NeuroImage
-
Irritable bowel syndrome (IBS) is a highly prevalent gastrointestinal disorder that is often accompanied by both visceral and somatic hyperalgesia (enhanced pain from colorectal and somatic stimuli). Neural mechanisms of both types of hyperalgesia have been analyzed by neuroimaging studies of IBS patients and animal analog studies of "IBS-like" rats with delayed rectal and somatic hypersensitivity. Results from these studies suggest that pains associated with both visceral and widespread secondary cutaneous hyperalgesia are dynamically maintained by tonic impulse input from the non-inflamed colon and/or rectum and by brain-to-spinal cord facilitation. ⋯ Yet these forms of hyperalgesia are also highly modifiable by placebo and nocebo factors (e.g., expectations of relief or distress, respectively). Our working hypothesis is that synergistic interactions occur between placebo/nocebo factors and enhanced afferent processing so as to enhance, maintain, or reduce hyperalgesia in IBS. This explanatory model may be relevant to other persistent pain conditions.
-
Identifying brain systems that regulate or modulate autonomic nervous system functions may identify pathways through which psychosocial factors can influence health and disease. Reduced high-frequency heart rate variability (HF-HRV) characterizes anxiety disordered patients and is predictive of adverse myocardial events. Sex differences in the prevalence of anxiety disorders and cardiac diseases implicate the possibility of sex specific neural regulation of HF-HRV. ⋯ These findings underscore the importance of the emotional division of the anterior cingulate cortex, the prefrontal cortex and the striatum in cardiovagal activity. The study replicates and extends results from published functional neuroimaging studies on cardioregulatory or modulatory areas in healthy subjects to men and women with social phobia. Moreover, caudate functions, possibly related to dopaminergic neurotransmission, have sexually dimorphic effects on vagal modulation of the heart.
-
Interrupting a continuous noxious heat by a greater noxious heat causes rapid and disproportionate pain reduction when the original noxious heat returns. This reduction in pain experience, known as offset analgesia, is believed to be the consequence of active descending inhibitory control of pain originating in the periaqueductal grey (PAG) and rostral ventromedial medulla (RVM). To test this possibility, brain activation was measured using fMRI in twelve healthy controls during an offset procedure. ⋯ PAG/RVM activation was observed during the final 6 s of offset trials but not during either of the control trials and this difference across trials was significant. Activation throughout the pain neuromatrix was inhibited during the final 6 s of the offset trials and was comparable to the activation observed when the heat returned to a non-noxious baseline. These findings provide strong evidence that offset analgesia engages an endogenous inhibitory mechanism originating in the PAG/RVM region, which inhibits pain experience and activation of the pain neuromatrix.
-
In human conditions, chronic pain is associated with widespread anatomical changes in the brain. Nevertheless, little is known about the time course of these changes or the relationship of anatomical changes to perception and behaviour. In the present study, we use a rat model of neuropathic pain (spared nerve injury, SNI) and 7 T MRI to determine the longitudinal supraspinal changes associated with pain-like and anxiety-like behaviours. ⋯ There was also decreased volume in retrosplenial and entorhinal cortices. We also explored areas that correlated with mechanical hyperalgesia and found that increased hyperalgesia was associated with decreased volumes in bilateral S1 hindlimb area, anterior cingulate cortex (ACC, areas 32 and 24), and insula. Overall, our results suggest that long-term neuropathic pain has widespread effects on brain anatomy related to the duration and magnitude of the pain.