Supraspinal terminations of visceral input

Standard anatomical and electrophysiological tracing methods have established widespread distribution of visceral input to the brain. The axons of second-order spinal neurons that receive visceral input have been shown to ascend the spinal cord to the brain with sites of termination in the medulla, pons, mesencephalon, hypothalamus, and thalamus. Neurons excited by visceral stimuli have likewise been identified at these same sites with extensive characterizations of neurons located within the ventral posterolateral, dorsomedial, and submedius nuclei of the thalamus, the locus coeruleus, parabrachial nucleus, ventrolateral medulla, and numerous brain stem and limbic sites.36,37,3839,40,41,42 Higher-order neurons excited by visceral stimuli have also been demonstrated to be present in the somatosensory and ventrolateral orbital cerebral cortices.43,44,45 A lack of visceral sensation has been noted in neurosurgical patients who have sustained damage to their frontal lobes.46,4748

Functional imaging of humans during visceral stimulation has revealed some consistencies, but the most common finding is that there is a multitude of sites which demonstrate increased regional blood flow in response to visceral stimulation. Rectal distension and urinary bladder distension both produce increased bloodflow in select areas of the thalamus, hypothalamus, mesencephalon, pons, and medulla (for example, Ref. 49). Cortical sites of processing include the anterior and midcingulate cortex, the frontal and parietal cortices and in the cerebellum.50 The most illustrative imaging study to date comparing visceral pain sensation with cutaneous pain sensation is that of Strigo et al.51 These investigators matched the intensity of pain sensation produced by esophageal distension with that produced by heating of the skin overlying the sternum. Whereas both cutaneous and esophageal pain sensations were associated with activation of the secondary somatosensory cortex, the parietal cortex, the thalamus, basal ganglia, and cerebellum, there was a higher activation of the anterior insular cortex bilaterally when cutaneous stimuli were used and the esophageal stimulus selectively activated the ventrolateral prefrontal cortex. Esophageal pain produced a broader bilateral cortical activation and produced activation of a more anterior locus of the anterior cingulate cortex than cutaneous pain. This all suggests some shared components of sensation from the same segmental structures, but also a selective activation of some structures by different types of pain.

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