Topographical features of cutaneous tactile hypoesthetic and hyperesthetic abnormalities in chronic pain

Moriwaki, Katsuyuki; Yuge, Osafumi

doi:10.1016/s0304-3959(98)00257-7

Cited by 69 publications

(46 citation statements)

References 32 publications

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“…Thus, DLPFC atrophy may lead to a disruption of its control over orbitofrontal activity, which in turn is critical in the perception of negative affect in general (Small, 2002;Goel and Dolan, 2003) and particularly in pain states (Price, 2000;Apkarian et al, 2004b). Thalamic atrophy in CBP is important, because it is a major source of nociceptive inputs to the cortex (although the peak decrease in gray matter seems more anterior than the medial thalamic target of spinothalamic terminations), and damage to this region may be a reason for the generalized sensory abnormalities commonly associated with chronic pain (Moriwaki and Yuge, 1999;Rommel et al, 2001;Fishbain et al, 2003;Giesecke et al, 2004). Moreover, the thalamic atrophy that we observe provides an explanation for repeated reports of decreased baseline and stimulus-evoked activity and for abnormal chemistry within the thalamus for diverse chronic pain states (Apkarian et al, 2004b).…”

Section: Discussionmentioning

confidence: 99%

Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density

Apkarian¹,

Sosa²,

Sonty³

et al. 2004

J. Neurosci.

1,217

853

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The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10 -20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm 3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.

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Section: Discussionmentioning

confidence: 99%

Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density

Apkarian¹,

Sosa²,

Sonty³

et al. 2004

J. Neurosci.

1,217

853

View full text Add to dashboard Cite

show abstract

“…For example, chronic pain is commonly associated with reduced tactile sensitivity (Moriwaki and Yuge, 1999;Moseley, 2008;Pleger et al, 2006) and disorganization in the somatosensory cortex Maihöfner et al, 2003;Tecchio et al, 2002). Moreover, tactile discrimination training, which should promote organized somatosensory maps, reduces chronic pain (Flor et al, 2001;Moseley et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Congruency of body-related information induces somatosensory reorganization

Cardini

Longo

2016

Neuropsychologia

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Chronic pain and impaired tactile sensitivity are frequently associated with "blurred" representations in the somatosensory cortex. The factors that produce such somatosensory blurring, however, remain poorly understood. We manipulated visuotactile congruence to investigate its role in promoting somatosensory reorganization.To this aim we used the mirror box illusion that produced in participants the subjective feeling of looking directly at their left hand, though they were seeing the reflection of their right hand. Simultaneous touches were applied to the middle or ring finger of each hand. In one session, the same fingers were touched (for example both middle fingers), producing a congruent percept; in the other session different fingers were touched, producing an incongruent percept. In the somatosensory system, 3

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“…Mirror-image pain occurs in chronic pain conditions, including reflex sympathetic dystrophy (Maleki et al, 2000), causalgia (Shir and Seltzer, 1991), atypical facial pain (Woda and Pionchon, 2000), idiopathic facial arthromyalgia (Woda and Pionchon, 2000), and stomatodynia (Woda and Pionchon, 2000). It is typically characterized by mechanical allodynia (Moriwaki and Yuge, 1999;Baron, 2000). That is, mirror-image pain is perceived in response to light touch/ pressure stimuli such as clothing and bed sheets (Slart et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

et al. 2003

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Mirror-image allodynia is a mysterious phenomenon that occurs in association with many clinical pain syndromes. Allodynia refers to pain in response to light touch/pressure stimuli, which normally are perceived as innocuous. Mirror-image allodynia arises from the healthy body region contralateral to the actual site of trauma/inflammation. Virtually nothing is known about the mechanisms underlying such pain. A recently developed animal model of inflammatory neuropathy reliably produces mirror-image allodynia, thus allowing this pain phenomenon to be analyzed. In this sciatic inflammatory neuropathy (SIN) model, decreased response threshold to tactile stimuli (mechanical allodynia) develops in rats after microinjection of immune activators around one healthy sciatic nerve at mid-thigh level. Low level immune activation produces unilateral allodynia ipsilateral to the site of sciatic inflammation; more intense immune activation produces bilateral (ipsilateral ϩ mirror image) allodynia. The present studies demonstrate that both ipsilateral and mirrorimage SIN-induced allodynias are (1) reversed by intrathecal (peri-spinal) delivery of fluorocitrate, a glial metabolic inhibitor; (2) prevented and reversed by intrathecal CNI-1493, an inhibitor of p38 mitogen-activated kinases implicated in proinflammatory cytokine production and signaling; and (3) prevented or reversed by intrathecal proinflammatory cytokine antagonists specific for interleukin-1, tumor necrosis factor, or interleukin-6. Reversal of ipsilateral and mirror-image allodynias was rapid and complete even when SIN was maintained constantly for 2 weeks before proinflammatory cytokine antagonist administration. These results provide the first evidence that ipsilateral and mirror-image inflammatory neuropathy pain are created both acutely and chronically through glial and proinflammatory cytokine actions.

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Topographical features of cutaneous tactile hypoesthetic and hyperesthetic abnormalities in chronic pain

Cited by 69 publications

References 32 publications

Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density

Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density

Congruency of body-related information induces somatosensory reorganization

Spinal Glia and Proinflammatory Cytokines Mediate Mirror-Image Neuropathic Pain in Rats

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