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

This review summarizes 169 cerebral vascular accidents in women taking oral contraceptives: 94 arterial (including 13 of the authors' cases), 20 venous, 37 neuroophthalmologic (5 of the authors'), and 18 undetermined diagnoses. The arterial accidents involved the carotid in 56, the vertebrobasilar in 27. Few were fatal; most were considered thromboses; none were due to hemorrhage; few could have been due to emboli or dissecting aneurisms. Aggravation or appearance of migraine was noted in 34 and transient focal cerebral ischemia in 28 cases before arterial accident. No definite time span was obvious, but many occurred 1-6 months or over 2 years after starting pills. Venous accidents were usually fatal, often extended thromboses of the superior longitudinal sinus. Clinically there was severe headache (85%), vomiting, fever without rapid pulse, alteration of consciousness, papillary edema, focal cerebral signs. Ophthalmologic accidents included retinal, arterial, and venous occlusion; paralysis of oculomotor nerve; optic neuritis; and pseudo-tumor-cerebri. The authors recommended caution with oral contraceptives in case of cerebral vascular episodes, migraine, visual disturbances, chorea, hyperlipidemia, and hypertension.
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PMID:[Cerebrovacular accidents and oral contraceptives]. 443 14

Patients with classic migraine (69 women and 31 men) selected randomly from a practice list of over 1000 were matched for age, sex and neighbourhood with 100 people who did not have headache problems, and both groups underwent M-mode and two-dimensional echocardiography and clinical examination by cardiologists blinded to the subjects' clinical status. The mean ages were 34.9 +/- 11.3 years for the migraine group and 33.1 +/- 9.9 years for the control group. Definite and possible mitral valve prolapse (MVP), diagnosed according to predefined echocardiographic criteria, were found about twice as often in the migraine group as in the control group (in 15 v. 7 and 16 v. 8 patients respectively); the echocardiograms were definitely normal in 69 migraine patients and 85 controls (chi 2 = 8.39, p less than 0.025). Altogether 25% of the migraine group and 11% of the control group had evidence of MVP from a combination of the echocardiographic and auscultatory findings (chi 2 = 5.72, p less than 0.025). The odds ratio was 2.7, with 95% confidence limits of 1.17 and 6.29. The association between migraine and MVP has implications for the understanding of platelet abnormalities and episodes of cerebral ischemia occurring in both these conditions.
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PMID:Increased prevalence of mitral valve prolapse in patients with migraine. 649 1

A conceptual approach that relates vascular headaches, bowel and bladder dysfunction to abnormalities of the "ammonia potassium axis" is presented. Hypokalemia alters smooth muscle function of both the bowel and bladder and results in the elaboration of an alkaline urine. The occurrence of an alkaline urine, along with bladder dysfunction and urinary stasis, predisposes to recurrent urinary tract infections. Hypokalemia and/or alkalosis increases the renal return of ammonia, exposes the brain to chronically higher concentration of ammonia and facilitates its passage into the central nervous system. Increased levels of blood ammonia predispose to hyperventilation which results in a superimposed respiratory alkalosis on a pre-existing hypokalemia and/or alkalosis therefore causing intense cerebral vasoconstriction. Varying degrees of cerebral ischemia and hypoxia occur and give rise to higher brain concentrations of ammonia. Vasodilatation occurs during the headache phase and may be a consequence of the sudden increase of brain ammonia and/or due to the release of other vasoactive mediators. As a consequence of increased blood ammonia, a reduction of protein intake may result in the alterations of amino acid precursors for brain uptake and therefore further interferes with the modulation of cerebral blood flow and brain function.
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PMID:The hypokalemic, bowel, bladder, headache relationship; a new syndrome. The role of the potassium ammonia axis. 651 31

Twenty-three clinical cases are reported, illustrating the difficulties of diagnosing migrainous focal cerebrovascular accidents. Cases of constituted cerebral infarcts and transient cerebral ischemia occurring during the cephalalgic phase, without headache and in patients with no previous history of typical migrainous attacks are described. Migraine may be considered to be the cause on convincing clinical criteria, but the diagnosis can only be established after negative results of investigations to exclude other causes of focal cerebral ischemia.
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PMID:[Cerebrovascular accidents and migraine]. 661 10

A 23-month-old infant with an extensive dural arteriovenous malformation (AVM) developed a heart murmur and cardiomegaly. The AVM involved the occipital and suboccipital dura mater and the tentorium, bilaterally. We embolized the AVM with Gelfoam and polyvinyl alcohol particulates, subtotally resected it, and embolized residual vessels with isobutyl cyanoacrylate. In spite of this extensive therapy, the malformation was not totally eradicated and an occipital pial AVM developed. This infant and the eight infants with posterior dural AVMs reported previously emphasize the difficulty of eradicating these lesions in infancy. We contrast the clinical features and therapy of infants and adults with posterior dural AVMs. Infants develop heart failure and cranial bruits because of arteriovenous shunts, whereas adults complain of headache and intracranial bruits. Infants need therapy to prevent progressive heart failure, intracranial hypertension, and perhaps cerebral ischemia. Ligation of arterial tributaries is inadequate therapy for these lesions. Embolization and resection of the malformation, when feasible, offers the best chance of curing posterior dural AVMs with extensive arterial tributaries.
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PMID:Posterior dural arteriovenous malformations in infancy. 688 91

Patients with classical migraine whose auras included paraesthesiae or numbness in the hands have been reviewed. In 55 of 111 patients the symptoms were on the same side of the body as the headache and in only 20 on the opposite side to the headache. In the remaining 36 patients one or other was incompletely lateralised. Five right handed patients described dysphasia at the same time as paraesthesiae in the their non-dominant hand. These findings are incompatible with the notion that the headache is due to reactive hyperaemia following localised cerebral ischaemia, and it is suggested that the ischaemic and hyperaemic processes are both the result of some more generalised vasomotor disturbance.
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PMID:Asymmetry of the aura and pain in migraine. 731 Apr 27

Hypertension causes marked adaptive changes in the cerebral circulation. The excess risk of stroke associated with hypertension is eliminated in controlled trials of antihypertensive treatment. Such treatment may even prevent transient ischaemic attacks in the elderly. In rare cases, overzealous antihypertensive treatment may cause cerebral ischaemia, especially in the initial treatment of very severe hypertension. Headache may occasionally be caused by severe hypertension, which may also lead to the rare syndrome of acute hypertensive encephalopathy. Finally, the importance of white-matter lesions, or leukoaraiosis, in hypertension is not yet fully established.
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PMID:Cerebrovascular damage in hypertension. 760 37

Recent debate concerning the interpretation of studies of regional cerebral blood flow in migraine has re-emphasized that cerebral ischaemia may occur during attacks of migraine with aura. In this article we suggest that the presence of ischaemia during attacks makes it possible that migraine with aura causes neuronal damage in the long term. We argue that damage is likely to occur in the primary visual cortex, given that a recent high-resolution rCBF study has found flow reductions confined to this area. Furthermore, we hypothesize that the extent to which rCBF is reduced in migraine with aura is sufficient to cause damage only to GABA-ergic inhibitory interneurons in layer IV of this cortex. In animal models, similar cells are known to be selectively vulnerable to damage as a result of hypoxic conditions. Evidence consistent with our hypothesis is provided by recent studies of visual function in migraine. Some clinical and pathophysiological implications of this hypothesis are discussed.
Cephalalgia 1994 Dec
PMID:Might migraine damage the brain? 769 2

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. 779 22

One current view of migraine pathophysiology suggests that vasospasm causes cerebral ischemia and focal symptoms during an aura and that reactive hyperemia accompanies the headaches. Eight patients with acute migraine with sensory aura were studied with somatosensory evoked potential (SEP) to examine the vascular theory of acute migraine headache. All patients had sudden onset of hemiparesthesia as an aura followed by throbbing headaches. SEPs were obtained from the median nerve stimulation in two patients during the aura phase and six during the headache phase. SEPs were abnormal in both cases during the aura phase. The abnormality consisted of attenuation of amplitude and prolongation of N19 in the sensory cortex, resulting in prolongation of central conduction time, which gradually returned to normal during the headache phase. SEPs of six other patients obtained during the headache phase were also normal. The study concludes that: (1) there is a different pathophysiology between aura and headache phase; (2) the changes of SEPs during the aura may result from cerebral ischemia; and (3) normal SEPs during the headache phase suggest that reactive hyperemia may not alter SEP wave forms.
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PMID:Somatosensory evoked potentials in acute migraine with sensory aura. 788 44


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