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At least 19 recordsLinked to original sources
PubMed1987

Vascular headache.

Vascular headache is an extremely common disorder. Current evidence points to an underlying neurogenic etiology, and the associated vascular changes are believed to be epiphenomena. Vascular headache tends to begin at a young age, is more common in women, and is frequently associated with a positive family history. Characteristics of the headache frequently suggest the diagnosis. The history and physical examination are keys to the diagnostic evaluation. A computed tomography scan when indicated is the single test with the highest yield of information. Non-narcotic analgesics, ergot compounds, and metoclopramide are the most commonly used agents for acute attacks. Beta blockers and amitriptyline are the most widely used prophylactic medications. Nonpharmacologic measures are occasionally of great benefit.

Adolescent↗
PubMed1998

Is chronic tension-type headache a vascular headache? The relation between chronic tension-type headache and cranial hemodynamics.

Twenty-seven patients with chronic tension-type headache were studied as to end-tidal PCO2, heart rate, mean blood pressure, diameter and blood flow of the common carotid arteries, cranial vascular resistance, and headache intensity at supine rest, after administration of nitroglycerin, and at head down tilt. The results were compared to the results of nitroglycerin and head down tilt provocations in age- and sex-matched controls. During supine rest, no change in chronic tension-type headache occurred. Nitroglycerin and tilting induced significant increase of the headache intensity compared to baseline in patients with chronic tension-type headache (P=0.01 and P<0.05, respectively) in contradistinction to controls who did not develop significant headache. Common carotid artery blood flow changes were similar during nitroglycerin provocations in the two groups, but greater (P<0.05) during head down tilt in patients than in controls. Lumbar cerebrospinal fluid pressure was found to be greater than 20 but less than 26 cm H2O in 45% of the 22 patients studied with chronic tension-type headache. The results indicate that the pain in chronic tension-type headache is related to cranial hemodynamics, presumably to distention of intracranial veins.

Adult↗
PubMed1990

The role of antihistamine therapy in vascular headaches.

Migraine (vascular) headache is a complex syndrome that involves vascular hyperreactivity. The functions of systemic mediators in migraine are not fully understood. It is unclear which mediators provoke this probably atopic disorder and which represent an attempt to correct an imbalance. However, it has been demonstrated fairly conclusively that increased histamine levels correlate with migraine attacks in susceptible persons. Recent studies showing that histamine seems to have many different receptors and to adopt different conformations for different receptors may serve as a useful guide to future scientific investigation. 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.

Allergens↗
PubMed1988

Cluster headache pain vs. other vascular headache pain: differences revealed with two approaches to the McGill Pain Questionnaire.

We compared cluster headache pain and other vascular (migraine and mixed) headache pain on pain intensity ratings and the McGill Pain Questionnaire (MPQ). Cluster headache sufferers reported not only more intense pain and more affective distress, but also different pain qualities than did migraine and mixed headache sufferers. The pain qualities that best distinguished cluster headaches from other vascular headaches were the presence of punctate pressure and thermal sensations and the absence of dull pain. Although cluster headache sufferers and other vascular headache sufferers endorsed different sensory pain qualities, MPQ subscales proved no better than pain intensity ratings at distinguishing these two groups. This finding may have occurred because MPQ subscale scores include an intensity component and do not provide information about specific pain qualities such as that provided by MPQ sensory items. These findings provide evidence that cluster headaches are characterized by distinct pain qualities and are not simply a more intense version of the same vascular headache pain experienced by migraine and mixed headache sufferers. They further suggest than when the MPQ is used to assess specific pain qualities, sensory items and not the sensory subscale are the preferred units for analysis.

Adult↗
PubMed1989

Two studies of the potential mechanisms of action in the thermal biofeedback treatment of vascular headache.

Sixty vascular headache sufferers who underwent a standard protocol treatment of progressive relaxation and thermal biofeedback with autogenic training were studied for changes in hand temperature (the targeted response) and heart rate (a non-targeted response) to determine how such physiological change relates to reduction in headache activity. Overall, regardless of degree of improvement, subjects showed a significant, positive change over time in their ability to increase hand temperature. It was also found that inability to handwarm at session one of thermal biofeedback training was predictive of treatment success, as was the ability to achieve a fingertip temperature of at least 96.0 degrees F at any point in thermal biofeedback training. In addition, it was found that migraine headache sufferers who were treatment successes had significantly lowered their heart rates from pre- to post-treatment assessment.

Adolescent↗
PubMedDate not supplied

[Vascular headache and cerebral edema].

Headache is one of the commonest symptoms in neurology. It can be present among many other somatic illnesses. There are many aetiological factors. Pathogenetic mechanisms are unknown. There is a significant number of patients with headache, especially with vascular headache, (about 15%), and vascular headache associated with cerebrovascular ischaemic stroke. Therefore the new investigations of neurobiochemical and neurophysiological problems are necessary. A group of patients involved in our study with diagnosis of vascular headache was tested. The result of the study (especially neuroradiological results) show that many patients, prevalently young women, had cerebral oedema during the attack of vascular headache.

Adult↗
PubMed1993

New concepts of vascular headache.

The 'vascular' aetiology of headache is questioned. An alternative hypothesis based on sensitisation of sensory nerve endings by neurogenic plasma extravasation is discussed. The development of drugs which selectively inhibit the release of vasoactive neuropeptides from perivascular sensory nerves may benefit patients with head pain from a variety of causes.

Brain↗
PubMed1989

Pain mechanisms underlying vascular headaches. Progress Report 1989.

Vascular headaches are among the most prevalent yet poorly understood problems in clinical neurology. Headaches may develop in association with hypertension, seizures, stroke or without a recognizable pathophysiology such as during migraine and cluster headaches. Cephalic blood vessels (pial and dural vessels) are implicated as the most important source for all headaches and are innervated by sensory fibers which arise from ganglia innervating the forehead, scalp and neck. Sensory fibers contain vasoactive neuropeptides which become released from peripheral (perivascular) and central terminations to mediate vasodilation and pain, respectively. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The existence of such a system a) clarifies certain pain patterns which develop following stimulation of cephalic blood vessels, b) suggests a mechanism to explain the referral of pain to the forehead, c) provides a mechanism to explain the action of certain antimigraine drugs, d) suggests a local mechanism which enhances blood flow under certain pathological conditions. Hence, this review will update existing knowledge about the trigeminovascular system and its role in headache pathophysiology.

Animals↗
PubMed1989

[Clinical and experimental research on lutongning in treating vascular headache].

Observing the therapeutic effect of 350 cases of vascular headache patients treated with oral Lutongning decoction and goat horn compound separately, and comparing the effects of these two groups' patients, they showed that the former was much better than the latter. The author found that cure rates of these two groups were 75.3% and 56% respectively (P less than 0.01). The medicinal action of the former was also faster than that of the latter, and the time to recover was shorter. So, Lutongning was an effective prescription in the treatment of vascular headache. In order to research the effective mechanism of Lutongning on vascular headache, the animal experiment was carried out. The hot-plate method and acetic acid body-turning method were used for the experiment in rats. After perfusing Lutongning into the rat's stomach, the author found that the reaction times by hot-plate method and the turning times by acetic acid body-turning method were less than those of the control animals. The result showed that the analgetic effect of this decoction was more obvious.

Adolescent↗
PubMed1986

The pathogenesis of vascular headaches in patients with hypertension; the role of the ammonia-potassium axis.

Headaches may occur in as many as 25% of hypertensive patients and generally bears little relationship to level of diastolic blood pressure. Previous observations, in normotensive patients, suggested that abnormalities in both potassium and ammonia metabolism might be related to the pathogenesis of these headaches. The present study was undertaken to see whether these factors also occurred in hypertensive patients with headaches. The present observations were made in thirteen hypertensive patients with vascular headaches. The major findings include potassium levels of 3.45 +/- 0.25 mEq/L; CO2, 29.85 +/- 1.21 mEq/L; blood ammonia, 41 +/- 8.40 U mol/L and an alkaline pH of the urine. The blood ammonia levels, when factored by the BUN, yielded elevated ammonia to BUN ratios (3.81 +/- 1.82). These findings are similar to those previously observed in normotensive patients with vascular headaches. The profile of hypokalemia and/or alkalosis, increased blood ammonia to BUN ratios and a relatively alkaline urine appears to be a commonly observed pattern in patients with vascular headaches. These data suggest that a biochemical basis exists for the genesis of vascular headaches in patients with hypertension.

Ammonia↗