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

Distension of dural sinuses in man produces migraine-like pain. In eight alpha-chloralose anaesthetized cats mechanical distension of the superior sagittal sinus with a small intraluminal device was used to activate single units in the dorsolateral C2 spinal cord. Units in this region have been shown to respond to electrical stimulation of the superior sagittal sinus in the cat model. Linked responses to mechanical dilatation could only be obtained with very rapid stretching stimuli or high amplitudes of distension of the vessel. Lower thresholds for transduction of distension in the vessel wall may depend on transferral to the dura or biochemical or neural pre-sensitization of the superior sagittal sinus. These data are consistent with the view that migraine is not primarily a vascular disorder but requires at least humoral or neural facilitation.
Cephalalgia 1992 Jun
PMID:Activation of the trigeminovascular system by mechanical distension of the superior sagittal sinus in the cat. 162 3

Fibromuscular dysplasia (FMD) is a non-atheromatous, non-inflammatory, segmental arteriopathy of unknown etiology. Fibroplasia of the tunica media is most common. After the renal arteries, the carotid arteries are most frequently affected. Angiographically beaded and tubular stenoses are seen. Complete occlusions and spontaneous dissection of the carotid arteries occur. The angiopathy causes general symptoms such as headache and vertigo, but also recurrent TIA and ischemic cerebral infarction. We examined 15 patients (12 female) suffering from FMD and stroke. The diagnosis of FMD was based on angiographic findings in all cases. 13 patients made a good recovery and seven of them could be discharged from hospital without any neurological deficit. Apart from conservative treatment, primary percutaneous or operative angioplasty may be necessary in some cases in spite of the mostly benign outcome of the disease. Acetylsalicylic acid should be given in all cases.
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PMID:[Fibromuscular dysplasia as a cause of cerebral infarct]. 163 15

Clinical, radiological, and immunohistochemical findings in brain biopsy specimens from six patients with cerebral amyloid angiopathy-associated intracerebral hemorrhage were reviewed. Acute clinical presentations included headache, nausea and vomiting, loss of consciousness, and focal neurological deficits such as hemiplegia and blindness. Transient ischemic attacks experienced by one patient and referable to one hemisphere did not indicate impending hemorrhage in that region. Computed tomographic scans revealed acute, irregular, superficial, lobar hemorrhage with occasional ring enhancement. Immunohistochemical studies were performed on biopsy specimens using primary antibodies against portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (the vascular amyloid protein in patients with hereditary cerebral hemorrhage with amyloidosis-Icelandic type). In all patients, anti-A4 and anti-gamma-trace labeled cerebral microvessels. Immunoreactive senile plaques were few compared with the numbers of stained microvessels. Reactive astrocytes in some patients were labeled by both antiserum samples, suggesting uptake or production of these proteins by the astrocytes. This study demonstrates the heterogeneous clinical and radiological features of cerebral amyloid angiopathy-related brain hemorrhage and the value of anti-A4 and anti-gamma-trace immunohistochemical study of biopsy material from patients with suspected cerebral amyloid angiopathy-related intraparenchymal bleeding.
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PMID:Cerebral hemorrhage with biopsy-proved amyloid angiopathy. 172 64

I studied 9 patients with migraine and posterior circulation ischemia. Inclusion criteria were (1) brainstem or cerebellar infarcts or transient ischemic attacks, (2) satisfactory vertebrobasilar angiograms, and (3) migraine. Excluded were patients with only occipital lobe ischemia, known arteriosclerosis, or other nonmigrainous vascular disease. Two women and 7 men, ages 6 to 58 years (mean, 34.7), had transient attacks only (2), single strokes (4), single stroke followed by attacks (1), or multiple strokes (2). Five had antecedent classic, 2 common migraine, and classic migraine began only after the initial ischemic event in the other two. The 7 stroke patients all had CT- or MRI-documented brainstem (4) or cerebellar (6) infarcts. Angiography was normal (3) or demonstrated basilar artery (BA) narrowing (2) or occlusion (4), or branch occlusion (1). In 3 patients the initially occluded BA later reopened. At follow-up (average 4.3 years, range 1 to 9 years), 5 were normal and 4 had important clinical deficits. I conclude that (1) "basilar migraine" is not always benign; it affects both sexes and a wide age range; (2) the pattern of headaches, attacks, and strokes varies; (3) migraine may appear only after ischemia; (4) some patients have BA occlusion or diffuse narrowing; and (5) BA occlusion can be temporary.
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PMID:Migraine and vertebrobasilar ischemia. 192 34

A 49-year-old male was admitted to our hospital because of severe headache and dizziness which had occurred suddenly one day before admission. There was no past history contributory to cerebral hemorrhage but was family history of cerebrovascular accidents in his father and brother. Neurological examination revealed left homonymous hemianopsia, mild left hemiparesis, and left side hemi-neglect in simultaneous stimuli on bilateral extremities. Laboratory data including peripheral blood cells, coagulation tests, and serum chemistry were unremarkable. Brain CT and MRI demonstrated large lobar hematoma in the right parieto-occipito-temporal region. Cystatin C level in the CSF samples taken on the 39th and 59 th days (38 and 27 ng/ml respectively) were low, compared with the normal value (greater than 100 ng/ml). These findings suggest that the lobar cerebral hemorrhage of the present case might have been caused by cerebral amyloid angiopathy with cystatin C deposits.
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PMID:[A case of lobar cerebral hemorrhage with low concentration of CSF cystatin C]. 191 34

5-Hydroxytryptamine (5-HT; serotonin) has long been implicated in the aetiology of migraine but the evidence remains circumstantial and certainly not definitive. Numerous papers have reviewed the background which is briefly outlined here. Although the continued belief in the primary involvement of 5-HT in the genesis of a migraine attack has recently been questioned, many antimigraine drugs undeniably interact potently with 5-HT receptors. It can be argued, however, that their modest clinical benefit results from their pharmacological effects, be they mediated through 5-HT receptors or otherwise, independently of any pathophysiological involvement of endogenous 5-HT. Nevertheless, there seems convincing evidence that central release of 5-HT by various drug mechanisms causes migraine-like headache in migraineurs. It remains to be seen whether these drugs mimic the pathological event initiating the spontaneous migraine attack. Regardless of these considerations, the focus of research on 5-HT and migraine has proved to be enormously profitable over several decades, culminating recently in the identification of a novel, potentially important, antimigraine drug for the treatment of the acute attack. This drug, sumatriptan, is a selective cranial vasoconstrictor which mediates this effect by specifically activating a particular 5-HT1 receptor subtype. Undoubtedly a precise understanding of its clinical mechanism of action, which is currently being studied by a number of groups, will lead to a better understanding of the pathogenesis of migraine. Perhaps this in turn will help in finally determining whether migraine is a vascular disease and whether or not a disturbance of 5-HT is just epiphenomenal or is truly the primary initiating pathological event.
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PMID:5-Hydroxytryptamine and the pathophysiology of migraine. 204 30

While headache frequently arises from local dysfunction, there are many systemic diseases in which headache may be the initial or sole manifestation of the underlying process. These include infectious disease, vascular disease, drug or heavy metal intoxication, metabolic abnormalities, migraine, cluster headache, headache associated with ENT disease and cranial neuralgias (these disease entities are described in detail in the International Headache Society Classification). The work up of a patient with headache must include a consideration of these entities.
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PMID:Headache as an initial manifestation of systemic disease. 209 55

Consumption of monosodium glutamate has long been considered to precipitate headaches in susceptible patients. In this study the direct effects of glutamate and its metabolite, glutamine, on arterial contractility were examined using rings of rabbit aorta. In a high concentration glutamate caused significant concentration-dependent contractions (EC50, 10(-1)M; maximum tension, 188.4 +/- 33.3 mg wt tension/mg tissue). Agonists and antagonists for alpha-adrenergic, histaminergic, serotonergic, cholinergic, and GABA-nergic receptors as well as inhibition of prostaglandin synthesis failed to influence glutamate contractions. At high concentrations (10(-5)M) the calcium channel blocker, verapamil, inhibited the glutamate response. Glutamate and glutamine both exhibited concentration dependent relaxation of norepinephrine (NE), phenylephrine (PE), histamine, serotonin (5-HT), and prostaglandin F2 alpha (PGF2 alpha)-induced contractions. Kainic acid (10(-4)M), an agonist of one subpopulation of central glutamate receptor, potentiated glutamate-induced vasoconstriction; a higher concentration (10(-3)M) produced an irreversible inhibition of glutamate contractility. Only the central glutamate receptor antagonist, ketamine (10(-4)-10(-2)M), induced a reversible, concentration dependent inhibition of glutamate-induced contractions. Glutamate contractility was not dependent on extracellular calcium, an intact endothelium or neuronal function. These results demonstrate a direct effect of glutamate on peripheral arterial tone. Dietary consumption of large quantities of MSG may represent a serious health hazard to certain individuals with pre-existing vascular disease.
Headache 1990 Sep
PMID:Vasospasm contributes to monosodium glutamate-induced headache. 226 10

We studied five patients with cerebral hemorrhage limited to the head of the caudate nucleus. This rare localization represents 11% of central nuclei hemorrhages. This entity has various clinical expressions; some are similar to a subarachnoid hemorrhage, others show the same manifestations associated with hemiparesis and neuropsychological findings, while still in others, the neuropsychological syndrome with speech, behaviour or memory disturbances predominates. Recovery depends on the patient's previous clinical status and on the presence of associated lesions at the time of hemorrhage. Typical warning signs, like headache, are often absent in the elderly and debilitated. Meningismus is explained by the intraventricular extension of the hemorrhage. Motor deficit, usually moderate, is probably due to impairment of the anterior portion of the posterior arm of the internal capsule. Destruction of the head of the left caudate nucleus, which is part of the circuit causing "subcortical aphasias", is responsible for non specific speech disturbances, that are however remarkably rich in semantic paraphasias. These dysfunctions could be caused by a "cortical diaschisis" as suggested by SPECT analysis. Memory dysfunction as a result of caudate lesion is questioned. However confusion and behavioural disturbances, like preservations, transitory mutism and self neglect, seem characteristic. As shown by cerebral blood flow (CBF) studies, these disturbances might represent a frontal dysfunction caused by the interruption of the dorso-latero-prefrontal and orbito-frontal circuits. When the hemorrhage extends beyond the head of the caudate nucleus, behavioural changes occur due to the involvement of neighbouring structures such as the thalamus, internal capsule, temporal lobe and nucleus accumbens. Caudate hemorrhages occur mostly in the elderly, often with long-standing arterial hypertension causing lesions of the lenticulo-striate arteries. Severe stenosis or complete occlusion of the middle cerebral artery with a fragile anastomotic circuit or angiopathies in younger individuals (particularly Asiatics: moyamoya disease) are less frequent, but they should be considered and investigated by arteriography. Vascular malformations are a rare cause and a relationship with amyloid angiopathy can only be suspected.
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PMID:[Hematoma of the head of the caudate nucleus]. 229 Oct 35

Forty six patients aged 18-39 years with transient ischaemic attacks (TIA) were studied; two thirds were women. Twenty five patients had attacks accompanied by headache, and seven gave a history of common migraine. Only four of 27 angiograms were abnormal; no operable carotid lesion was demonstrated. Over a mean follow up period of 10 years stroke or myocardial infarction (AMI) occurred in all four patients who presented major cerebrovascular risk factors, but in only two of the remaining 42 patients. Thus irrespective of age thromboembolic TIA is a harbinger of stroke or AMI. However, most TIAs under the age of 40 years are caused by a non-embolic benign vascular disorder. The clinical characteristics, long-term prognosis, and possible pathogenesis, for such attacks are often indistinguishable from those of classical migraine. In the absence of cardiovascular risk factors, arteriography does not provide much diagnostic and prognostic information.
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PMID:Transient ischaemic attacks in young patients: a thromboembolic or migrainous manifestation? A 10 year follow up study of 46 patients. 229 92


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