Innovations In Clinical Neuroscience

MAY-JUN 2017

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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Innovations in CLINICAL NEUROSCIENCE [ V O L U M E 1 4 , N U M B E R 5 – 6 , M A Y – J U N E 2 0 1 7 ] 15 by a cerebral lesion causing subsequent s pontaneous firing of damaged neurons. Injury to the area of the brain supplied by the middle cerebral artery, internal capsule, or thalamus—and even the parietal lobe in one patient—has been s hown to cause contralateral pruritus. 1 1 Additionally, multiple imaging studies of human brains have shown several cortical regions that are significantly involved in the perception of itch. In these studies, the primary and secondary somatosensory cortices (S1, S2), the insula and anterior cingulate cortex (ACC) and prefrontal cortex (PFC) were frequently activated, commonly in a bilateral manner. Activation of the ACC and insula reflects the affective and emotional elements of the itch experience, with linkage to the limbic system and areas regulating evaluative functions and decision-making, such as the dorsolateral prefrontal cortex (DLPFC). 29,30 Regions of the brain involved in memory retrieval, visuospatial processing, and self-awareness, such as the precuneus (medial parietal cortex), are activated by the sensation of itch more significantly than during pain processing. The claustrum, a discrete gray matter area connected to many areas of the cortex with a role in the analysis, comparison, and integration of sensory information, has recently been shown to be involved in itch processing. Premotor, motor, and supplementary motor areas as well as the cerebellum are also involved in controlling actual or planned scratching. The activation of both the premotor cortex and supplementary motor area (SMA) areas occurred in most studies, even when the act of scratching itself was prohibited. 30 Areas of the midbrain involved in the reward system, such as the ventral tegmentum (VTA), substantia nigra, and nucleus accumbens (NAc), and its connections to the insula, ACC, and striatum might contribute to the urge to scratch and the relief provided by scratching, as summarized in Table 2. 29 BRAIN PROCESSING OF NAUSEA Once nausea is recognized, sustained brain activation is demonstrated in a broader network of interoceptive (e.g., stomach awareness), limbic, somatosensory, and cognitive processing brain areas. A correlation analysis demonstrated that subjects who had greater anterior insula activation on neuroimaging following transition to strong nausea also demonstrated greater activation in midcingulate cortex. 3 1 This finding suggests a closer linkage between these specific regions within the brain circuitry supporting the perception of nausea. These results are consistent with the characterization of nausea as a multidimensional perceptual state encompassing interoceptive, emotional, and cognitive domains. 31 GI sensation elicited by inflated balloon distention has facilitated mapping of visceral interoceptive circuits, which most consistently show activation of the anterior and posterior insula, as well as midcingulate cortex. However, it should be noted that visceral balloon inflation stimuli typically produce pain sensations instead of nausea. Thus, while interoception from the esophagus and stomach likely play an important role in the perception of nausea, such afferent signals might be necessary but are not sufficient to produce nausea. 31 Previous studies have reported that higher-level stimuli (e.g., visual scenes of vomiting) could induce emotional disgust and nausea via activation of the anterior insula and midcingulate cortex. These structures have also been implicated in salience detection, which relates to assigning homeostatic relevance for both internal and external sensory inputs to the brain. Hence, we can further postulate that nausea emerges from activation in a broad brain network that includes salience-processing regions, which alter interoceptive signaling in order to alert the suffering individual to enact the appropriate autonomic/motor response. 31 Increasing sustained activation common to affective/emotional circuitries was also noted in perigenual (pg) ACC, OFC, NAcc, and VTA. These structures likely support the aversive nature of nausea, and the OFC in particular might attribute hedonic valence to interoceptive afference. The pgACC is an important subregion of the ACC that is also strongly related to emotion. 31 Brain activity in bilateral prefrontal cortical regions (PFC), especially dorsolateral, demonstrated sustained TABLE 1. Summary of major pain-related brain areas BRAIN AREA FUNCTION R ostral anterior cingulate cortex (rACC) P ain modulation (inhibitory), response selection, reward associated with pain relief Amygdala A defense mechanism involved in recruitment of descending inhibition Periaqueductal grey (PAG) Receives projections from ACC and amygdala, pain modulation (inhibitory) Primary (S1) and secondary (S2) somatosensory cortices Coding intensity and location of pain Hippocampus Aversive drive and motivational dimension of pain Orbitofrontal cortex (OFC) Evaluation of noxious events and motivation to respond, central for placebo analgesia, anticipation of pain relief Insula Interoception, relaying sensory information to the limbic system, autonomic regulation

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