![]() Patients included in this study were screened for an over-arching investigation of the premonitory phase of GTN-induced migraine. We conducted positron emission tomography (PET) scans as a marker of neuronal activity in the premonitory phase of migraine to be able to compare patients with and without nausea. We hypothesized that central brain structures involved in nausea and emesis, in particular, the NTS, is activated in migraine patients who experience nausea in the absence of pain in the premonitory phase. Premonitory symptoms, such as tiredness, difficulty in concentration, mood changes, yawning and cravings, suggest the origin of the problem is likely to be within the brain, and therefore, nausea could also be a predominantly centrally driven symptom. Premonitory symptoms represent the earliest clinical change in migraineurs. The presence of nausea before pain suggests it can occur independent of pain. In a previous study, nausea in the premonitory phase correctly predicted headache in a quarter of migraineurs. However, nausea can already be present in the premonitory phase, before the appearance of headache. Nausea is often associated with the pain in migraine and in this regard, connections between trigeminal neurons and nucleus tractus solitarius (NTS) are thought to explain the occurrence of nausea with headache. The neurobiology of nausea in migraine is not well understood. Nausea is a common and disabling symptom of migraine, which is listed in the International Classification of Headache Disorders-III-beta (ICHD-III-beta) as a key symptom of an attack. We conclude that nausea is a centrally driven symptom in migraine. This is associated with activation of brain structures known to be involved in nausea. The results demonstrate that nausea can occur as a premonitory symptom in migraine, independent of pain and trigeminal activation. ![]() The rostral dorsal medullary area included the nucleus tractus solitarius, dorsal motor nucleus of the vagus nerve and the nucleus ambiguus, all of which are thought to be involved in brain circuits mediating nausea. The results showed activation in rostral dorsal medulla and periaqueductal grey (PAG) in the nausea group, which was absent in the no nausea group. We performed positron emission tomography scans with H 2 15O PET in premonitory phase of nitroglycerin-induced migraine and compared patients with and without nausea. However, nausea occurs as a premonitory symptom in about a quarter of patients, suggesting that a primary brain alteration unrelated to the experience of pain may be the reason for nausea. The origin of nausea is not well understood although functional connections between trigeminal neurons and the nucleus tractus solitarius may explain occurrence of nausea with pain. Nausea is a common and disabling symptom of migraine. ![]()
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