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

It has been suggested that magnesium (Mg) may play a role in the pathogenesis of headaches. Serum and intracellular measurements of Mg in headache patients have produced inconsistent results. The recent development of an ion-selective electrode for Mg2+ allowed precise measurement of serum ionized magnesium (IMg2+) in patients with various headache syndromes. Low serum IMg2+ and a high ICa2+/IMg2+ ratio were found in 42% of patients having an attack of migraine, but only in 23% of patients with a severe continuous headache. Total serum Mg was normal in both groups of patients. However, in patients with low serum IMg2+ total serum Mg was lower than in patients with normal serum IMg2+. These results are compatible with the serotonin and vascular concepts of migraine pathogenesis. Low IMg2+ and a high ICa2+/IMg2+ would result in cerebral vasospasm and reduced blood flow in the brain. The activity of serotonin receptors can also be affected by changes in IMg2+ levels. The finding of a difference in IMg2+ levels in two different headache types suggests a possible novel classification of headaches and that migraine patients with a low serum IMg2+ or a high ICa2+/IMg2+ ratio may benefit from Mg supplementation.
Headache 1993 Mar
PMID:Deficiency in serum ionized magnesium but not total magnesium in patients with migraines. Possible role of ICa2+/IMg2+ ratio. 848 10

Previous studies have shown that migraine with aura is associated with the reduction of regional cerebral blood flow (rCBF). However, the question of whether the reduction of rCBF during migraine aura is caused by cerebral vasospasm or is secondary to the neural depression (spreading depression) is still disputed. We measured rCBF by high resolution SPECT method during the attack of migraine and examined whether the reduction in flow corresponds to the cerebral vascular territory. Fourteen patients with migraine with aura (7 men and 7 women, 34.7 +/- 17.8 years) were studied. In all the patients rCBF was measured during the interictal period and in four patients rCBF was measured during the aura of migraine. SPECT measurements of rCBF was performed using Tc-99m-PAO (740 MBq) as a tracer. During the aura of scintillation scotoma in the unilateral visual field rCBF was reduced in the opposite occipital, temporal and thalamic regions which corresponded clearly to the region of the posterior cerebral arterial territory. The reduction of rCBF was by 31 approximately 49% compared with the opposite hemisphere. Cerebral spinal fluid lactate level during the headache measured in one patient was higher (38 mg/dl) than the interictal period (12 mg/dl). Our data indicated that the reduction of rCBF during the aura is caused by ischemia probably due to the cerebral vasospasm and is not secondary to the neuronal depression. It was also suggested that the primary site of rCBF reduction during the visual aura is the occipital association cortex which is reported to be responsible for the visual hallucination.
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PMID:[Regional cerebral blood flow during migraine]. 875 89

In a 23-year-old woman, gravida 1, para 1-0-0-1, headaches and seizures developed 1 week after an uncomplicated delivery. Cerebral angiography revealed severe, diffuse cerebral vasospasm. Her symptoms resolved with hyperosmolar, hypervolemic therapy and nimodipine. Magnetic resonance angiography on postpartum day 23 confirmed persistent, severe vasospasm, and repeat magnetic resonance angiography on postpartum day 33 demonstrated interval improvement. This report documents the time course of a case of postpartum vasospasm and its response to hypervolemic, hyperosmolar therapy and nimodipine.
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PMID:Postpartum cerebral vasospasm treated with hypervolemic therapy. 894 24

Published medical evidence pertaining to the management of aneurysmal subarachnoid hemorrhage (SAH) was critically reviewed in order to prepare practice guidelines for this condition. SAH should be considered as a possible cause of all sudden and/or unusual headaches, and every attempt should be made to recognize mild SAHs, as they are still frequently misdiagnosed. The first test for SAH is computed tomography (CT), followed by lumbar puncture when the CT is negative for intracranial bleeding (the case in only several per cent of patients within 24 hours of aneurysm bleeding). Urgent cerebral angiography is necessary to detect the underlying cerebral aneurysm. The advantage of rapid diagnosis of SAH followed by early aneurysm repair is minimizing the risk of catastrophic aneurysm rebleeding. Early surgery for aneurysm repair is often possible and is recommended, unless the aneurysm location or size renders it technically difficult to expose in clot-laden subarachnoid cisterns beneath an acutely swollen brain. Aneurysm ablation is optimally accomplished with open microsurgery and clipping of the aneurysm neck, although other options include proximal parent artery occlusion, "trapping" of the aneurysmal segment of the artery, and embolization of thrombogenic materials (e.g., platinum "microcoils") directly into the aneurysm dome using endovascular techniques. Neurological outcome following SAH is also optimized through the prevention of secondary SAH complications, and further management specific for ruptured cerebral aneurysms can include anticonvulsants, neuroprotectants, and various agents and techniques to prevent or reverse delayed-onset cerebral vasospasm. All patients with aneurysmal SAH should be treated with the calcium antagonist nimodipine, and in certain circumstances patients should receive anticonvulsants. Induced arterial hypertension, hypervolemia and in some instances percutaneous balloon angioplasty are recommended to reverse vasospasm causing symptomatic cerebral ischemia prior to cerebral infarction.
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PMID:Current management of aneurysmal subarachnoid hemorrhage guidelines from the Canadian Neurosurgical Society. 916 96

Vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is correlated with the thickness of blood within the basal cisterns on the initial computerized tomography (CT) scan. To identify additional risk factors for symptomatic vasospasm, the authors performed a prospective analysis of 75 consecutively admitted patients who were treated for aneurysmal SAH. Five patients who died before treatment or were comatose postoperatively were excluded from the study. Of the remaining 70 patients, demographic (age, gender, and race) and clinical (hypertension, diabetes, coronary artery disease, smoking, alcohol abuse, illicit drug use, sentinel headache, Fisher grade, Hunt and Hess grade, World Federation of Neurological Surgeons grade, and ruptured aneurysm location) parameters were evaluated using multivariate logistic regression to determine factors independently associated with cerebral vasospasm. All patients were treated with hypervolemic therapy and administration of nimodipine as prophylaxis for vasospasm. Cerebral vasospasm was suspected in cases that exhibited (by elevation of transcranial Doppler velocities) neurological deterioration 3 to 14 days after SAH with no other explanation and was confirmed either by clinical improvement in response to induced hypertension or by cerebral angiography. The mean age of the patients was 50 years. Sixty-three percent of the patients were women, 74% were white, 64% were cigarette smokers, and 46% were hypertensive. Ten percent of the patients suffered from alcohol abuse, 19% from sentinel bleed, and 49% had a Fisher Grade 3 SAH. Twenty-nine percent of the patients developed symptomatic vasospasm. Multivariate analysis demonstrated that cigarette smoking (p = 0.033; odds ratio 4.7, 95% confidence interval [CI] 2.4-8.9) and Fisher Grade 3, that is, thick subarachnoid clot (p = 0.008; odds ratio 5.1, 95% CI 2-13.1), were independent predictors of symptomatic vasospasm. The authors make the novel observation that cigarette smoking increases the risk of symptomatic vasospasm after aneurysmal SAH, independent of Fisher grade.
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PMID:Cigarette smoking-induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. 952 31

A 64-year-old female came to our department because of a sudden onset of bilateral deafness 2 days before. She had sudden onset of mild headache, nausea and vomiting 9 days before, but was diagnosed as food poisoning by her home doctor. Her symptoms disappeared on the following day. Neurological examination revealed bilateral deafness, right facial palsy of central type and very slight neck stiffness. CT showed inconspicuous subarachnoid hemorrhage, but lumber puncture revealed definite subarachnoid hemorrhage. Another important finding of CT was old left temporal lobe infarction. Cerebral angiography detected right middle cerebral artery aneurysm at the trifurcation and moderate cerebral vasospasm of the right M2 portion. Neck clipping was successfully performed, but small size of right temporal lobe infarction was found on postoperative CT, which was due to cerebral vasospasm. Postoperative MRI showed bilateral temporal lobe infarction, especially including bilateral auditory cortex. This finding suggests that her deafness was cortical in origin.
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PMID:[A case of subarachnoid hemorrhage complaining of deafness]. 962 67

The authors present a case of aneurysmal subarachnoid hemorrhage that were verified as cerebral vasospasm by using both three-dimensional CT angioraphy (3 D-CTA) and conventional angiography. A 45-year-old man was referred to our department 4th day after sudden onset of a severe headache. On admission, emergency 3 D-CTA showed the cerebral vasospasm involving M 1 segment. Conventional angiography performed at the same day of the left internal carotid artery confirmed the cerebral vasospasm of the same vessel as 3 D-CTA, and furthermore demonstrated the left middle cerebral artery (MCA) and anterior cerebral artery (ACA) genu aneurysms. The former was seen as a ruptured aneurysm from brain CT findings (Fisher group 3). On the 10th day after the onset, 3 D-CTA demonstrated the remaining severe cerebral vasospasm of the supraclinoid portion of left ICA and M 1 segment. Findings at the conventional angiography subsequently performed were concordant with those of 3 D-CTA. The patient was successfully treated with delayed surgical clipping for both aneurysms without the symptoms related to the cerebral vasospasm and discharged without neurological abnormality. We consider that 3 D-CTA shows promise as a minimally invasive method of evaluating the cerebral vasospasm and would take the place of the conventional angiography.
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PMID:[A case of subarachnoid hemorrhage verified as cerebral vasospasm by using three-dimensional CT angiography (3 D-CTA): reference to comparison with conventional angiography]. 1051 60

Cerebral blood vessels are innervated by sensory nerves that store several neurotransmitters among which calcitonin gene-related peptide (CGRP) is the most abundant. In primary headaches, there is a clear association between the head pain and the release of CGRP. In cluster headache there is an additional release of vasoactive intestinal peptide (VIP). In connection with administration of triptans, the headache subsides and the neuropeptide release normalises, in part via a presynaptic effect. In subarachnoid hemorrhage (SAH), CGRP is released to counterbalance the blood-induced vasospasm. In severe cases, the stored CGRP may be exhausted while infusion of CGRP may limit cerebral vasospasm. Thus, interactions with the trigeminovascular system at CGRP receptors may be a useful target for understanding of cerebrovascular disease and to design novel treatments.
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PMID:Calcitonin gene-related peptide (CGRP) in cerebrovascular disease. 1280 34

The difficult types of preeclampsia and eclampsia are presented with the neurological symptoms. The break of cerebral autoregulation mechanism plays the most important role in pathogenesis of cerebral vasospasm. Nevertheless, eclampsia isn't just an ordinary hypertensive encephalopathy because other pathogenic mechanisms are involved in its appearance. The main neuropathologic changes are multifocal vasogenic edema, perivascular multiple microinfarctions and petechial hemorrhages. Neurological clinical manifestations are convulsions, headache, visual disturbances and rarely other discrete focal neurological symptoms. Eclampsia is a high-risk factor for onset of hemorrhagic or ischemic stroke. This is a reason why neurological diagnostic tests are sometimes needed. The method of choice for evaluation of complicated eclampsia is computerized brain topography that shows multiple areas of hypodensity in occipitoparietal regions. These changes are focal vasogenic cerebral edema. For differential diagnosis of eclampsia and stroke other diagnostic methods can be used--fundoscopic exam, magnetic resonance brain imaging, cerebral angiography and cerebrospinal fluid exam. The therapy of eclampsia considers using of magnesium sulfate, antihypertensive, anticonvulsive and antiedematous drugs.
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PMID:[Neurologic aspects of eclampsia]. 1460 66

Bathing headache is rarely described in literature. We report four middle-aged Taiwanese women who developed severe throbbing headache with maximum intensity of onset during bathing. Diffuse cerebral vasospasm was demonstrated in one of them. All their headaches resolved spontaneously (n = 1) or after nimodipine treatment (n = 3). Except for one patient with vasospasm in whom reversible posterior leukoencephalopathy and an asymptomatic cerebellar infarction developed, the others recovered without any complications. The clinical profile of bathing headache points to idiopathic thunderclap headache. It may not be as benign as previously reported. Nimodipine might be effective in treatment of this special headache syndrome.
Cephalalgia 2003 Nov
PMID:Bathing headache: a variant of idiopathic thunderclap headache. 1461 25


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