Differences of Anti-Nociceptive Mechanisms of Migraine Drugs on the Trigeminal Pain Processing during and Outside Acute Migraine Attacks

Katsarava, Zaza; Limmroth, Volker; Baykal, Orhan; Akguen, D; Hc, Diener; Kaube, Holger

doi:10.1111/j.1468-2982.2004.00730.x

Cited by 18 publications

(11 citation statements)

References 28 publications

(40 reference statements)

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“…An increased excitability of the R3 component, which is suggested nociceptive quality, was documented during attack, 15 while decreased habituation of R2 component was detected 16 . Recently, the “nociceptive” BR (nBR), which is highly sensitive to changes in trigeminal nociception, has been established 17 and the studies 18–21 indicate an abnormal trigeminal nociceptive processing in migraine.…”

Section: Commentsmentioning

confidence: 99%

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Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Shibata¹,

Yamane²,

Iwata³

2006

Headache

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For BR, there were no significant differences in the ratio of the area of the R2 between the sides of stimulation, and the sides of headache. AM patients had less suppression of the R2 at the ISI of 150 and 300 ms when compared with the NA patients and HS. For PVEP, at 0.5, there were significant differences of amplitude between AM patients and HS, and between NA patients and HS in low and high contrast. At 4.0 cpd, there were significant differences of amplitude between AM patients and HS in low contrast, and between AM patients and HS, and NA patients and HS in high contrast. In AM patients, there was a significant difference of amplitude ratio between 0.5 and 4.0 cpd. Conclusions.-Our BR and PVEP study showed that migraine patients exhibiting allodynia may show central sensitization of brainstem trigeminal neuron and have contrast modulating dysfunction during the cortical visual processing of striate and extrastriate on visual cortex in-between attacks.

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Section: Commentsmentioning

confidence: 99%

“…However, clinical and neurophysiological manifestations of information processing associated with central sensitization are little known. Numerous studies have explored the trigeminal system and visual function by using the BR 11–22 and PVEP 8–10,23–25 . To our knowledge, no study has used BR and PVEP to examine migraine exhibiting allodynia.…”

mentioning

confidence: 99%

Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Shibata¹,

Yamane²,

Iwata³

2006

Headache

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“…Of the included studies, 12 reported reflex threshold (Boureau et al, 1991;Coffin et al, 2004;De Marinis et al, 2007;Sterling et al, 2008;Courtney et al, 2009Courtney et al, , 2010Lim et al, 2012;Neziri et al, 2012;Rhudy et al, 2013;Smith et al, 2013Smith et al, , 2014Curatolo et al, 2015), six reported reflex peak magnitude or AUC or both Avramidis et al, 1998;De Marinis et al, 2007;Peddireddy et al, 2009;Rhudy et al, 2013;Kofler and Halder, 2014), six reported reflex latency (Avramidis et al, 1998;Katsarava et al, 2004;De Marinis et al, 2007;Courtney et al, 2009;Peddireddy et al, 2009;Kofler and Halder, 2014), and two reported reflex duration (Courtney et al, 2009;Peddireddy et al, 2009). Pain populations included 'chronic pain', migraine, migraine without aura, tension type headache, chronic tension type headache, fibromyalgia, rheumatoid arthritis, chronic upper back pain, chronic low back pain, knee osteoarthritis, chronic whiplash associated disorder, irritable bowel syndrome, chronic lateral epicondylalgia ('tennis elbow'), and a combination of idiopathic pain, myofascial pain, and headache (see Table 1 for study details).…”

Section: Included Studiesmentioning

confidence: 99%

“…Six studies (Avramidis et al, 1998;Katsarava et al, 2004;De Marinis et al, 2007;Courtney et al, 2009;Peddireddy et al, 2009;Kofler and Halder, 2014) (pooled n = 319) were included in the main analysis for latency of the reflex. One study (Avramidis et al, 1998) investigated two patient groups raising the number of group comparisons to seven.…”

Section: Latency Of Responsementioning

confidence: 99%

Defensive reflexes in people with pain – a biomarker of the need to protect? A meta-analytical systematic review

Wallwork

Grabherr

O’Connell

et al. 2017

Reviews in the Neurosciences

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AbstractUpregulation of defensive reflexes such as the nociceptive flexion reflex (NFR) has been attributed to sensitisation of peripheral and spinal nociceptors and is often considered biomarkers of pain. Experimental modulation of defensive reflexes raises the possibility that they might be better conceptualised as markers of descending cognitive control. Despite strongly held views on both sides and several narrative reviews, there has been no attempt to evaluate the evidence in a systematic manner. We undertook a meta-analytical systematic review of the extant English-language literature from inception. Thirty-six studies satisfied our a priori criteria. Seventeen were included in the meta-analysis. Reflexive threshold was lower in people with clinical pain than it was in pain-free controls, but reflex size, latency, and duration were unaffected. The pattern of difference was not consistent with sensitisation of nociceptive neurones, as these changes were not isolated to the affected body part but was more consistent with top-down cognitive control reflective of heightened protection of body tissue. The pattern of modulation is dependent on potentially complex evaluative mechanisms. We offer recommendations for future investigations and suggest that defensive reflex threshold may reflect a biomarker of a broader psychological construct related to bodily protection, rather than sensitisation of primary nociceptors, spinal nociceptors, or pain.

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“…Nonetheless, in the present study we could not reveal a significant difference in BOLD signal changes in response to trigeminal-nociceptive stimulation in the trigeminal nuclei after ASA administration compared to the saline condition. We note, that ASA and triptans inhibit the nociceptive blink reflex in the acute migraine attack, but seem to have no effect on trigeminal pain in migraineurs in the interictal state or in healthy volunteers [42], suggesting a modulatory effect on the trigeminal nociceptive system which occurs only in the migraine attack but not in the healthy system nor in the interictal phase [42], for example by blocking sensitization.…”

Section: Discussionmentioning

confidence: 99%

Central effects of acetylsalicylic acid on trigeminal-nociceptive stimuli

Kröger

May

2014

J Headache Pain

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BackgroundAcetylsalicylic acid is one of the most used analgesics to treat an acute migraine attack. Next to the inhibitory effects on peripheral prostaglandin synthesis, central mechanisms of action have also been discussed.MethodsUsing a standardized model for trigeminal-nociceptive stimulation during fMRI scanning, we investigated the effect of acetylsalicylic acid on acute pain compared to saline in 22 healthy volunteers in a double-blind within-subject design. Painful stimulation was applied using gaseous ammonia and presented in a pseudo-randomized order with several control stimuli. All participants were instructed to rate the intensity and unpleasantness of every stimulus on a VAS scale. Based on previous results, we hypothesized to find an effect of ASA on central pain processing structures like the ACC, SI and SII as well as the trigeminal nuclei and the hypothalamus.ResultsEven though we did not find any differences in pain ratings between saline and ASA, we observed decreased BOLD signal changes in response to trigemino-nociceptive stimulation in the ACC and SII after administration of ASA compared to saline. This finding is in line with earlier imaging results investigating the effect of ASA on acute pain. Contrary to earlier findings from animal studies, we could not find an effect of ASA on the trigeminal nuclei in the brainstem or within the hypothalamic area.ConclusionTaken together our study replicates earlier findings of an attenuating effect of ASA on pain processing structures, which adds further evidence to a possibly central mechanism of action of ASA.

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Differences of Anti-Nociceptive Mechanisms of Migraine Drugs on the Trigeminal Pain Processing during and Outside Acute Migraine Attacks

Cited by 18 publications

References 28 publications

Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

Defensive reflexes in people with pain – a biomarker of the need to protect? A meta-analytical systematic review

Central effects of acetylsalicylic acid on trigeminal-nociceptive stimuli

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