Background: The relationship between migraine and depression has been thoroughly investigated, indicating a bidirectional comorbidity. The exact temporal relationship between acute depressive... Show moreBackground: The relationship between migraine and depression has been thoroughly investigated, indicating a bidirectional comorbidity. The exact temporal relationship between acute depressive symptoms (mood changes) and the various phases of the migraine attack has not yet been examined. Methods: We performed a prospective diary study in n = 487 participants with migraine. Participants filled out a daily diary on migraine and acute depressive symptoms during a 1-month period. We randomly selected one migraine attack per participant, consisting of six days around an attack, including the interictal, premonitory, ictal, and postdromal phases. Acute depressive symptoms covered five major items from the DSM-5 classification. Primary analysis was performed using a mixed model with post-hoc testing. We also tested whether lifetime depression influenced the presence of acute depressive symptoms. Results: During a migraine headache day, patients scored higher on acute depressive symptoms than on all other days of the migraine attack (p < 0.001). There were no early warning signs for an upcoming headache attack through acute depressive symptomatology. Migraine patients with lifetime depression scored overall higher during the migraine attack than those without lifetime depression (p < 0.001). Limitations: Migraine attacks were based on self-reported migraine and one migraine attack per patient was randomly selected.Conclusion: We now clearly demonstrate that during the migraine headache phase, but not in the prodromal phase, patients report increased depressive symptomatology. No evidence was found for mood changes as an early warning sign for an upcoming migraine attack. Show less
Hoewel voorheen al onderzoek is verschenen naar verschillende onderdelen van de migrainedriehoek: chronificatie, depressie, en medicatieafhankelijkheid, waren er nog altijd ontbrekende stukken van... Show moreHoewel voorheen al onderzoek is verschenen naar verschillende onderdelen van de migrainedriehoek: chronificatie, depressie, en medicatieafhankelijkheid, waren er nog altijd ontbrekende stukken van de puzzel. Dit proefschrift onderzocht verschillende aspecten van deze driehoeksrelatie, waarbij wij ons richtten op:• klinische determinanten van depressie in migrainepatiënten (hoofdstuk 2 en 3),• de associatie van depressie met migraine aanvalsfrequentie, zowel in dwarsdoorsnede onderzoek (hoofdstuk 2) als in longitudinale studieopzet (hoofdstuk 3),• de rol van allodynie van de huid in zowel de comorbiditeit met depressie alsook migraine chronificatie (hoofdstuk 2 en 3),• symptoomdimensies van affectieve stoornissen in migrainepatiënten, in vergelijking met personen zonder migraine met en zonder affectieve aandoeningen (hoofdstuk 5),• de comorbiditeit van depressie in hemiplegische migraine, als een monogenetisch migraine fenotype (hoofdstuk 4),• genetische factoren die betrokken zijn bij migraine chronificatie (hoofdstuk 7),• de comorbiditeit van depressie in clusterhoofdpijn, als een ernstige episodische primaire hoofdpijnvorm anders dan migraine (hoofdstuk 8), en• de behandeling van medicatieafhankelijke hoofdpijn. Show less
In this dissertation clinical genetic investigations on migraine, related syndromes and comorbid conditions are described. The first migraine syndrome studied is Familial Hemiplegic Migraine (FHM),... Show moreIn this dissertation clinical genetic investigations on migraine, related syndromes and comorbid conditions are described. The first migraine syndrome studied is Familial Hemiplegic Migraine (FHM), a monogenic migraine variant. The clinical spectrum of FHM1-3 and the relation with closely related diseases such as Alternating hemiplegia of Chilhood, Early Seizures and Cerebral Edema after Trivial Head Trauma, epilepsy and episodic ataxia were investigated. The second monogenic migraine syndrome studied is Retinal Vasculopathy with Cerebral Leukodystrophy (later renamed CHARIOT), where common migraine is part of the clinical spectrum. The identification of TREX1 as the causal gene for RVCL is described. Investigation of the clinical spectrum showed retinal, cerebral and internal organ involvement, without an apparent genotype-phenotype correlation. Endothelial dysfunction of large arteries was shown in RVCL patients and is proposed as a possible disease mechanism. Lastly, migraine patients were identified in a Dutch genetic isolate and the relation with depression and atherosclerosis was assessed. For depression it was shown that shared genetic factors, at least partly, underlie the comorbidity with migraine, in particular migraine with aura. These studies improve our insight in genetic factors and pathofysiological mechanisms involved in migraine, which may ultimately contribute to better treatment options for migraine patients Show less
