The medial pain system, cingulate cortex, and parallel processing of nociceptive information

Vogt, Brent A.; Sikes, Robert W.

doi:10.1016/s0079-6123(08)62141-x

Cited by 192 publications

(139 citation statements)

References 56 publications

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“…Motivational-affective processing is associated primarily with nociceptive pathways ascending from the dorsal horn of the spinal cord through the medial thalamic nuclei, which send projections to the ACC (Craig, 2003;Devinsky et al, 1995;Vogt & Sikes, 2000). In the ACC, nociceptive neurons are interspersed among cells that code for the aversive value of the stimulus (Koyama, Kato, Tanaka, & Mikami, 2001;Porro et al, 2003).…”

Section: Vicarious Pain As a Motivational-affective Representationmentioning

confidence: 99%

Vicarious responses to pain in anterior cingulate cortex: Is empathy a multisensory issue?

Morrison

Lloyd

Pellegrino

et al. 2004

Cognitive, Affective, & Behavioral Neuroscience

437

261

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Results obtained with functional magnetic resonance imaging show that both feeling a moderately painful pinprick stimulus to the fingertips and witnessing another person's hand undergo similar stimulation are associated with common activity in a pain-related area in the right dorsal anterior cingulate cortex (ACC). Common activity in response to noxious tactile and visual stimulation was restricted to the right inferior Brodmann's area 24b. These results suggest a shared neural substrate for felt and seen pain for aversive ecological events happening to strangers and in the absence of overt symbolic cues. In contrast to ACC 24b, the primary somatosensory cortex showed significant activations in response to both noxious and innocuous tactile, but not visual, stimuli. The different response patterns in the two areas are consistent with the ACC's role in coding the motivational-affective dimension of pain, which is associated with the preparation of behavioral responses to aversive events.

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Section: Vicarious Pain As a Motivational-affective Representationmentioning

confidence: 99%

Vicarious responses to pain in anterior cingulate cortex: Is empathy a multisensory issue?

Morrison

Lloyd

Pellegrino

et al. 2004

Cognitive, Affective, & Behavioral Neuroscience

437

261

View full text Add to dashboard Cite

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“…It has been proposed that the cortex may reduce pain by interrupting the transmission of noxious information from the spinal cord level by activating descending pain modulatory systems located in the brainstem [6] . Recent studies have shown that the anterior cingulate cortex (ACC), the insular cortex, the primary (SI) and secondary (SII) somatosensory cortices, the ventrolateral orbital cortex (VLO) and the motor cortex are involved in pain modulation [3][4][5][7][8][9][10][11] . These cortical structures constitute, respectively, the medial and lateral pain systems, the nucleus submedius (Sm)-VLO-periaqueductal gray (PAG) system and the motor cortex system [3][4][5][7][8][9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that the anterior cingulate cortex (ACC), the insular cortex, the primary (SI) and secondary (SII) somatosensory cortices, the ventrolateral orbital cortex (VLO) and the motor cortex are involved in pain modulation [3][4][5][7][8][9][10][11] . These cortical structures constitute, respectively, the medial and lateral pain systems, the nucleus submedius (Sm)-VLO-periaqueductal gray (PAG) system and the motor cortex system [3][4][5][7][8][9][10][11] . Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine transmitters, are involved in the modulation of pain by these cortical structures [11][12][13][14][15] .…”

Section: Introductionmentioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary (SΙ) and secondary somatosensory (SΠ) cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.

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“…In patients with CPSP, it is proposed that a lesion of this pathway disinhibits a proposed medial STT pain-signaling pathway projecting to anterior cingulate cortex (ACC) via the medial dorsal nucleus (Craig, 2000) (cf. Vogt and Sikes, 2000). According to this hypothesis, lesions of VMpo lead to cold hypoesthesia and to the disinhibition of the ACC, which results in the burning pain of CPSP.…”

Section: Introductionmentioning

confidence: 99%

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

et al. 2007

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Central pain is neuropathic pain resulting from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)]. Lesions involving the posterior thalamus lead to reduction or loss of sensation and to CPSP, although the responsible nuclei have not been identified. We now examine the hypotheses that thalamic lesions must extend posterior to the ventral caudal nucleus (Vc) and include ventral medial posterior nucleus (VMpo), to result in loss of cold sensibility and CPSP. Patients with small thalamic strokes associated with CPSP were evaluated by atlas-based mapping of magnetic resonance imaging scans, and by somatosensory testing. All lesions involved posterior Vc; two lesions also involved nuclei posterior to Vc, but not VMpo. All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von Frey hairs. Three patients had altered cool sensation, and the patient with the least involvement of Vc had normal cool thresholds, suggesting that a critical volume of Vc must be involved before cool sensation is impaired. Perception of warm was impaired only in lesions involving nuclei posterior to Vc. Heat pain perception was never affected. In a subject with cold allodynia, a single-subject protocol PET study measured the responses to immersion of either hand in a 20°C waterbath. The scan during stimulation of the affected hand was characterized by intense activation of contralateral sensorimotor cortex. Therefore, there are modality-specific subnuclear structures in the posterior thalamus, but lesions of Vc not involving VMpo are sufficient to impair cold sensibility and to produce CPSP.

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The medial pain system, cingulate cortex, and parallel processing of nociceptive information

Cited by 192 publications

References 56 publications

Vicarious responses to pain in anterior cingulate cortex: Is empathy a multisensory issue?

Vicarious responses to pain in anterior cingulate cortex: Is empathy a multisensory issue?

Cerebral cortex modulation of pain

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

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