particularly important in older adults, as both dehydration and pain are prevalent in this population. Ten individuals (70 ± 4 years) completed two randomized and counterbalanced trials. They were exposed to passive heat until they lost 1% body mass through sweat and urine (~ 100 min), with the loss either unreplaced (sham infusion, HYPO) or fully replaced via 0.45% saline infusion (EUH). Nociceptive electrical stimulation was applied to the sural nerve (1) before heat exposure (baseline), (2) 60 min following hydration manipulation (R60, ~ 160 min after baseline); (3) after mouth rinsing with water (MR, ~ 170 min after baseline) and; (4) following water ingestion (ING, ~ 185 min after baseline). Pain-related event-related potentials were assessed using electroencephalography (EEG) at R60, MR, and ING. After hydration manipulation, body mass loss and plasma osmolality were greater, and plasma volumes was lower in HYPO compared to EUH, although thirst did not differ between the conditions. There were no differences between the two conditions regarding pain intensity and unpleasantness. Still, EEG analyses revealed that the peak-to-peak amplitude of the pain-related N200-P300 potential (~ 136 - 310 ms) was significantly greater in HYPO compared to EUH (p = 0.036), and significantly greater in R60 compared to both MR (p = 0.01) and ING (p = 0.03), either with HYPO and EUH. These results suggest that mild hypohydration in healthy older adults may influence some neurophysiological processes related to nociception without significantly affecting pain perception.
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