Disease relevance of Vascular Headaches

• Based on this experience, we would caution against the use of unopposed beta-blockade in this setting and suggest that the role of prazosin in the initial management of postendarterectomy hypertension and vascular headache be explored [1].
• Increases in LCBF were significantly asymmetric among migraine and cluster patients and provoked typical unilateral vascular headaches which responded to sumatriptan [2].
• Two unusual cases of vascular headache, one caused by jugular venous compression from a goiter and one triggered by flushing associated with a CGRP-producing renal tumour, are reported [3].

Psychiatry related information on Vascular Headaches

• It is recommended that physicians treating epilepsy, vascular headaches, or mood disorders with divalproate consider the diagnosis of PTC when their patients complain of new onset of headaches or an increase in frequency or severity of existing headaches--especially those associated with a visual disturbance--to prevent permanent visual loss [4].

High impact information on Vascular Headaches

• Further impetus may come from ongoing studies of H3 histamine receptors, which indicate that H3 agonists offer promise as prophylactic agents for people who suffer from vascular headaches [5].
• We treated 64 emergency room patients with a primary vascular headache with dihydroergotamine (DHE), meperidine, or butorphanol [6].
• The variable duration and intensity of the headache in different patients can be explained by the pressor and cranial vasoconstrictor effects of the secreted amines, which respectively enhance and diminish vascular headache [7].
• This study addresses possible interactions of the vasodilators nitric oxide (NO), calcitonin gene-related peptide (CGRP) and prostaglandins, which may be implicated in the generation of vascular headaches [8].
• Cocaine-related vascular headaches [9].

Chemical compound and disease context of Vascular Headaches

• Comparison of single-dose meperidine, butorphanol, and dihydroergotamine in the treatment of vascular headache [6].
• Both dihydroergotamine and sumatriptan are useful in the acute treatment of vascular headaches and bind with high affinity to 5-HT1D receptors [10].
• 5-Hydroxytryptamine receptor agonists for the abortive treatment of vascular headaches block mast cell, endothelial and platelet activation within the rat dura mater after trigeminal stimulation [10].
• Nitric oxide (NO) and the dura mater are implicated in the pathogenesis of vascular headache [11].
• The thermographically observed effects of hyperoxia on vascular headache patients and non-headache individuals [12].

Biological context of Vascular Headaches

• Localized reduction in the expected blood flow surge after CO2 inhalation, most often noted posteriorly, was seen in 8 of the 13 vascular headaches, but in none of the musculoskeletal headache group [13].

Anatomical context of Vascular Headaches

• The development of sumatriptan has been based on a vascular theory of migraine and its high degree of efficacy in the treatment of migraine strengthens the argument that dilatation of cranial blood vessels is the cause of vascular headache [14].

Gene context of Vascular Headaches

• Because 5-HT1-like agonists, which are useful for treating migraine and related headaches, share similar inhibitory properties in this in vivo model, the significance of prejunctional alpha 2, histamine H3 and somatostatin receptors to treatment of vascular headaches is suggested [15].
• The MS patients had tension headaches or vascular headaches of the migraine type; there was no distinctive "MS headache." Seven of these patients had headaches with their first MS symptoms, but in only one did headaches recur with disease activity [16].

References