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Impaired trigeminal nociceptive processing in patients with trigeminal neuralgia

Impaired trigeminal nociceptive processing in patients with trigeminal neuralgia
Impaired trigeminal nociceptive processing in patients with trigeminal neuralgia
Background: Trigeminal neuralgia (TN) usually leads to paroxysms of short lasting but very severe pain. Between the attacks the patient is usually asymptomatic, but a constant dull background pain may persist in some cases. The mechanisms associated with the development of this chronic pain are not well understood. Objective: To determine trigeminal nociceptive fiber impairment in patients with TN comparing symptomatic and nonsymptomatic sides using the nociceptive blink reflex (nBR) and pain-related evoked potentials (PREP) and to identify possible central mechanisms of pain chronicity. Methods: We investigated 24 patients with TN without and 18 patients with TN with concomitant chronic facial pain. PREP and nBR were investigated following nociception specific electrical stimulation on both sides of the face and in each division of the trigeminal nerve (V1, V2, and V3). Results: We found prolonged PREP and nBR latencies and reduced amplitudes comparing symptomatic and nonsymptomatic sides in all patients with TN. In patients with chronic facial pain, however, PREP amplitudes were larger and latencies shorter compared to patients with TN without facial pain, while nBR results were similar across groups. Conclusion: The data suggest an impairment of the trigeminal nociceptive system due to demyelination and/or axonal dysfunction on the symptomatic side and locate this defect close to the root entry zone in the brainstem. Moreover, central facilitation of trigeminal nociceptive processing was observed in patients with trigeminal neuralgia with concomitant chronic facial pain indicating overactivation of central sensory transmission. This may represent a possible adaptive mechanism for the development of chronic pain
mechanisms, cortical reorganization, tension-type headache, stimulation, central sensitization, carbamazepine, impairment, evoked-potentials, migraine, phantom-limb pain, dysfunction, system, blink reflex
0028-3878
835-841
Obermann, M.
cc1138d3-5491-4788-ba43-02982aa5f2f1
Yoon, M.S.
3dc63ba8-cb06-4624-bd89-466b16fbcf86
Ese, D.
49097354-4579-45d3-a29d-d8a780e3628a
Maschke, M.
0bd9b588-6978-4778-a839-5bdaec1dc2c7
Kaube, H.
77be5a18-5ca2-4d97-b90c-0ba9bf978f6d
Diener, H.C.
7df1797f-31a6-4f72-8632-a1d3a8e54bd6
Katsarava, Z.
2c88871f-d7a7-4424-a9d5-51f2234d1c92
Obermann, M.
cc1138d3-5491-4788-ba43-02982aa5f2f1
Yoon, M.S.
3dc63ba8-cb06-4624-bd89-466b16fbcf86
Ese, D.
49097354-4579-45d3-a29d-d8a780e3628a
Maschke, M.
0bd9b588-6978-4778-a839-5bdaec1dc2c7
Kaube, H.
77be5a18-5ca2-4d97-b90c-0ba9bf978f6d
Diener, H.C.
7df1797f-31a6-4f72-8632-a1d3a8e54bd6
Katsarava, Z.
2c88871f-d7a7-4424-a9d5-51f2234d1c92

Obermann, M., Yoon, M.S., Ese, D., Maschke, M., Kaube, H., Diener, H.C. and Katsarava, Z. (2007) Impaired trigeminal nociceptive processing in patients with trigeminal neuralgia. Neurology, 69 (9), 835-841.

Record type: Article

Abstract

Background: Trigeminal neuralgia (TN) usually leads to paroxysms of short lasting but very severe pain. Between the attacks the patient is usually asymptomatic, but a constant dull background pain may persist in some cases. The mechanisms associated with the development of this chronic pain are not well understood. Objective: To determine trigeminal nociceptive fiber impairment in patients with TN comparing symptomatic and nonsymptomatic sides using the nociceptive blink reflex (nBR) and pain-related evoked potentials (PREP) and to identify possible central mechanisms of pain chronicity. Methods: We investigated 24 patients with TN without and 18 patients with TN with concomitant chronic facial pain. PREP and nBR were investigated following nociception specific electrical stimulation on both sides of the face and in each division of the trigeminal nerve (V1, V2, and V3). Results: We found prolonged PREP and nBR latencies and reduced amplitudes comparing symptomatic and nonsymptomatic sides in all patients with TN. In patients with chronic facial pain, however, PREP amplitudes were larger and latencies shorter compared to patients with TN without facial pain, while nBR results were similar across groups. Conclusion: The data suggest an impairment of the trigeminal nociceptive system due to demyelination and/or axonal dysfunction on the symptomatic side and locate this defect close to the root entry zone in the brainstem. Moreover, central facilitation of trigeminal nociceptive processing was observed in patients with trigeminal neuralgia with concomitant chronic facial pain indicating overactivation of central sensory transmission. This may represent a possible adaptive mechanism for the development of chronic pain

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More information

Published date: 2007
Keywords: mechanisms, cortical reorganization, tension-type headache, stimulation, central sensitization, carbamazepine, impairment, evoked-potentials, migraine, phantom-limb pain, dysfunction, system, blink reflex

Identifiers

Local EPrints ID: 62528
URI: http://eprints.soton.ac.uk/id/eprint/62528
ISSN: 0028-3878
PURE UUID: dedebac2-eeea-48c9-b645-bc50084c9e5a

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Date deposited: 12 Sep 2008
Last modified: 26 Apr 2022 21:41

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Contributors

Author: M. Obermann
Author: M.S. Yoon
Author: D. Ese
Author: M. Maschke
Author: H. Kaube
Author: H.C. Diener
Author: Z. Katsarava

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