Sensitization of trigeminal nociception specific for migraine but not pain of sinusitis

Katsarava, Zaza; Lehnerdt, Goetz; Duda, B.; Ellrich, Jens; Hc, Diener; Kaube, Holger

doi:10.1212/wnl.59.9.1450

Cited by 69 publications

(28 citation statements)

References 9 publications

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“…The association between migraine and TMD may be due to multiple biopsychosocial factors, such as shared physiology, genetics, psychological traits, and environmental influences. Both migraine and TMD pain are mediated by the trigeminocervical complex [16,19] and migraine-specific sensitization of trigeminal nociception [28] is likely to facilitate the onset of TMD. Dysregulation of pain modulatory mechanisms in the central and peripheral nervous systems has been reported in both conditions [3,33,38,43].…”

Section: Discussionmentioning

confidence: 99%

Temporal change in headache and its contribution to the risk of developing first-onset temporomandibular disorder in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study

Tchivileva

Ohrbach

Fillingim

et al. 2016

Pain

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While cross-sectional studies have demonstrated an association between headache and temporomandibular disorder (TMD), whether headache can predict the onset of TMD is unknown. The aims of this study were to evaluate the contribution of headache to the risk of developing TMD and describe patterns of change in headache types over time. An initially TMD-free cohort of 2410 persons with low frequency of headache completed quarterly questionnaires assessing TMD and headache symptoms over a median 3.0-year follow-up period. First-onset TMD was confirmed by clinical examination in 199 participants. Baseline reports of migraine (hazard ratio [HR] = 1.67, 95% confidence interval [CI]: 1.06-2.62) or mixed headache types (HR = 4.11, 95% CI: 1.47-11.46), or headache frequency (HR = 2.13, 95% CI: 1.31-3.48) predicted increased risk of developing TMD. In addition, headache dynamics across the follow-up period before the TMD onset were evaluated in a nested case–control study where 248 incident TMD cases were matched to 191 TMD-free controls. Both headache prevalence and frequency increased across the observation period among those who developed TMD but not among controls. Patients with TMD were more likely to experience worsening in the headache type compared with that by controls, eg, prevalence of definite migraine among TMD cases increased 10-fold. Among all headache types experienced by patients with TMD before the TMD onset, migraine had the highest odds of progression relative to remission (odds ratio = 2.8, 95% CI: 1.6-4.8), whereas for controls this ratio was significant only for the tension-type headache (odds ratio = 2.1, 95% CI: 1.2-3.9). The important clinical implication of these findings is that adequate treatment of migraine may reduce the risk for developing TMD.

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Section: Discussionmentioning

confidence: 99%

Temporal change in headache and its contribution to the risk of developing first-onset temporomandibular disorder in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study

Tchivileva

Ohrbach

Fillingim

et al. 2016

Pain

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“…In this animal model of headache, application of inflammatory mediators to the dura leads to mechanical hypersensitivity to both cranial and extracranial regions as well as sensitization of both dural primary afferent and MDH neurons (Drummond, 1987; Strassman et al, 1996; Burstein et al, 1998; Burstein et al, 2000; Katsarava et al, 2002; Kaube et al, 2002; de Tommaso et al, 2003; Katsarava et al, 2003; Valeriani et al, 2003; Weissman-Fogel et al, 2003; Oshinsky and Gomonchareonsiri, 2007; Edelmayer et al, 2009). As with prolonged morphine exposure, inflammation of the dura increased cutaneous receptive field sizes and lowered dural activation thresholds.…”

Section: Discussionmentioning

confidence: 99%

Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Okada-Ogawa

Porreca²,

Meng³

2009

J. Neurosci.

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Overuse of medications used to treat migraine headache can produce a chronic daily headache, termed medication overuse headache (MOH). Although “overuse” of opioids, triptans, and over-the-counter analgesics can all produce MOH, the neuronal mechanisms remain unknown. Headache pain is likely to be produced by stimulation of primary afferent neurons that innervate the intracranial vasculature and the resulting activation of medullary dorsal horn (MDH) neurons. The present study compared the receptive field properties of MDH dura sensitive neurons in rats treated with morphine to those given vehicle. Animals were implanted with osmotic mini-pumps or pellets for sustained subcutaneous administration of morphine or vehicle 6–7 days prior to recording from dura-sensitive neurons. Electrical and mechanical activation thresholds from the dura were significantly lower in chronic morphine treated animals when compared to vehicle controls. In addition, sustained morphine increased the cutaneous receptive field sizes. The presence of diffuse noxious inhibitory controls (DNIC) was examined by placing the tail in 55°C water during concomitant noxious thermal stimulation of the cutaneous receptive field, usually located in the ophthalmic region. The DNIC stimulus produced significant inhibition of heat-evoked activity in vehicle, but not chronic morphine treated animals. Inactivation of the rostral ventromedial medulla (RVM) with 4% lidocaine reinstated DNIC in chronic morphine treated animals. These results are consistent with studies demonstrating a loss of DNIC in patients that suffer from chronic daily headache and may partially explain why overuse of medication used to treat migraine can induce headaches.

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“…Data from imaging studies showing that the periaqueductal gray region seemed to be activated during a migraine attack, 17 together with evidence of functional impairment in chronic migraine, 18 suggest that a failure of descending pathways that slow down pain transmission could contribute to further increase of afferent input by the nociceptive dorsal horn to the thalamus and cortex. Reduced inhibitory control over the trigeminal nociceptive reflexes has also been suggested to occur during migraine attack: in previous studies, the later components of the blink reflex were enhanced on the pain side, 19 while facilitation of the nociceptive blink reflex response was observed in migraine, but not in sinusitis, suggesting that it may be specific for migraine rather than a consequence of peripheral pain 20 . The finding of a prevalent enhancement of the amplitude of the later LEP responses suggests that the subjective attentive attitude to the painful stimuli during migraine may increase the effect of the pain transmission disinhibition and further ease pain processing via a facilitation mechanism of cortical origin 21 .…”

mentioning

confidence: 98%

Topographic and Dipolar Analysis of Laser‐Evoked Potentials During Migraine Attack

Tommaso¹,

Guido²,

Libro³

et al. 2004

Headache

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Sensitization of trigeminal nociception specific for migraine but not pain of sinusitis

Cited by 69 publications

References 9 publications

Temporal change in headache and its contribution to the risk of developing first-onset temporomandibular disorder in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study

Temporal change in headache and its contribution to the risk of developing first-onset temporomandibular disorder in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study

Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Topographic and Dipolar Analysis of Laser‐Evoked Potentials During Migraine Attack

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