Whole‐body reversible neuropathic pain associated with right parieto‐temporal operculum single inflammatory lesion in a patient with multiple sclerosis: A case report

Abstract

Background The posterior insula and the medial parietal operculum (PIMO) are part of the pain network. Pain can be induced by direct stimulation of the PIMO, but the clinical consequence of lesions in this brain area is not well known. Case report We report the case of a patient with multiple sclerosis who presented a relapse characterized by isolated widespread neuropathic pain. The MRI displayed a single new inflammatory lesion in the juxta cortical white matter of the opercular region. This lesion was extended to the parietal operculum and was associated with the pain syndrome. The patient was treated with high‐dose intravenous methylprednisolone, and the pain disappeared progressively. Diffusion‐tensor MRI showed that some of the fibres passing through the lesion ended in the PIMO. Conclusion Based on diffusion‐tensor MRI we hypothesize that the partial disconnection from afference to the PIMO can lead to widespread neuropathic pain. Significance Most of the data concerning the functional role of the PIMO come from stereoelectroencephalography in presurgical evaluation of epilepsy, or from functional imaging (PET or fMRI). There is, however, very few data on the consequences of the lesion of the PIMO. Here, we report the first case of a transient widespread pain syndrome associated to a single, small and reversible inflammatory lesion of the PIMO. Thus, this case highlights the key role of the PIMO in spatial perception of pain.

Sensory and pain modulation profiles of ongoing central neuropathic extremity pain in multiple sclerosis

“…A new mechanism‐based classification has recently been proposed consisting of nine pain types, and the most frequent central neuropathic extremity pain was defined as ongoing extremity deafferentation pain secondary to lesions in the spinothalamocortical pathways (Truini et al., 2013). There are, however, other lesions outside the spinothalamocortical pathway, such as those in the parietal operculum, that may cause central neuropathic pain in MS (Poncet‐Megemont et al., 2019). Additional studies of the natural history, mechanisms and treatment of central neuropathic extremity pain have been recommended and are of immediate concern, since most of the published studies have not specifically focussed on this type of MS‐associated pain (O'Connor et al., 2008; Svendsen et al., 2005).…”

Risk factors of neuropathic pain in multiple sclerosis: a retrospective case-cohort study

“…These neurons project bilaterally to the superficial dorsal horn of the lumbosacral region, which may contribute to the occurrence of pain ( 26 ). In addition, from anatomical and pathophysiological perspective, lesions in the thalamus and parietal cortex are likely related to neuropathic pain and these association were verified by some studies ( 27 , 28 ). However, in our study, we didn’t find the association of parietal lobe lesions as well as the thalamic lesions with the neuropathic pain which should be investigated by further studies.…”

Unique features of central neuropathic pain in multiple sclerosis: Results of a cluster analysis

“…A sensory profile similar to that of Cluster 1 was reported for people with CNP due to other etiologies although not in all cases (e.gDefrin et al, 2001; Klit et al, 2011; Ofek & Defrin, 2007; Tuveson et al, 2009) and therefore may characterize a CNP subtype. MS lesions along the spinothalamic‐thalamocortical pathways, as well as in brain regions that receive their input, may lead to pathological processes in the vicinity of, and within, deafferented nociceptive neurons, and in turn, to CNP emergence (He et al, 2021; Poncet‐Megemont et al, 2019; Wu et al, 2013). Unexpectedly, however, poor pain inhibition did not characterize the CNP group in the cluster analysis, despite reports of poor inhibition among other CNP patients (Albu et al, 2015; Gruener et al, 2016, 2020; Naugle et al, 2020; Tuveson et al, 2009).…”