Using functional MRI, Moulton

and collaborators104 measur

Using functional MRI, Moulton

and collaborators104 measured brainstem function in episodic migraineurs during the interictal phase after heat stimulation. These patients with migraine had a hypofunctional response in an area possibly corresponding to the nucleus cuneiformis (a component of pain modulatory circuits) compared with non-migraine controls, which indicates that brainstem dysfunction leads to decreased nociceptive inhibition and could contribute to central sensitization. The PAG, which modulates somatic pain transmission, also shows evidence of interictal functional and structural abnormalities in migraine patients. These abnormalities may result in a hyperexcitability of spinal and trigeminal nociceptive Rapamycin order pathways and lead to the migraine attack. Resting-state functional MRI studies found stronger connectivity between the PAG and several brain this website areas within nociceptive and somatosensory processing pathways in migraineurs vs controls.105 In addition, as the monthly frequency of migraine attacks worsens, the strength of the connectivity in some areas within these pathways increases, while a significant decrease occurs in functional resting-state connectivity between the PAG and brain regions with a predominant role in pain modulation (prefrontal cortex, anterior cingulate, amygdala). Finally, migraineurs with a history of allodynia exhibit significantly reduced connectivity between

PAG, prefrontal regions, and anterior cingulate compared with migraineurs without allodynia. These data reveal interictal dysfunctional dynamics within pain pathways in migraine, manifested as an impairment of the descending pain modulatory circuits likely leading to loss of pain inhibition, and hyperexcitability primarily in nociceptive areas. In voxel-based statistical parametric

selleck chemicals llc mapping analyses of 18F-FDG PET, interictal migraine patients had significant hypometabolism in several regions involved in central pain processing, such as bilateral insula, bilateral anterior and posterior cingulate cortex, left premotor and prefrontal cortex, and left primary somatosensory cortex.106 In addition, regional metabolism of the insula and anterior cingulate cortex showed significant negative correlations with disease duration and lifetime headache frequency. These observations suggest that repeated migraine attacks over time lead to metabolic abnormalities of selective brain regions belonging to the central pain matrix. Tessitore and colleagues107 explored the pain processing network in patients with migraine during trigeminal nociceptive stimulation and found that patients exhibit a greater activation in the perigenual area of anterior cingulate cortex at 51°C and less activation in the bilateral somatosensory cortex at 53°C compared with HCs. These findings were confirmed in a subsequent study that also revealed a region in the pons showing divergent responses in patients and HCs.

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