Excretion of Free and Conjugated 5-Hiaa and Vma in Urine and Concentration of 5-Hiaa and Hva in CSF During Migraine Attacks and Free Intervals

Kangasniemi, P; Sonninen, V.; Rinne, U. K.

doi:10.1111/j.1526-4610.1972.hed1202062.x

Cited by 37 publications

(27 citation statements)

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“…We cannot explain the lower total protein content in the presence of the normal protein fractions. Kangasniemi (22) found an increased HVA concentration in almost every case, but the mean values were not statistically significant. The values of total protein, HVA, and 5-HIAA concentration in the CSF.…”

Section: Con1 Rolmentioning

confidence: 82%

Cerebrospinal Fluid (CSF) Investigations in Migraine

Kovacs¹,

Bors²,

Tothfalusi³

et al. 1989

Cephalalgia

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A normal cell count as well as normal CSF pressure levels were found in both classic and common migraine patients during and between attacks. Total protein content was significantly lower in the migraine patients than in the controls, but no changes were found in the CSF protein fractions. The CSF 5-hydroxyindoleacetic acid level of the migraine patients proved to be higher than in the controls, whereas the homovanillic acid concentration was within the control limits.

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Section: Con1 Rolmentioning

confidence: 82%

Cerebrospinal Fluid (CSF) Investigations in Migraine

Kovacs¹,

Bors²,

Tothfalusi³

et al. 1989

Cephalalgia

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“…(1) Serotonin.-At first glance, a triggering role of serotonin appeared appealing for at least the following two reasons: -Sicuteri et al (29) reported an increase in urinary excretion of 5-HIAA, the main metabolite of serotonin, during a migraine attack in 15 patients. Subsequent investigators have only partially been able to confirm these findings (30,31), however.…”

Section: Factors Involved In the Genesis Of Brain Hypoxiamentioning

confidence: 98%

Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

Amery

1982

Cephalalgia

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The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack of migraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be provoked by different mechanisms in different patients; the potential role of decreased oxygen supply and of increased oxygen need are reviewed and excess sympathetic drive is considered a potential key mechanism in a majority of patients. Whether or not focal hypoxia leads to a genuine migraine attack, depends largely upon the quality of the whirlpool of biochemical, vascular and hematological changes that follow the hypoxic episode. These changes are discussed and it is concluded that those which have been reported to occur during migraine attacks could be due to a preceding hypoxic event. Finally, the hypoxia viewpoint is confronted with some popular theories about the pathogenesis of migraine. It is found that the other points of view are compatible with the hypoxia hypothesis.

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“…l ess than 2 years old, 6-8 and in one series, 18 per cent were less than 5 years old,' but most migraine in childhood starts between 6 and 10 years.&dquo;' Bille Wolff postulated that migraine was the result of altered blood supply to the brain and divided attacks into 4 phases.-3 The. l ess than 2 years old, 6-8 and in one series, 18 per cent were less than 5 years old,' but most migraine in childhood starts between 6 and 10 years.&dquo;' Bille Wolff postulated that migraine was the result of altered blood supply to the brain and divided attacks into 4 phases.-3 The.…”

mentioning

confidence: 96%