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

Eleven patients with primary thunderclap headache (TCH) were treated with oral nimodipine 30 to 60 mg every 4 hours or IV nimodipine 0.5 to 2 mg/h if the oral regimen failed or images showed cerebral vasospasm. With oral nimodipine, headache did not recur in the nine patients without vasospasm. IV nimodipine was given in two patients with vasospasm, including one who developed ischemic stroke. Nimodipine may be effective for TCH. Vasospasm may warrant IV nimodipine.
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PMID:Nimodipine for treatment of primary thunderclap headache. 1511 86

Prophylactic activity of flunarizine in migraine is attributed to its antioxidant properties and to the relief of cerebral vasospasm in which nitric oxide (NO) is involved. We investigated the antimigraine activity of flunarizine and its influence on NO and oxidative marker bioavailability in 25 subjects suffering from migraine without aura and in 25 healthy controls. Urinary samples collected before and after treatment with flunarizine (5 mg orally per day for 6 months) were assayed for NO stable metabolites (NOx) and thiobarbituric acid reactive substances (TBARS). Urinary levels of NOx and TBARS were higher in migraine sufferers before treatment than in healthy controls. No differences were observed in NOx levels in migraine sufferers, before and after flunarizine treatment; urinary TBARS levels were decreased after flunarizine treatment (P < 0.05) and remained persistently higher than in healthy controls (P < 0.05). Our results suggest that flunarizine did not prevent NO-mediated vasodilatation, while it proved effective in limiting the oxidative reactions occurring in migraine sufferers.
Cephalalgia 2004 Jul
PMID:Flunarizine effects on oxidative stress in migraine patients. 1519 94

Cilostazol, an inhibitor of phosphodiesterase (PDE) type 3, is used clinically in peripheral artery disease. PDE3 inhibitors may be clinically useful in the treatment of delayed cerebral vasospasm after subarachnoid hemorrhage. The authors present the first results on the effect of cilostazol on cerebral hemodynamics in normal participants. In this double-blind, randomized, crossover study, 200 mg cilostazol or placebo was administered orally to 12 healthy participants. Cerebral blood flow was measured using 133Xe inhalation and single photon emission computerized tomography. Mean flow velocity in the middle cerebral arteries (VMCA) was measured with transcranial Doppler, and the superficial temporal and radial arteries diameters were measured with ultrasonography. During the 4-hour observation period, there was no effect on systolic blood pressure (P = 0.28), but diastolic blood pressure decreased slightly compared with placebo (P = 0.04). VMCA decreased 21.5 +/- 5.7% after cilostazol and 5.5 +/- 12.2% after placebo (P = 0.02, vs. placebo), without any change in global or regional cerebral blood flow. The superficial temporal artery diameter increased 17.6 +/- 12.3% (P < 0.001 vs. baseline) and radial artery diameter increased 12.6 +/- 8.6% (P < 0.001 vs. baseline). Adverse events, especially headache, were common. The findings suggest that cilostazol is an interesting candidate for future clinical trials of delayed cerebral vasospasm.
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PMID:The phosphodiesterase 3 inhibitor cilostazol dilates large cerebral arteries in humans without affecting regional cerebral blood flow. 1562 9

Delayed cerebral ischemia as a result of cerebral vasospasm is the most common cause of death and disability after aneurysmal subarachnoid hemorrhage (SAH). It leads to death or permanent neurologic deficits in over 17-40% of SAH patients. The initial and main symptom of cerebral vasospasm is diffuse headache and may be accompanied with a slight increase in discomfort from neck stiffness and fever. The clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness or a new focal neurologic deficit. There has been a great progress in identifying the patients at risk, putative mechanisms, and possible treatment options for cerebral vasospasm. However, the problem is by no means solved, mainly due to a limited understanding of the pathologic mechanisms of this complex disease. The iatrogenic factors that can increase the risk of cerebral vasospasm include prolongation of the subarachnoid clot by antifibrinolytic drugs, hypotension, inappropriate treatment of hyponatremia, hypovolemia, hyperthermia and increased intracranial pressure. Nimodipine has been shown to improve neurologic outcome and decrease the incidence of cerebral vasospasm. Triple H therapy is a treatment designed to augment cerebral blood flow for patient with cerebral vasospasm. Hypervolemic hypertension is induced with intravenous volume expansion with crystalloid or colloid to increase cardiac output and raise blood pressure. However, small randomized trials showed no clear benefit. Recently, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators has emerged as the primary intervention for treating medically refractory ischemia from cerebral vasospasm and in many centers is being used as a first-line treatment or even prophylactically. In addition, promising new treatments for cerebral vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia; however, all still need further clinical trials. Newly recognized mediators of cerebral vasospasm after SAH include endothelium-derived mediators, vascular smooth-muscle-derived mediators, proinflammatory mediators involved in blood-brain barrier disruption, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Moreover, observations in the laboratory have, in many circumstances, matched those of reported small series. Larger, prospective, randomized trials are needed to verify several hypotheses of molecular pathophysiology and clinical treatment regimens.
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PMID:Treatment of cerebral vasospasm after subarachnoid hemorrhage--a review. 1567 31

Administration of sumatriptan in subarachnoid haemorrhage (SAH) patients, misdiagnosed as migraine patients, may induce symptomatic cerebral vasospasm with potentially dangerous consequences. Over a 5-year period, we observed three patients with a 3-15-year history of migraine, who received sumatriptan for acute headache. Two patients received 6 mg sumatriptan subcutaneously on days 4 and 6, and one patient 3 x 100 mg sumatriptan orally on day 1 after an acute headache episode. In all three cases, an alleviation of headache intensity from severe to moderate was observed. When headache recurred and meningeal signs appeared, SAH was diagnosed by computed tomography in all three cases. No neurological deficits occurred during the further course of the disease. In both patients with a SAH caused by an aneurysm, transcranial Doppler sonography demonstrated vasospasm of the basal cerebral arteries. An antinociceptive effect of sumatriptan can be observed in SAH patients in good clinical condition, which suggests a specific craniovascular antinociceptive action. This may lead to misdiagnosis as migraine and delayed appropriate diagnosis and treatment.
Cephalalgia 2006 Mar
PMID:The risks of sumatriptan administration in patients with unrecognized subarachnoid haemorrhage (SAH). 1647 39

Primary thunderclap headache (TCH) is sometimes associated with cerebral vasospasm. However, the role of vasospasm in relation to the development of reversible or irreversible posterior leukoencephalopathy among patients with primary TCH has never been fully addressed. This paper includes a report on a 51-year-old woman with primary TCH complicated with posterior leukoencephalopathy and a literature review of 16 further patients with the same illness. Their magnetic resonance or conventional angiographic findings were clearly described. Our review found that all these 17 patients showed evidence of cerebral vasospasm. Eleven (65%) of them developed permanent ischaemic infarctions, almost exclusively located at the watershed zones. We suggest that the presence of vasospasm might be requisite for posterior leukoencephalopathy as well as for permanent infarctions in these patients. Therefore, searching for any clue of vasospasm is mandatory in treatment of patients with primary TCH. Absence of an accompanying vasospasm might predict a good outcome.
Cephalalgia 2006 May
PMID:Is vasospasm requisite for posterior leukoencephalopathy in patients with primary thunderclap headaches? 1667 61

After the demonstration that spinal cord stimulation (SCS) can improve peripheral blood flow it was Hosobuchi ('86) who first studied the effect of SCS on cerebral blood flow (CBF) in human beings. Our group found that SCS can produce either an increase of CBF or a reduction or no effect. In patients studied with both SPECT technique and TCD, the sign of the induced variations, when present in both, was the same. Cervical stimulation produces more frequently an increase in CBF (61% of cervical stimulations). Our experimental studies confirm that SCS and CO2 interact with the mechanism of regulation of CBF in a competitive way and produce a reversible functional sympathectomy. Further experimental reports suggest that SCS 1) drastically prevents cerebral infarction progression in cats; 2) improves clinical symptoms of patients in persistent vegetative states; 3) suppress headache attacks in migraneous patients; 4) significantly reduces ischemic brain oedema in rats. Following these clinical and experimental observations, Hosobuchi first used cervical SCS for the treatment of cerebral ischemia in man ('91). More recently we confirmed the therapeutic effect of SCS on ischemic stroke in humans, experimental brain injury and cerebral vasospasm in rabbits.
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PMID:Spinal cord stimulation and cerebral haemodynamics. 1737 Jul 75

The anaesthetist may be involved at various stages in the management of subarachnoid haemorrhage (SAH). Thus, familiarity with epidemiological, pathophysiological, diagnostic, and therapeutic issues is as important as detailed knowledge of the optimal intraoperative anaesthetic management. As the prognosis of SAH remains poor, prompt diagnosis and appropriate treatment are essential, because early treatment may improve outcome. It is, therefore, important to rule out SAH as soon as possible in all patients complaining of sudden onset of severe headache lasting for longer than an hour with no alternative explanation. The three main predictors of mortality and dependence are impaired level of consciousness on admission, advanced age, and a large volume of blood on initial cranial computed tomography. The major complications of SAH include re-bleeding, cerebral vasospasm leading to immediate and delayed cerebral ischaemia, hydrocephalus, cardiopulmonary dysfunction, and electrolyte disturbances. Prophylaxis and therapy of cerebral vasospasm include maintenance of cerebral perfusion pressure (CPP) and normovolaemia, administration of nimodipine, triple-H therapy, balloon angioplasty, and intra-arterial papaverine. Occlusion of the aneurysm after SAH is usually attempted surgically ('clipping') or endovascularly by detachable coils ('coiling'). The need for an adequate CPP (for the prevention of cerebral ischaemia and cerebral vasospasm) must be balanced against the need for a low transmural pressure gradient of the aneurysm (for the prevention of rupture of the aneurysm). Effective measures to prevent or attenuate increases in intracranial pressure, brain swelling, and cerebral vasospasm throughout all phases of anaesthesia are prerequisite for optimal outcome.
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PMID:Aneurysmal subarachnoid haemorrhage and the anaesthetist. 1752 49

Posterior reversible encephalopathy syndrome (PRES) is a rare neurological condition identifiable by clinical presentation and MRI appearance.1 Patients present with headache, seizures, loss of vision and altered mental function. The pathogenesis of the syndrome is poorly understood. One hypothesis is that cerebral vasospasm results in cerebral ischaemia and subsequent development of T2 hyperintensity, and the other is a temporary failure of the autoregulatory capabilities of the cerebral vessels, leading to hyperperfusion, breakdown of the blood-brain barrier, and consequent vasogenic oedema. It is believed that a rapid rise in blood pressure overcomes cerebral autoregulatory mechanisms with abrupt dilatation of cerebral arterioles. We report a patient with systemic lupus erythematosus and PRES after recurrent spontaneous abortion.
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PMID:Seizures and loss of vision in a patient with systemic lupus erythematosus. 1765 17

Patients who survive an Aneurysmal Subarachnoid Haemorrhage or ASAH describe it as being the worst headache ever, multiplied one hundred-times over. It is a debilitating and life threatening condition, which affects approximately 6.5 people per 100,000 throughout Australia and New Zealand every year (The ACROSS group, 2000). When caring for a patient post Aneurysmal Subarachnoid Haemorrhage or ASAH meticulous monitoring of the patient's neurological, cardiovascular, hepatic, endocrine, renal, and respiratory functions are vital. Due to both the initial ASAH and its complications such as rebleed, cerebral vasospasm, hydrocephalus, cerebral oedema, seizures as well as adverse reactions to counteract these potential problems. All of, which can cause significant long-term morbidity as well as potential mortality if left, undiagnosed and untreated. The following article presets a composite patient highlighting clinical manifestations of ASAH, its associated complications as well as various methods of detecting, preventing and treating them.
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PMID:Aneurysmal subarachnoid haemorrhage--part 1: Pre-operative nursing management diagnosis, complications and treatment: a composite case study. 1792 38


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