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A patient with long standing sustained unilateral headache ("background vascular") and occasional multiple jabs received prompt and lasting relief from indomethacin. The effectiveness of the drug was tested in a placebo controlled double-blind trial. Indomethacin may be of value in some types of sustained headache.
Recent evidence has demonstrated that neurogenic vascular headaches are a combination of neurological primary events and secondary vasomotor changes. The neurological events involve the hypothalamus and sensory cortex with sympathetic hypofunction and noradrenergic abnormalities. A platelet theory has been proposed but has not really been confirmed as a legitimate cause of the neurogenic vascular headaches. Food and chemicals in foods can act as a precipitating factor in the food-sensitive neurogenic vascular headache patient. In these patients evidence is now being demonstrated to confirm this, but larger patient studies are needed. The food-sensitive migraine patient and cluster headache patient must give a good history and food diary to go along with active challenges and provocative testing in order to determine the causative foods. Any concomitant allergies of inhalants or environmentals must also be treated. The treatment modalities of elimination and rotation diets or provocation neutralization may successfully control the headaches without the need for continuous medications.
A complex network of neurotransmission systems underlies the control of the cerebral circulation. Classical neurotransmitters, vasoactive peptides and receptors have been found in cerebral arteries. Central and peripheral structures are also probably involved in the neurogenic control of the cerebral circulation. Vascular and neurotransmission changes reported in vascular headaches suggest that an alteration of the neurogenic control of the brain circulation may be implicated in vascular headaches. In particular, locus coeruleus, which may control the intracerebral adrenergic pathway, can induce vascular changes similar to those of migraine. Moreover, the trigeminal ganglion, which may induce the release of substance P, can change the extracranial and intracranial vasodilator activity. The vascular theory of migraine, proposed by Wolff, is re-evaluated on the grounds of a possible mediation of the vascular responses by neurotransmitters. It is hypothesized that a deficient modulation by enkephalins may cause alterations of locus coeruleus and/or trigeminal ganglion. The problem of pain in vascular headaches is also considered: whether it is of vascular origin or whether it is due to a dysfunction of the central nociceptive pathway. Knowledge of the neurogenic control of the cerebral circulation may be useful in understanding some pathogenetic mechanisms of vascular headaches.
A behavioral package was used to shape and maintain the adherence of 5 subjects with vascular headache to a program of aerobic exercise training. Repeated measures of exercise behavior were examined through the use of a bidirectional changing criterion design. Repeated measures of headache activity were also collected. Results demonstrated a functional relationship between the behavioral package and exercise adherence, because all 5 subjects showed exercise behavior that matched bidirectional changing exercise criteria. The results also indicated clinically significant collateral reductions in vascular headache activity in 4 subjects. Subjects whose aerobic fitness levels were not masked by vasoactive medication also showed measurable increases in aerobic fitness. The results are discussed in terms of the methodology used to demonstrate a functional relationship between the adherence package and exercise behavior and the possible mechanism(s) by which aerobic exercise activity might affect vascular headache activity.
The clinical utility of Tellegen's Absorption Scale was examined using a sample of 32 chronic vascular headache patients drawn from a larger treatment study investigating the efficacy of thermal biofeedback with vascular headache. A regression analysis found that acquisition of the hand-warming response was directly related to increase in capacity for absorption. Conversely, a trend was found for absorption capacity to be inversely related to reductions in headache frequency and intensity. Reasons for these differences in process and outcome variables are discussed.
The dispute about whether migraine and cluster headache are one disorder--the "unified theory"--or two facets of a spectrum of "vascular headache" has not yet been settled. The author discusses various clinical features that unite or divide migraine and cluster headache in this respect: so-called "mixed forms" of vascular headache, corneal indentation pulse amplitudes, partial Horner's syndrome and possible aberrations in histamine metabolism. Evidence is presented showing that there may exist subunits of cluster headache, such as chronic paroxysmal hemicrania (C.P.H.) and a hitherto unreported type that co-exists with recurring bouts of retrobulbar neuritis and a partial factor XII deficiency.
The molecular mechanisms of migraine pain remain to be determined. Our studies of glyceryl trinitrate (GTN)-induced and histamine-induced headaches have led us to propose that nitric oxide (NO) may be the causative molecule in migraine pain. We also propose that substances capable of inducing experimental vascular headache do so with NO as the common mediator. Finally, we suggest that drugs with antimigraine activity inhibit NO and the cascade of intracellular reactions triggered by NO. We believe these observations provide new insight into the mechanisms of vascular headache. The importance of NO as a potential initiator of the migraine attack indicates new directions for the pharmacological treatment of migraine and other vascular headaches.
The antimigraine efficacy of dihydroergotamine methanesulphonate in the pharmaceutical form of planned release capsules has been evaluated. Forty-nine subjects were treated, 39 suffering from common migraine 10 from tension vascular headache, for a period of 90 days, with an oral dose of 15 mg twice daily. The product was found to be efficacious in 71% of the common migraine cases, while unsatisfactory or nil results were obtained in the remaining 29%. In the tension-vascular headache cases, efficacy was 40% compared to 60% unsatisfactory or nil results. Tolerance was good in 43 cases, while transient digestive disorders (nausea and vomiting) occurred in 6; in 2 cases the treatment had to be withdrawn for allergic erythema. The results demonstrate that the drug is indicated in cases of common migraine, while it does not appear to significantly influence the course of attacks of tension-vascular headache.
Three cases are reported of vascular headache following trauma and which failed to respond adequately to standard therapy for migraine. In each case the effect of ligation of the arteries involved has been dramatic, with complete and lasting relief in two cases.
One-hundred-sixteen patients suffering from vascular headache (migraine or combined migraine and tension) were, after 4 weeks of pretreatment baseline headache monitoring, randomly assigned to one of four conditions: (a) thermal biofeedback with adjunctive relaxation training (TBF); (b) TBF plus cognitive therapy; (c) pseudomediation as an ostensible attention-placebo control; or (d) headache monitoring. The first three groups received 16 individual sessions over 8 weeks, while the fourth group continued to monitor headaches. All groups then monitored headaches for a 4-week posttreatment baseline. Analyses revealed that all treated groups improved significantly more than the headache monitoring group with no significant differences among the three treated groups. On a measure of clinically significant improvement, the two TBF groups had slightly higher (51%) degree of improvement than the meditation group (37.5%). It is argued that the attention-placebo control became an active relaxation condition.
Nitric oxide (NO) may play a key role in migraine and other vascular headaches since glyceryl trinitrate (a donor of NO) and histamine (which probably activates endothelial NO formation) both cause a pulsating dose-dependent headache with several migrainous characteristics. At relatively high doses of glyceryl trinitrate, migraine sufferers develop stronger and more migraine-like headaches and more pronounced cerebral arterial dilatation than controls. After the infusion of glyceryl trinitrate, non-migraineurs remain headache-free while migraineurs develop a migraine-like attack. In this review, Jes Olesen, Lars Thomsen and Helle Iversen suggest that migraine may be caused by increased amounts and/or affinity of an enzyme in the NO-triggered cascade of reactions. NO may also be involved in the pathogenesis of other vascular headaches.
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The following three unusual complications of carotid endarterectomy developed in a 64-year-old woman: vascular headaches, delayed hypertension, and seizures. beta-Blockade with propranolol hydrochloride had no beneficial effect on either the hypertension or the headaches. Peripheral alpha-blockade with prazosin hydrochloride resulted in prompt improvement in the patient's condition. Altered autonomic vascular control secondary to carotid sinus trauma is proposed as a possible causative mechanism for all three complications. The therapeutic implications are discussed. 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.
We report a series of 11 patients who developed headaches during intracranial endovascular procedures performed for the treatment of arteriovenous malformations (10 cases) or aneurysms (1 case). Headache was precipitated either by balloon inflation (3 cases) or by embolization (8 cases), and had a very constant pattern. In all cases the pain started suddenly, reaching maximum intensity at once. Headache was focal, unilateral, ipsilateral to the occluded artery, nonthrobbing and short-lasting (usually less than 10 minutes). It was not associated with gastrointestinal, autonomic, or aura-like symptoms. Headache localization depended upon the catheterized artery, being constant for each of the major vascular territories. Yet, in all patients pain was felt in the cutaneous territory of the ophthalmic division of the trigeminal nerve. The occurrence of headache was not associated with cortical deficit nor cortical irritation (assessed both clinically and by the EEG) and therefore seems to be directly related to the stimulation of the arterial wall. This type of pain can be used as a model of pure vascular headache. Its study can contribute not only to understand the pattern of intracranial vascular innervation but also to understand or to refute the vascular components of migraine.
Vascular headache of migraine-type may be a presenting symptom of multiple sclerosis (MS), a condition usually not considered in the differential diagnosis of a severe headache accompanied by neurological signs. We reviewed records of 1,113 patients with MS seen from 1967-1987 and found 44 cases whose initial attack or subsequent exacerbations were heralded by a migraine-type headache. Twenty-seven patients had no prior history of migraine, and of these, 12 presented simultaneously with their first headache and MS attack. Twenty-three patients had symptoms of a posterior fossa mass lesion. The significance of these results and possible pathogenesis is discussed.
To develop a reliable experimental model of vascular headache, we studied the dose-response relationship between headache and i.v. nitroglycerin (NTG) in 10 healthy subjects. NTG was infused intravenously over periods of 10 min separated by wash-out periods. Doses of 0.25, 0.50, 1.00 and 2.00 micrograms/kg/min were applied successively with one placebo infusion and wash-out period inserted randomly and double blindly. The subjects scored their headache intensity on a scale 0-10. After 1-8 weeks a retest was performed. Nine subjects developed headache already at 0.25 microgram/kg/min, whereas one had no headache at any dose. Headache severity did not increase with doses above 0.5 microgram/kg/min. This ceiling effect was reproducible. The headache was moderate, usually throbbing, bifrontal and not associated with other migrainous features. It reached maximum within 2.5-5.5 min (medians) at various doses and declined rapidly after NTG discontinuation. Wash-out periods of 10-20 min were sufficient. The reproducibility of headache intensity and character was satisfactory in the retest experiment. There were no unpleasant side effects and no visible flushing. Thus blindness was maintained. I.v. NTG is suitable as an experimental headache model. A constant infusion of 0.5 microgram/kg/min will be suitable for studies of arterial diameter, pulsations, blood flow, etc. Comparative studies of sensitivity should use the present infusion schedule but with the two highest doses substituted by 0.06 and 0.125 microgram/kg/min.