Pain System

Historically, the involvement of the cerebral cortex in the perception of pain (nociception) was an issue of controversy due to failure to elicit a painful response during stimulation of areas of the cortex as well as the lack of analgesia following cortical lesions. However, electrophysiological recording and neuroimaging techniques clearly indicate that numerous areas of the cerebral cortex do act synchronously to mediate the perception of pain and the responses to it. Such techniques have identified several cortical areas that are involved in nociception, including the primary and secondary somatosensory (SI and SII), the inferior and superior parietal, the insular, anterior cingulate, and medial prefrontal cortices.

There are believed to be two pathways, or streams, that mediate the perception of somatic pain, namely the medial and lateral pain pathways. The lateral pain pathway includes the ventral posterolateral and ventral posteromedial nuclei of the thalamus and their projections to SI of the parietal cortex. These thalamic nuclei and SI encode the type, temporal pattern, intensity, and topographic localization of a painful stimulus. Thus, the lateral pain pathway is believed to mediate the sensory-discriminate component of pain perception. Conversely, the medial pain pathway is thought to be concerned with the affective or emotional component of pain. Nociceptive information from the ventral posteroinferior, mediodorsal, and intralaminar nuclei of the thalamus is relayed to cortical areas such as SII, inferior parietal cortex, insular, anterior cingulate, and prefrontal cortices. The neurons in these areas generally have large, bilateral receptive fields and poor, or absent, somato-topic organization, consistent with their role in the affective-emotional dimension of pain perception.

Pain perception at the level of the cerebral cortex is complex and mediated by numerous interacting systems. For instance, all of the previously mentioned areas, particularly those involved in the affective-emotional component of pain processing, also have connections with diffuse areas of the limbic system and influence the ascending pain pathways. These connections likely mediate factors such as cognition, mood, and attention in response to a noxious stimulus.

There is an increasing amount of information regarding the neurochemistry of nociceptive connections at the cortical level. In the somatosensory cortices, excitatory amino acids acting on NMDA, AMPA, and metabotropic glutamate receptors likely mediate the transfer of nociceptive information from the thalamus to the cortex. In addition, there are large pools of GABAergic inhibitory interneurons in the sensory cortices that may modulate this transfer. Moreover, cytokines and neurotrophins may influence neurotransmission via glutamate NMDA and GABA receptors.

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