Fundamental Neuroscience for Basic and Clinical Applications: with STUDENT CONSULT Online Access (Haines,Fundamental Neuroscience for Basic and Clinical Applications) by Duane E. Haines

Author:Duane E. Haines [Haines, Duane E.]
Language: eng
Format: azw3
Publisher: Elsevier Health Sciences
Published: 2012-11-27T16:00:00+00:00

IMAGING OF THE PAIN PATHWAY

Electroencephalography (EEG), PET, fMRI, and magnetoencephalography (MEG) have provided insight into the localization of brain regions responsible for the processing of pain signals. EEG recordings show patterns of increased brain activity after the application of painful stimuli. This increased activity is especially prevalent in the somatosensory cortex and the frontal cortex.

When PET is used to identify changes in regional cerebral blood flow, painful stimuli are found to activate SI and SII cortices as well as the anterior cingulate cortex, the anterior insula, the supplemental motor area of motor cortex, and different thalamic nuclei. The cingulate cortex and the anterior insula are connected with nontraditional somatosensory brain regions, including the limbic cortex. This widespread cortical activation may provide a morphologic basis for integrating the location of painful stimuli with memory and emotion. PET has also been used to study possible gender differences in pain perception to noxious heat stimuli. Similar increases in cortical activation in the posterior insula and anterior cingulate cortex as well as in the cerebellar vermis have been described for both sexes. However, increases in the contralateral prefrontal cortex activity, contralateral insula, and thalamus noted in female subjects suggest that pain perception and processing may be different in males and females.

fMRI techniques reveal increased thalamic and cortical activation in response to application of innocuous (tactile, cool, and warm) and nociceptive (cold and hot) stimuli. Regions of increased activity in response to innocuous stimuli included the contralateral thalamus (VPL), posterior insula, and bilateral SII cortex. Application of innocuous thermal stimuli fails to activate SII. Painful thermal stimuli, however, activate the anterior insular cortex as well as the contralateral SII cortex.

With use of a carbon dioxide laser to activate Aδ and C nociceptors, MEG revealed that both the contralateral SI and bilateral SII cortices are involved in the processing of pain stimuli. These results support the view that SI provides a mechanism to code spatial, temporal, and intensity qualities of a painful stimulus. These various methods are providing a more complete identification of structures included in pain pathways and responsible for the processing of painful stimuli.

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