Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy

Simon Haroutiunian; Lone Nikolajsen; Thomas F Bendtsen; Nanna B Finnerup; Anders D Kristensen; Jørgen B Hasselstrøm; Troels S Jensen

doi:10.1016/j.pain.2014.03.022

Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy

Simon Haroutiunian, Lone Nikolajsen, Thomas F Bendtsen, Nanna B Finnerup, Anders D Kristensen, Jørgen B Hasselstrøm, Troels S Jensen

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

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Abstract

Central sensitization following peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (seven with unilateral foot pain due to peripheral nerve injury and seven with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients presented with sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10 min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (± 31.7%), and reduced mechanical and thermal hypersensitivity in most patients who displayed such signs, but the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrates that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.

Original language	English
Journal	Pain
Volume	155
Issue	7
Pages (from-to)	1272-1279
ISSN	0304-3959
DOIs	https://doi.org/10.1016/j.pain.2014.03.022
Publication status	Published - 2014

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10.1016/j.pain.2014.03.022

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title = "Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy",

abstract = "Central sensitization following peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (seven with unilateral foot pain due to peripheral nerve injury and seven with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients presented with sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10 min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (± 31.7%), and reduced mechanical and thermal hypersensitivity in most patients who displayed such signs, but the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrates that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.",

author = "Simon Haroutiunian and Lone Nikolajsen and Bendtsen, {Thomas F} and Finnerup, {Nanna B} and Kristensen, {Anders D} and Hasselstr{\o}m, {J{\o}rgen B} and Jensen, {Troels S}",

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AU - Haroutiunian, Simon

AU - Nikolajsen, Lone

AU - Bendtsen, Thomas F

AU - Finnerup, Nanna B

AU - Kristensen, Anders D

AU - Hasselstrøm, Jørgen B

AU - Jensen, Troels S

N1 - Epub 2 April 2014.

PY - 2014

Y1 - 2014

N2 - Central sensitization following peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (seven with unilateral foot pain due to peripheral nerve injury and seven with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients presented with sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10 min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (± 31.7%), and reduced mechanical and thermal hypersensitivity in most patients who displayed such signs, but the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrates that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.

AB - Central sensitization following peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (seven with unilateral foot pain due to peripheral nerve injury and seven with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients presented with sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10 min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (± 31.7%), and reduced mechanical and thermal hypersensitivity in most patients who displayed such signs, but the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrates that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.

U2 - 10.1016/j.pain.2014.03.022

DO - 10.1016/j.pain.2014.03.022

M3 - Journal article

C2 - 24704366

SN - 0304-3959

VL - 155

SP - 1272

EP - 1279

JO - Pain

JF - Pain

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ER -

Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy

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