Parietal and cingulate processes in central pain. A combined positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) study of an unusual case

Abstract

Parietal, insular and anterior cingulate cortices are involved in the processing of noxious inputs and genesis of pain sensation. Parietal lesions may generate central pain by mechanisms generally assumed to involve the 'medial' pain system (i.e. medial thalamic nuclei and anterior cingulate cortex (ACC)). We report here PET and fMRI data in a patient who developed central pain and allodynia in her left side after a bifocal infarct involving both the right parietal cortex (SI and SII) and the right ACC (Brodmann areas 24 and 32), thus questioning the schematic representation of cortical pain processing. No rCBF increase was found in any part of the residual cingulate cortices, neither in the basal state (which included spontaneous pain and extended hypoperfusion around the infarct), nor during left allodynic pain. Thus, as previously observed in patients with lateral medullary infarct, neither spontaneous pain nor allodynia reproduce the cingulate activation observed after noxious pain in normal subjects. Conversely, both PET and fMRI data argue in favour of plastic changes in the 'lateral discriminative' pain system. Particularly, allodynia was associated with increased activity anteriorly to the infarct in the right insula/SII cortex. This response is likely to be responsible for the strange and very unpleasant allodynic sensation elicited on the left side by a non-noxious stimulation.

Transcranial Direct Current Stimulation Targeting Primary Motor Versus Dorsolateral Prefrontal Cortices: Proof-of-Concept Study Investigating Functional Connectivity of Thalamocortical Networks Specific to Sensory-Affective Information Processing

“…2A). We chose to stimulate the right hemisphere in our right-handed participants because evidence suggests that pain matrix is mainly lateralized to the right hemisphere, although networks across both hemispheres constitute the pain matrix (Casey, 1999;Peyron et al, 2000) irrespective of the side affected by pain (Borckardt et al, 2012;Symonds et al, 2006).…”

Insula-specific responses induced by dental pain. A proton magnetic resonance spectroscopy study

“…Brain-specific mechanisms of experimentally induced acute pain have already been described in several studies, inter alia with the assistance of functional magnetic resonance imaging (fMRI), neuroelectrophysiological and neurosurgical procedures [1][2][3][4][5][6][7][8]. Structures involved in processing the multidimensional aspect of pain perception are often summarised with the term "pain matrix", and include several regions consistently found within investigations [1,8,9], hence accommodating the complex neurosignature pattern of pain [10].…”

Deconstructing Central Pain with Psychophysical and Neuroimaging Studies

“…As noted above, a PET study of patients with Wallenburg strokes did not find activation of the ACC in response to stimuli which produced allodynia (Peyron et al, 1998), although such activation is often found in response to acute pain stimuli in healthy controls (Apkarian et al, 2005;Lenz et al, 2010). A combined PET and fMRI study of a unique patient with strokes of both the ACC and parietal cortex demonstrated cold allodynia, in the absence of hyperactivity in the remaining ACC (Peyron et al, 2000). In contrast, one fMRI study of a patient with CPSP resulting from a stroke of the posterolateral thalamus and adjacent internal capsule found activation of the ACC, the posterior parietal cortex, and the putamen during allodynia evoked by a cool stimulus (Seghier et al, 2005).…”