Afferent and spinal mechanisms of joint pain

Schaible, Hans‐Georg; Grubb, Blair D.

doi:10.1016/0304-3959(93)90183-p

Cited by 560 publications

(326 citation statements)

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“…The localized inflammatory condition appears, using neurophysiological criteria, to induce a similar type of receptor sensitization to that seen in rats with full polyarthritis (Grubb et al, 1988). The duration of the inflammatory lesion is restricted to between 2 and 4 weeks (see Schaible & Grubb, 1993). In the present work, the injection of Freund's adjuvant in one paw led to a unilateral, localized inflammation which reached its peak between 2 and 3 weeks, as already reported Donaldson et al, 1993 (Millan et al, 1987) and rats bearing a carrageenin-induced hindlimb inflammation (Hargreaves et al, 1988).…”

Section: Discussionmentioning

confidence: 92%

“…In the present study, the alternative method of unilateral intraplantar injection of a low dose of Freund's complete adjuvant into one hind paw of Lewis rats has been used. This method is known to produce the local acute reaction but limits or abolishes the development of the secondary phase such that secondary lesions do not occur (see Schaible & Grubb, 1993). The localized inflammatory condition appears, using neurophysiological criteria, to induce a similar type of receptor sensitization to that seen in rats with full polyarthritis (Grubb et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

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Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system

Malcangio

Bowery

1994

British J Pharmacology

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1 Monoarthritis was induced in Lewis rats by interdermal injection in the left hind paw of a suspension of Mycobacterium tubercolusis in mineral oil (500 jig 100 IW'). Controls were injected with 100 fil mineral oil. 2 Withdrawal latencies to thermal stimuli of the inflamed paw, the contralateral and both paws of control rats were measured at daily intervals after injection by the plantar test. 3 After detection of the pain threshold, rat spinal cords were removed and horizontal dorsal slices were mounted in a 3-compartment bath to measure electrically-evoked release of substance P-like immunoreactivity (SP-LI). 4 The inflamed paw of monoarthritic rats exhibited a lower pain threshold to thermal stimuli than the contralateral paw of the same animals and both paws of control rats. Inflamed paw hyperalgesia was maximal two days after injection, and declined gradually between 7 to 21 days with no evidence of excitability of withdrawal reflexes after 28 days. 5 During the 28 days study, monoarthritic rats gained less weight than control rats. 6 Electrical stimulation of the dorsal roots attached to rat isolated spinal cord slices induced a significant increase (174 ± 18% of basal outflow which was 30.3 fmol 8 ml-', n = 5) in SP-LI release. 7 One-week after induction of inflammation no differences in the amount of SP-LI released from the spinal cord of incomplete Freund's adjuvant-treated rats (IFA) and Freund's adjuvant-treated rats (CFA) were detected. Two weeks after, CFA spinal cord tended to release more SP-LI than IFA cords and, 21 days after injection, the spinal cord of CFA rats released significantly more peptide than IFA rats (17.8 ± 2.8 fmol ml1', n = 12 and 6.9 ± 3.2 fmol ml-', n = 9, respectively). 8 Twenty-one days after treatment, the evoked release from monoarthritic rat spinal cords was increased by 263 + 42% (n = 3) in the presence of the GABAB receptor antagonist, CGP 36742 (100 fLM) which also significantly potentiated monoarthritis-induced hyperalgesia up to 45 min after injection (100mgkg-', i.p.). 9 These findings may provide a basis for a novel approach to chronic pain therapy but also an explanation for the lack of analgesia produced by the GABAB agonist, baclofen, in chronic as compared to acute pain.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system

Malcangio

Bowery

1994

British J Pharmacology

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“…Local injury yields the release of a variety of factors that alter sensitivity of the primary afferent fibers innervating the damaged tissue, and among these factors that are important components of this peripheral sensitization are prostaglandins (Schaible and Grubb, 1993). Prostaglandins are lipidic acids that are locally synthesized by the cyclooxygenase enzymes after focal tissue injury and that sensitize peripheral nerve endings and enhance pain behavior in both animals and humans (Masferrer et al, 1994;Vane et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Constitutive Spinal Cyclooxygenase-2 Participates in the Initiation of Tissue Injury-Induced Hyperalgesia

Ghilardi¹,

Svensson²,

Rogers³

et al. 2004

J. Neurosci.

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Inhibitors of the isozyme cyclooxygenase-2 (COX-2) represent an important advance in pain management, although where and when these inhibitors can exert their antihyperalgesic actions are not completely understood. Here we show that unlike many peripheral tissues in which COX-2 is only expressed in physiologically significant levels after tissue injury, in the normal rat lumbar spinal cord, the majority of neurons and radial glia constitutively express high levels of COX-2 protein. Immediately after peripheral tissue injury and before any measurable upregulation of COX-2 protein in peripheral tissue or spinal cord, inhibition of constitutively expressed spinal COX-2 reduced injury-induced activation of primary afferent neurons, activation of spinal neurons, and the mechanical and thermal hyperalgesia that normally occurs after peripheral tissue injury. The present data demonstrate that constitutively expressed spinal COX-2 plays an important role in the initial hyperalgesia that follows peripheral tissue injury. These results suggest that blocking constitutive spinal COX-2 before tissue injury may reduce the initial peripheral and central sensitization that occurs after tissue injury.

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“…5,6 Moreover, it has been demonstrated that stimulation of afferents from deep somatic tissues such as joints and muscles is more effective than cutaneous input in generating central hyperexcitability. 7,8 More specifically, provocation of the deep paraspinal tissues at the level of the atlanto-axial (C1-2) spinal segment was shown to induce central sensitization in medullary and C1-C2 dorsal horns. 9 Together, these findings suggest that hyperexcitability of nociceptive second-order neurons in the TCN could result from noxious afferent information from dysfunctional spinal segments, thereby increasing sensitivity to subclinical afferent information from the trigeminal field.…”

mentioning

confidence: 99%

Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex

Watson

Drummond

2014

Headache

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Objective.-To investigate cervical, interictal reproduction of usual head pain and its effect on the nociceptive blink reflex in migraineurs.Background.-Anatomical and neurophysiological studies in animals and humans have confirmed functional convergence of trigeminal and cervical afferent pathways. Migraineurs often present with occipital and neck symptoms, and cervical pain is referred to the head in most cases, suggesting that cervical afferent information may contribute to headache. Furthermore, the effectiveness of greater occipital nerve blockade in migraine and demonstrable modulation of trigeminal transmission following greater occipital nerve blockade suggest an important role for cervical afferents in migraine. However, to what extent cervical afferents contribute actively to migraine is still unknown.Methods.-The passive accessory intervertebral movements of the atlanto-occipital and C2-3 spinal segments of 15 participants (14 females, 1 male; age 24-44 years, mean age 33.3 years) with migraine were examined interictally. During 1 session, either the atlanto-occipital or C2-3 segment was examined, resulting in referred usual head pain, while in another session, pressure was applied over the common extensor origin (lateral epicondyle of the humerus) of the ipsilateral arm. Each intervention was repeated 4 times. The nociceptive blink reflex to a supraorbital electrical stimulus was elicited ipsilaterally during both sessions before and during each intervention. The main outcome variables were the number of recorded blinks, area under the curve and latencies of the R2 components of the nociceptive blink reflex. Participants also rated the intensity of referred head pain and the supraorbital stimulus on a scale of 0-10, where 0 = "no pain" and 10 = "intolerable pain," and rated the intensity of applied pressure where 0 = "pressure but no pain" and 10 = "intolerable pain."Results.-Participants reported a significant reduction in local tenderness ratings across the 4 trials for the cervical intervention but not for the arm (P = .005). The cervical intervention evoked head pain in all participants. As the cervical intervention was sustained, head pain decreased significantly from the beginning to the end of each trial (P = .000) and from the beginning of the first trial to the end of the last (P = .000). Pain evoked by the supraorbital stimulus was consistent from baseline to across the 4 trials (P = .635) and was similar for the cervical and arm interventions (P = .072). The number of blinks decreased significantly across the experiment (P = .000) and was comparable in the cervical and arm interventions (P = .624). While the R2 area under the curve decreased irrespective of intervention (P = .000), this reduction was significantly greater for the cervical intervention than when pressure was applied to the arm (P = .037). Analysis of the R2 latencies revealed a notable increase across the experiment (P = .037). However, this increase was significantly greater following the cervical than arm intervention (P ...

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Afferent and spinal mechanisms of joint pain

Cited by 560 publications

References 340 publications

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system

Constitutive Spinal Cyclooxygenase-2 Participates in the Initiation of Tissue Injury-Induced Hyperalgesia

Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex

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Afferent and spinal mechanisms of joint pain

Cited by 560 publications

References 340 publications

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABAB receptor system

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABAB receptor system

Constitutive Spinal Cyclooxygenase-2 Participates in the Initiation of Tissue Injury-Induced Hyperalgesia

Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex

Contact Info

Product

Resources

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Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system

Spinal cord SP release and hyperalgesia in monoarthritic rats: involvement of the GABA_B receptor system