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

A 22-year old female with Takayasu disease, who underwent bilateral aorto-carotid bypass surgery developed hyperperfusion syndrome postoperatively. Following the operation, convulsion and headache developed and mean velocity in the middle cerebral artery, measured by transcranial doppler, elevated. Mean velocity gradually decreased on the 10th postoperatively day and became a plateau at 200% of preoperative value. Pulsatility index as a index of cerebral vascular resistance was low just after the operation, became normal the following day and gradually increased 10 days after the operation. These changes seem to be recovery of cerebral autoregulation. On the 20th postoperative day, computed tomography scan was examined and multiple low density areas were found in the basal ganglia regions, but these changes disappeared 2 months after the operation. These reversible changes of CT scan might show ischemic changes or cerebral edema induced by cerebral vasospasm.
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PMID:[Hyperperfusion syndrome following bilateral aorto-carotid bypass--a study of transcranial Doppler]. 168 Mar 60

We present two cases of severe headache associated with the use of bromocriptine for lactation suppression in otherwise healthy women. In each case, the additional use of a therapeutic sympathomimetic agent resulted in extreme worsening of symptoms with development of hypertension and life-threatening complications (ventricular tachycardia and cardiac dysfunction in one case, seizures and cerebral vasospasm in the other). Sympathomimetics in combination with bromocriptine in patients with a bromocriptine-associated headache during the puerperium may be dangerous.
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PMID:Bromocriptine-associated headache: possible life-threatening sympathomimetic interaction. 192 36

Tissue plasminogen activator (t-PA) is expected to be used for cisternal drainage in subarachnoidal hemorrhage, for dissolving of the residual hematoma after stereotactic evacuation of a cerebral hematoma, and for regional intraarterial injection therapy for occlusion of the primary cerebral artery. This is because the drug exerts a very potent and immediate dissolving-effect on a hematoma when it is locally administered. However, the solubility of t-PA is rapidly decreased at pH 5 or more. At pH 7 or more, precipitation of crystals is observed when the concentration of t-PA exceeds 20 x 10(4) IU/ml. The pH of the t-PA general-purpose solution (for intravenous injection) is adjusted at 4.6 to 4.8 because of its solubility and stability, and the osmotic pressure is also increased with an increase in concentration of t-PA. When the concentration of t-PA is 750 x 10(4) IU/ml, the osmotic ratio is 30 and the pH is 4.82. These features suggest that a locally administered t-PA solution at high concentration may induce meningeal irritation leading to headache and vomiting, and exacerbation of symptomatic cerebral vasospasm when it is used for cisternal drainage. Furthermore, the t-PA solution administered intraarterially at high concentration may induce adverse effects such as dessiocyte and echinocyte deformation of erythrocytes and the sludging phenomenon of leukocytes in the cerebral microcirculation, and a sensation of fever and pain upon injection. Therefore, the dose and method of administration of the t-PA for local intracranial use should be determined by taking into consideration its pH and osmotic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intracranial administration of tissue plasminogen activator and its important factors involved concerning the pH and osmotic pressure]. 194 89

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

Many patients with a ruptured berry aneurysm report an intense sentinel headache of sudden onset in the weeks before rupture. Such headaches have been attributed to a leak of blood, which implies that partial rupture has occurred. A case is reported of a patient who had severe headaches which seemed to be caused by an unruptured cerebral aneurysm, accompanied by diffuse cerebral vasospasm. Headache episodes with the thunderclap profile may require angiography for diagnosis even if the cerebrospinal fluid is bloodless.
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PMID:Thunderclap headache: symptom of unruptured cerebral aneurysm. 287 33

A new classification of calcium antagonists has been developed by a WHO expert committee. Substances acting primarily via the inhibition of calcium entry into the cell have been divided into four distinct classes. The pharmacological characteristics of these classes that may be relevant for the use in various neurological disorders are highlighted in this paper. Some main differences concern the effects on vascular smooth muscle cells and brain cells. The well-documented clinical applications in neurology are still limited to migraine prophylaxis and vertigo. The evidence concerning the usefulness in cerebral vasospasm secondary to subarachnoid haemorrhage was regarded as reasonable, whereas several neurological indications should still be regarded as being under examination. There is little doubt that calcium antagonists will gain importance in the treatment of several neurological diseases.
Cephalalgia 1988
PMID:The classification of calcium antagonists by the WHO expert committee: relevance in neurology. 318 Feb 2

The present studies show that nimodipine prevents and/or improves permanent ischemic neurological deficits in patients with subarachnoid hemorrhage. This was particularly marked in four double-blind, placebo-controlled studies in which statistically significant reductions in mortality and morbidity as consequence of cerebral vasospasm were found. The drug has been shown to increase cerebral blood flow, to reduce vasoconstriction, although not to fully prevent angiographic vasospasm, and to improve central conduction time. Nimodipine did not increase the rate of rebleeding. Its administration during anesthesia does not result in management problems. In general, nimodipine was well tolerated. Side effects were recorded mainly in open studies using the intravenous formulation and consisted mainly of decreases in blood pressure and headaches. Transient increases in liver enzymes may be due to the organic solvent. Hence, all results indicate that patients with subarachnoid hemorrhage will benefit from preventive or therapeutic nimodipine treatment.
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PMID:Survey of clinical experience with nimodipine in patients with subarachnoid hemorrhage. 332 2

Calcium-channel entry blockers are drugs with different chemical properties and a common pharmacological characteristic. Calcium is very important in many physiological mechanisms and could be involved in neuronal damage following cerebral ischemia. Thus, calcium-channel blockers agents could be of interest in medical treatment of cerebrovascular diseases, headache and subarachnoid hemorrhage. Calcium-channel blockers seem to have a direct protective role against neuronal ischemic damage and/or a direct action on cerebral vessels. Some clinical experiences have suggested a protective role of nimodipine in the prevention of ischemic complications related to cerebral vasospasm after subarachnoid hemorrhage.
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PMID:[Vascular and neuronal mechanisms of calcium antagonists. Significance in neurological therapy]. 372 33

A case of fatal cerebral vasospasm after transsphenoidal removal of a pituitary macroadenoma with suprasellar extension is reported. On the second postoperative day the patient developed headache, lethargy, and cardiorespiratory arrest. Five days later, after recovery from this episode, she developed signs of involvement of the left hemisphere. At that time she demonstrated severe cerebral vasospasm, which was worse in the left supraclinoid segment of the internal carotid artery, and she died 19 days postoperatively. Postmortem examination showed left hemispheric and hypothalamic infarction with subsequent herniation. In addition, pathologic arterial changes usually related to use of oral contraceptives were present.
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PMID:Vasospasm following transsphenoidal tumor removal associated with the arterial changes of oral contraception. 687 8

Calcium antagonists are currently most widely used for chronic cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH). However, the vasodilatory effects of systemically administered calcium antagonists can be limited secondary to hypotension. We previously compared intrathecal and intravenous routes of administration of nicardipine. Intrathecal administration of nicardipine significantly dilated spastic basilar arteries on day 7 in a two-haemorrhage canine model of vasospasm. In the present communication, the effects of prophylactic, serial administration of intrathecal nicardipine on vasospasm was examined in 50 patients. Patients were classified as Fisher SAH group 3 and all had their aneurysms clipped within 3 days of SAH. Following placement of a cisternal drain, 2 mg of nicardipine was injected, three times each day for an average of 10 days. The control group consisted of 91 similar patients with cisternal drainage not treated with nicardipine. Intrathecal administration of nicardipine decreased the incidence of symptomatic vasospasm by 26%, angiographic vasospasm by 20% and increased good clinical outcome at one month after the haemorrhage by 15%. Postoperative angiograms revealed that patients in the nicardipine group showed less vasospasm of major cerebral arteries, near the tip of a drain in the basal cistern, but vasospasm in the A2 and M2 segments was not decreased. Radio-isotope cisternography suggested that nicardipine might not reach the subarachnoid space around A2 and M2 segments. Nine patients complained of headache probably secondary to nicardipine induced vasodilation. Two patients suffered from meningitis, both were successfully treated. Intrathecal administration nicardipine appears to be effective in the treatment of vasospasm, but side effects were significant.
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PMID:Effects of prophylactic intrathecal administrations of nicardipine on vasospasm in patients with severe aneurysmal subarachnoid haemorrhage. 770 81


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