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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The current view that the migraine aura arises from spasm of the major cerebral arteries and the ensuing headache from extracranial arterial vasodilatation is examined and refuted. It is proposed that the headache is due to stimulation of nociceptive nerve-endings in the walls of meningeal vessels (arterioles, venules, and particularly the dural venous sinuses); and that the aura arises from calibre changes in meningeal vessels that penetrate the outer cortex, resulting in localised inhibition or excitation. It is suggested that there are two types of migraine patients--vasodilators and vasoconstrictors.
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PMID:Migraine: A vasomotor instability of the meningeal circulation. 8 93

Various types of disorders of the cervical region may produce headache. In many of these increased tension of the neck musculature plays an important role. The following mechanisms underlying headache are described and differentiated: 1. Headache due to faulty muscle pattern (stereotype) resulting in overstrain of the upper fixators of the shoulder girdle (upper part of the m.trapezius and levator scapulae); faulty respiration with the aid of the upper auxillary muscles even at rest is pointed out. 2. A forward drawn head position producing static overstrain in the posterior neck muscles and compensatory retroflexion of the cranio-cervical junction resulting in blockage in this region. 3. Anteflexion and ligament pain mainly due to faulty position at work and jolting. 4. Static disturbance in the frontal plain due to obliquity producing asymmetrical strain in the neck musculature. 5. Increased muscular tension due to psychological stress. 6. Blockage in the regions of the cervical spine, shoulder girdle and upper ribs with reflex muscular spasm. 7. Reflex spasm of the neck musculature in visceral disorders causing in addition blockage of the cervico-thoracic junction (heart, gall bladder). 8. Pain arising from the posterior arch of the atlas (here described for the first time). 9. Headache due to vertebral artery involvement. The type of headache seems to be determined rather by the individual mode of reaction than by the mechanism underlying it. As a rule a combination of mechanisms is actually found.
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PMID:[Pathomechanisms of cervical headaches]. 60 87

In contradistinction to all currently available water-soluble contrast media, metrizamide (Amipaque) is not a salt, but a substituted amide and therefore does not dissociate in solution. This unique property results in solutions of high iodine content yet with low osmolality. Metrizamide probably has a lower neurotoxicity than any other known water-soluble contrast agent. A clinical trial of metrizamide lumbar myelography in 201 patients in three clinical centres represents the first clinical assessment of this new contrast medium in the United Kingdom. The technique of the radiological procedure and the adverse reactions encountered are presented and discussed. There were no serious adverse effects: no muscle spasm or epilepsy. Minor adverse reactions--headache, vomiting and nausea occur with approximately the same frequency as with meglumine iocarmate: 43 percent of patients complained of headache. In 118 patients, the lower dorsal subarachnoid space was also examined with no increase in toxic reactions. It is concluded that metrizamide is a safe contrast medium for lumbar and lower dorsal myelography. Water-soluble media will probably largely replace oil products for these investigations. Further clinical trials are being extended to include examination of the upper dorsal and cervical subarachnoid space.
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PMID:Lumbar myelography with metrizamide-a new non-ionic contrast medium. 79 73

Computerized axial tomography of the cranium has been carried out in 46 patients referred because recurring migrainous headaches. Increasing frequency or severity of headaches or a change in headache pattern were the usual reasons for referral. Abnormalities were found in 37 cases and fell into 4 categories. The most frequent (21 cases) consisted of a mild degree of oedema in the white matter of one or both cerebral hemispheres. This was usually bi-frontal (15 patients) but was more extensive in 2 patients. Varying degrees of cerebral atrophy, as determined by widening of the Sylvian, brain-stem and interhemispheric cisterns, and/or widening of the third and lateral ventricles as compared to a group of normal scans, was found in 8 cases. Areas of occipital infarction were found in 4 patients with permanent visual field defects. Unexpected small areas of infarction were found in the temporal lobe in 2 other cases. Cerebral tumours were found in 2 cases. The significance of these findings is discussed, as well as the possible role of migrainous vaso-spasm with consequent changes in cerebral blood flow in the pathogenesis of oedema and atrophy in migraine subjects.
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PMID:Computerized axial tomography findings in a group of patients with migrainous headaches. 102 5

Severe extremity ischemia developed in four patients who had ingested methysergide maleate or ergot for the relief of headache. Symptoms involved the upper extremity in two patients and the lower extremity in two. Spontaneous reversal of the ischemic picture was obtained by simple discontinuation of ergot in most instances, although intra-arterial vasodilators were used in one case. Angliography disclosed arterial spasm and was a useful adjunct in confirming the cause of ischemia in each of the patients. It was especially useful when a history or ergot ingestion was not immediately available.
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PMID:Ergotism. 115 59

The author reports the results of electromyographic investigations of the muscles of the nape and temporal muscles in 132 patients with headaches of different aetiology (migraine, cervical migraine, vasomotor headache, symptomatic headaches) and in 51 controls who had never had headaches. In the healthy subjects no bioelectric activity was observed when the patients relaxed completely. On the other hand, in most patients with headaches continuous bioelectric activity was observed at rest in these muscles indicating their involuntary contraction. This phenomenon is called by the author "cephalalgic" spasm of head and neck muscles, which is rather characteristic of various headaches.
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PMID:[Electromyographic studies of nape and temporal muscles in headaches of various etiology]. 116 32

A 68-year-old woman was admitted to Nagasaki University Hospital complaining of gait disturbance. She had suffered from hemifacial spasm since the age of 56 and had undergone neurovascular decompression for the spasm in another hospital five years before admission. At surgery, the vertebral and posterior inferior cerebellar arteries had been separated from the facial nerve with cotton string and attached to the clivus with alpha-cyanoacrylate monomer. Although the hemifacial spasm had improved postoperatively, the patient had suffered from gait disturbance and headache for two months after surgery, and hearing disturbance and hemifacial palsy on the same side as the hemifacial spasm for seven months after surgery. At the time of the present admission, contrast-enhanced CT scan revealed a mass at the left cerebello-pontine angle. In the T1-weighted inversion recovery sequence of MRI, the mass showed a slightly lower intensity than that of surrounding tissues. In the T2-weighted spin echo sequence of MRI, it showed a heterogenously low intensity with some high intensity spots. We diagnosed this mass as a foreign-body granuloma and treated it with dexamethasone injected intramuscularly. Edema decreased around the granuloma, and her gait disturbance improved markedly. But the hearing disturbance and hemifacial palsy did not improve at all, indicating that these two symptoms might not be caused only by brain edema but also by direct damage due to granuloma or inflammation. We thought that the steroid hormone elicited good results in the treatment of inoperable foreign-body granuloma.
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PMID:[A case of foreign-body granuloma treated with steroid hormone]. 130 Feb 60

For several years, cerebral blood flow (CBF) studies have been fueling the controversy surrounding the pathophysiology of migraine headache. The earliest studies focused mainly on migraine with aura (MA+) and provided evidence in support of the classical hemodynamic theory: a decrease in blood flow during the aura is followed by reactive vasodilation during the headache phase. Studies in migraine without aura (MA-), although less numerous, consistently demonstrated an increase in CBF during the attack. Olesen et al., gave rise to a heated debate by suggesting that hemodynamic manifestations are different in MA+ and MA-; in their view, CBF remains unchanged in MA-, whereas MA+ is associated with a wave of posterior blood flow deficiency which slowly spreads forwards in a manner reminiscent of experimental spreading depression; they interpret this hemodynamic pattern as evidence that the attack is mainly caused by a neural mechanism rather than a vascular spasm. This concept of MA- with no hemodynamic changes suggests that the pathophysiology of MA- may be completely different from that of MA+. However, most studies using stationary detectors or single photon emission computerized tomography (SPECT) with Xenon 133 or HMPAO as the tracer have demonstrated increased CBF during migraine attacks. The increase was not correlated with the side of the pain suggesting that vasodilatation is not the only cause of the pain. Current data do not seem to support the view that MA- and MA+ are different pathophysiologic entities; whether the mechanism of the attack is neural or vascular cannot be determined on the basis of CBF data.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral blood flow in migraine without aura]. 149 16

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
Headache 1992 Jan
PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

In an open clinical trial, thirty patients 14 to 44 years old and with acute uncomplicated falciparum malaria were given halofantrine hydrochloride 500 mg (2 tablets) 6-hourly for 3 doses, a total dose of 1500 mg. All 30 patients were cured, with a mean asexual parasite clearance time of 47.6 hours and mean fever clearance time of 36.6 hours. Post-dosing side-effects occurred in 6 patients consisting of mild to moderate headache, dizziness and abdominal muscle spasm. Drug-induced hemolysis did not occur in two G6PD deficient patients. Twenty-three out of 28 isolates tested (82%) were resistant to amodiaquine, 3 (11%) were resistant to the sulfadoxine-pyrimethamine combination, and all were sensitive to chloroquine, quinine and mefloquine by in vitro microtests. The study confirms the efficacy of halofantrine hydrochloride as a blood schizonticide in falciparum malaria.
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PMID:Halofantrine in the treatment of acute uncomplicated falciparum malaria in the Philippines. 181 90


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