Migraine with aura shows gadolinium enhancement which is reversed following prophylactic treatment

Arnold, G.; Reuter, Uwe; Kinze, Stephan; Wolf, Tilo; Km, Einhäupl

doi:10.1046/j.1468-2982.1998.1809644.x

Cited by 30 publications

(19 citation statements)

References 8 publications

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“…Nissila et al (1996), although hampered by resolution problems, failed to demonstrate extravasation in the meninges during an acute migraine attack using gadolinium enhanced magnetic resonance imaging. However, Arnold et al (1998), demonstrated gadolinium enhancement in the white matter near to the middle cerebral artery in one migraineur and Crawford and Konkol (1997) detected enhancement in the meninges in a patient with familial hemiplegic migraine. More recently, Pappagallo et al (1999) used Single Photon Emission Computerized Tomography (SPECT) to detect mild to marked increases in activity in extraparenchymal regions close to the region of the headache in three patients, suggesting some inflammatory component to the headache, although whether this is true for a larger sample remains to be determined.…”

Section: Other Clinical Studies On Neurogenic Inflammationmentioning

confidence: 99%

Neurogenic inflammation in the context of migraine

Williamson

Hargreaves

2001

Microscopy Res & Technique

203

144

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Despite considerable research into the pathogenesis of idiopathic headaches, such as migraine, the pathophysiological mechanisms underlying them remain poorly understood. Although it is well established that the trigeminal nerve becomes activated during migraine, the consequences of this activation remain controversial. One theory, based on preclinical observations, is that activation of trigeminal sensory fibers leads to a painful neurogenic inflammation within the meningeal (dural) vasculature mediated by neuropeptide release from trigeminal sensory fibres and characterized by plasma protein extravasation, vasodilation, and mast cell degranulation. Effective antimigraine agents such as ergots, triptans, opioids, and valproate inhibit preclinical neurogenic dural extravasation, suggesting that this activity may be a predictor of potential clinical efficacy of novel agents. However, several clinical trials with other agents that inhibit this process preclinically have failed to show efficacy in the acute treatment of migraine in man. Alternatively, it has been proposed that painful neurogenic vasodilation of meningeal blood vessels could be a key component of the inflammatory process during migraine headache. This view is supported by the observation that jugular plasma levels of the potent vasodilator, calcitonin gene-related peptide (CGRP) are elevated during the headache and normalized by successful sumatriptan treatment. Preclinically, activation of trigeminal sensory fibers evokes a CGRP-mediated neurogenic dural vasodilation, which is blocked by dihydroergotamine, triptans, and opioids but unaffected by NK1 receptor antagonists that failed in clinical trials. These observations suggest that CGRP release with associated neurogenic dural vasodilation may be important in the generation of migraine pain, a theory that would ultimately be tested by the clinical testing of a CGRP receptor antagonist.

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Section: Other Clinical Studies On Neurogenic Inflammationmentioning

confidence: 99%

Neurogenic inflammation in the context of migraine

Williamson

Hargreaves

2001

Microscopy Res & Technique

203

144

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“…What if BBB openings vary in size during migraine aura or pain, or it depends on the severity of aura? Thus, two studies have reported gadolinium enhancement over the symptomatic cerebral hemisphere during severe and prolonged attacks of familial hemiplegic migraine (31,32). This indicates that the severity and duration of CSD may influence outcome in imaging studies.…”

Section: Blood-brain Barrier In Migrainementioning

confidence: 99%

Matrix metalloproteinases during and outside of migraine attacks without aura

et al. 2009

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To test the hypothesis that permeability of the blood-brain barrier (BBB) is altered during migraine attack due to enhanced activation of matrix metalloproteinases (MMPs), we investigated MMP-3, MMP-9 and tissue inhibitor of metalloproteases (TIMP)-1 in the external jugular vein during and outside of migraine attacks in 21 patients with migraine without aura. In addition, we measured plasma levels of several other proteins including MMP-7, -8, -10 and TIMP-2. We used Rules-Based Medicine multi-analyte profiling and protein array technologies to study plasma concentration of MMPs. There was no difference in MMP-9 and TIMP-1 levels between ictal and interictal periods. We found significantly decreased plasma levels of MMP-3 in the external jugular (P = 0.002) and cubital (P = 0.008) vein during attacks compared with outside of attacks. We found no correlation of ictal or interictal MMP-3, MMP-9 and TIMP-1 to migraine duration and frequency analysed in 21 patients (P > 0.05). There was no difference between ictal and interictal plasma levels of MMP-7, -8, -10 and TIMP-2 (P > 0.05). Our data suggest that plasma MMP-9 cannot be used as a biomarker of BBB disruption in migraine without aura. Decreased MMP-3 levels are an interesting and unexpected finding warranting further investigation.

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“…Such neurogenic inflammatory reactions were thought to trigger headache via a stimulation of trigeminal afferents (4,5). Consistent with this theory, vasogenic leakage (6,7) and an increase in calcitonin generelated peptide in the jugular vein (8) have been reported in migraine patients during migraine attack. However, recent clinical trials have shown that several drugs that selectively inhibit plasma protein extravasation in rodents have failed to reduce pain severity in patients with migraine (9).…”

mentioning

confidence: 73%

¹¹C-PK11195 PET for the In Vivo Evaluation of Neuroinflammation in the Rat Brain After Cortical Spreading Depression

Cui¹,

Takashima²,

Takashima-Hirano³

et al. 2009

J Nucl Med

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Neurogenic inflammation triggered by extravasation of plasma protein has been hypothesized as a key factor in the generation of the pain sensation associated with migraine. The principal immune cell that responds to this inflammation is the parenchymal microglia of the central nervous system. Methods: Using a PET technique with 11 , a PET ligand for peripheral type-benzodiazepine receptor, we evaluated the microglial activation in the rat brain after generation of unilateral cortical spreading depression, a stimulation used to bring up an experimental animal model of migraine. Results: We found a significant increase in the brain uptake of 11 C-PK11195, which was completely displaceable by the excess amounts of unlabeled ligands, in the ipsilateral hemisphere of the spreading depressiongenerated rats. Moreover, the binding potential of 11 C-PK11195 in the spreading depression-generated rats was significantly higher than that in the sham-operated control rats. Conclusion: These results suggest that as an inflammatory reaction, microglial cells are activated in response to the nociceptive stimuli induced by cortical spreading depression in the rat brain. Therefore, the 11 C-PK11195 PET technique could have a potential for diagnostic and therapeutic monitoring of neurologic disorders related to neuroinflammation such as migraine.

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Migraine with aura shows gadolinium enhancement which is reversed following prophylactic treatment

Cited by 30 publications

References 8 publications

Neurogenic inflammation in the context of migraine

Neurogenic inflammation in the context of migraine

Matrix metalloproteinases during and outside of migraine attacks without aura

¹¹C-PK11195 PET for the In Vivo Evaluation of Neuroinflammation in the Rat Brain After Cortical Spreading Depression

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Migraine with aura shows gadolinium enhancement which is reversed following prophylactic treatment

Cited by 30 publications

References 8 publications

Neurogenic inflammation in the context of migraine

Neurogenic inflammation in the context of migraine

Matrix metalloproteinases during and outside of migraine attacks without aura

11C-PK11195 PET for the In Vivo Evaluation of Neuroinflammation in the Rat Brain After Cortical Spreading Depression

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Product

Resources

About

¹¹C-PK11195 PET for the In Vivo Evaluation of Neuroinflammation in the Rat Brain After Cortical Spreading Depression