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

Arteriographic findings suggestive of inflammation are described in a 26-year-old woman presenting with headache and syncope. There were no clinical findings of angitis, and a diagnosis of status migrainosus was eventually made. We present her case, as well as a review of previous cases of arterial changes in patients with headache. Most previous cases report arterial narrowing, felt to reflect spasm, whereas our patient demonstrated segmental stenoses and dilatations, perhaps implicating inflammation. The inflammatory process has been postulated as the pathogenesis of migraine pain. As most migraineurs do not undergo arteriography, the incidence of arterial change in these patients is unknown. This finding has therapeutic implications for selecting the optimal anti-migraine agent.
Headache 1991 Jun
PMID:An unusual angiographic picture in status migrainosus. 188 82

Coronary spasm is an important etiologic mechanism in the pathogenesis of myocardial ischemia. Provocative test of coronary spasm during coronary arteriography is clinically useful. The ergonovine test has gained widespread use, and we have examined the efficacy and safety of intracoronary ergonovine application with a fixed dose of 16 micrograms. We studied 119 patients undergoing coronary arteriography. Coronary spasm was induced in 34 cases by intracoronary administration of 16 micrograms of ergonovine maleate. Coronary spasm was readily resolved by intracoronary administration of isosorbide dinitrate. None of the cases negative to the intracoronary ergonovine applications could be induced by additional systemic administration of 0.4 mg of ergonovine. Side effects of ergonovine such as elevation of blood pressure, headache and chest symptoms were infrequent in the intracoronary ergonovine test. We conclude that our method of intracoronary ergonovine application is sensitive and safe for the diagnosis of coronary spasm.
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PMID:[Intracoronary administration of ergonovine maleate for detecting vasospastic angina; one dose method]. 189 59

A 25 year old patient presented with recurrent prolonged episodes of life-threatening coma varying from 3 to 10 days. The clinical recovery was slow. The history and technical examinations led to the diagnosis of basilar artery migraine (BAM). The etiology of the coma episodes is thought to be related to ischemic dysfunction of the rostral part of the brainstem due to severe spasm of the basilar artery demonstrated by arteriography. Exceptional are the recurrent prolonged coma episodes of sudden onset, the severe spasm of the basilar artery, and the suppression-burst and FIRDA pattern on the EEG examinations during the coma episodes.
Headache 1991 Feb
PMID:Recurrent prolonged coma due to basilar artery migraine. A case report. 203 77

Three women with well-documented migraine associated with intracerebral hemorrhage are described. In each case, migraine headaches began during adulthood. Unusually severe and protracted headache heralded the onset of fixed neurological deficits associated with lobar intracerebral hemorrhage. Striking carotid artery tenderness was characteristic. Except for a history of migraine, no cause for intracerebral hemorrhage could be established. In each case arteriography showed extensive spasm of the appropriate extracranial or intracranial artery. Surgical pathology following evacuation of two hematomata demonstrated signs of vessel wall necrosis associated with subacute inflammatory changes. Vasospasm associated with severe migraine attacks may result in ischemia of intracranial vessel walls, leading to necrosis and subsequent vessel rupture when perfusion pressure is restored.
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PMID:Migraine with vasospasm and delayed intracerebral hemorrhage. 198 18

A 35-year-old woman presented 9 days postpartum with severe headache, arterial hypertension, and left parietal symptoms. A cerebral angiogram revealed widespread irregular areas of narrowing and dilatation, highly suggestive of vasculitis. The hypertension was treated successfully. A repeat angiogram 9 days later was almost completely normal. As this course is inconsistent with isolated cerebral vasculitis, and because the angiogram normalized with antihypertensive therapy, it is likely that the angiographic findings were secondary to hypertension. Experimental data in fact show that acute hypertension can produce areas of cerebrovascular spasm and dilatation. Recognition that angiographic findings suggestive of cerebral vasculitis are nonspecific and may be due to hypertension should prevent unnecessary treatment for vasculitis in such patients.
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PMID:Acute blood pressure elevation can mimic arteriographic appearance of cerebral vasculitis--(a postpartum case with relative hypertension). 231 80

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

Segmental arterial narrowing has rarely been angiographically demonstrated in patients with migraine. One new case is reported and 12 previous cases are reviewed. Though often referred to as vasospasm, arteriographic stenosis may result from edema of the vessel wall, arterial dissection, the effects of puerperium or arteritis. A biphasic course of spasm, similar to the pattern noted with subarachnoid hemorrhage, has been recorded in some migraineurs. The current neurogenic and biochemical concepts of "spasm" developed for subarachnoid hemorrhage are reviewed. Arterial narrowing may be important in several phenomena associated with migraine. It may account for migrainous cerebral infarction or hemorrhage. Vasoconstriction has also been invoked to explain the aura and other features of migraine. But the site of stenosis does not always correlate with the headache or focal neurologic features in location or timing. The angiographic changes are probably an epiphenomena rather than a primary mechanism of migraine. These changes may result from altered sympathetic neuronal activity; factors supporting that concept are reviewed.
Headache 1990 Jan
PMID:Arterial stenosis in migraine: spasm or arteriopathy? 240 21

Within the last decade it became obvious that the treatment of angina pectoris alone is not sufficient. Modern goals include the optimization of anti-ischemic treatment ("silent myocardial ischemia") without compromising quality of life, as well as the reduction of fatal and non-fatal cardiac events. The failure of nitrates to continuously protect from myocardial ischemia ("nitrate tolerance") requires a modification of the current step-care recommendations for medical treatment. Numerous combinations of nitrates, betablockers and calcium channel blockers compensate for each other regarding their effects on heart rate, contractility, peripheral resistance and coronary blood flow. Recommendations for combination therapy decisively depend on the choice of the first-line drug. Only nitrates reduce myocardial preload by venodilation and substitute for EDRF-deficiency. After headaches disappear, nitrates do not affect quality of life and they are cheap. The nitrate-induced acceleration of heart rate should be compensated by the addition of beta-blockers or heart rate-decreasing calcium channel blockers. Therefore, the combination of nitrates with heart-rate-increasing calcium channel blockers, such as nifedipine, should be avoided. Many studies have proven the superiority of different double and triple therapies, as compared to their single components. A few reports, however, did not confirm this increase of anti-ischemic efficacy with combination therapy. The improvement of prognosis is proven for beta blockers without ISA in subgroups of patients with acute or post myocardial infarction and can be assumed for nitrates as well. With regard to prognosis, calcium channel blockers were inferior to nitrates and beta blockers. The combination of nitrates with a non-ISA betablocker should be preferred in post myocardial infarction patients with ventricular arrhythmias, whereas the combination of nitrates with a heart rate decreasing calcium channel blocker should be preferred in patients with COPD, severe peripheral arterial disease or severe diabetes. The combination of nitrates with a heart-rate-increasing calcium channel blocker should be considered in patients with sinus bradycardia, first degree AV-block, or proven coronary spasm. In patients with congestive heart failure, betablockers and calcium channel blockers should be avoided. To optimize medical treatment of ischemic heart disease, intermittent high dosage ISDN plus a beta blocker without ISA or ISDN plus a calcium channel blocker like verapamil are recommended. Frequently, however, the patient decides by himself, based on unacceptable side effects.
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PMID:[Combination of anti-angina drugs]. 257 81

Benign headaches related to sexual activity and exertion are being recognised with increasing frequency. We wish to report a case of benign sexual headache (Type 2) and benign exertional headache, occurring sequentially in the same patient. Multiple areas of cerebral arterial spasm were demonstrable on angiography. This observation would support the concept that benign sexual headache (Type 2) and benign exertional headache may have a similar pathophysiology.
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PMID:Angiographically demonstrated arterial spasm in a case of benign sexual headache and benign exertional headache. 259 98

It's about a therapeutic method, particular to the author, which gets its universality from an optic prescription with a prismatic aspect. The ophthalmic headache's crisis is caused, in fact, by a spasm of convergence on an unknown exophory of which the amplitude of fusion is satisfying, and the presence of which can only be seen with test under screen.
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PMID:[Universal treatment of ophthalmic migraine]. 259 Sep 81


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