Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy

Elena Enax-Krumova; Nadine Attal; Didier Bouhassira; Rainer Freynhagen; Janne Gierthmühlen; Per Hansson; Bianca M. Kuehler; Christoph Maier; Juliane Sachau; Märta Segerdahl; Thomas Tölle; Rolf Detlef Treede; Lise Ventzel; Ralf Baron; Jan Vollert

doi:10.1212/WNL.0000000000012229

Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy

Elena Enax-Krumova, Nadine Attal, Didier Bouhassira, Rainer Freynhagen, Janne Gierthmühlen, Per Hansson, Bianca M. Kuehler, Christoph Maier, Juliane Sachau, Märta Segerdahl, Thomas Tölle, Rolf Detlef Treede, Lise Ventzel, Ralf Baron, Jan Vollert

Department of Clinical Medicine - The Danish Pain Research Center

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

22 Citations (Scopus)

Abstract

OBJECTIVE: To test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms. METHODS: We analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area. RESULTS: Among 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function. CONCLUSION: Mechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.

Original language	English
Journal	Neurology
Volume	97
Issue	4
Pages (from-to)	e389-e402
Number of pages	15
ISSN	0028-3878
DOIs	https://doi.org/10.1212/WNL.0000000000012229
Publication status	Published - Jul 2021

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Enax-Krumova, E., Attal, N., Bouhassira, D., Freynhagen, R., Gierthmühlen, J., Hansson, P., Kuehler, B. M., Maier, C., Sachau, J., Segerdahl, M., Tölle, T., Treede, R. D., Ventzel, L., Baron, R., & Vollert, J. (2021). Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy. Neurology, 97(4), e389-e402. https://doi.org/10.1212/WNL.0000000000012229

@article{e2c9d6d6a42b4d95bf6763f92e948561,

title = "Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy",

abstract = "OBJECTIVE: To test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms. METHODS: We analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area. RESULTS: Among 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function. CONCLUSION: Mechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.",

author = "Elena Enax-Krumova and Nadine Attal and Didier Bouhassira and Rainer Freynhagen and Janne Gierthm{\"u}hlen and Per Hansson and Kuehler, {Bianca M.} and Christoph Maier and Juliane Sachau and M{\"a}rta Segerdahl and Thomas T{\"o}lle and Treede, {Rolf Detlef} and Lise Ventzel and Ralf Baron and Jan Vollert",

note = "Publisher Copyright: {\textcopyright} 2021 American Academy of Neurology.",

year = "2021",

month = jul,

doi = "10.1212/WNL.0000000000012229",

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volume = "97",

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Enax-Krumova, E, Attal, N, Bouhassira, D, Freynhagen, R, Gierthmühlen, J, Hansson, P, Kuehler, BM, Maier, C, Sachau, J, Segerdahl, M, Tölle, T, Treede, RD, Ventzel, L, Baron, R & Vollert, J 2021, 'Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy', Neurology, vol. 97, no. 4, pp. e389-e402. https://doi.org/10.1212/WNL.0000000000012229

TY - JOUR

T1 - Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy

AU - Enax-Krumova, Elena

AU - Attal, Nadine

AU - Bouhassira, Didier

AU - Freynhagen, Rainer

AU - Gierthmühlen, Janne

AU - Hansson, Per

AU - Kuehler, Bianca M.

AU - Maier, Christoph

AU - Sachau, Juliane

AU - Segerdahl, Märta

AU - Tölle, Thomas

AU - Treede, Rolf Detlef

AU - Ventzel, Lise

AU - Baron, Ralf

AU - Vollert, Jan

PY - 2021/7

Y1 - 2021/7

N2 - OBJECTIVE: To test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms. METHODS: We analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area. RESULTS: Among 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function. CONCLUSION: Mechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.

AB - OBJECTIVE: To test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms. METHODS: We analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area. RESULTS: Among 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function. CONCLUSION: Mechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.

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U2 - 10.1212/WNL.0000000000012229

DO - 10.1212/WNL.0000000000012229

M3 - Journal article

C2 - 34011572

AN - SCOPUS:85112489034

SN - 0028-3878

VL - 97

SP - e389-e402

JO - Neurology

JF - Neurology

IS - 4

ER -

Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy

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