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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(1) For patients aged over 60 years who have essential thrombocythaemia, and are considered to be at increased risk of thromboembolism, the standard cytotoxic agent is hydroxycarbamide (hydroxyurea), which reduces the risk of thrombocytosis but adversely affects other blood cell lines. It may also increase the risk of progression to cancer. (2) Anagrelide, initially studied as an antiplatelet drug, was approved in Europe for the treatment of essential thrombocythaemia in high-risk patients when other treatments fail or are poorly tolerated. (3) Evaluation data includes a trial versus hydroxycarbamide that was prematurely halted because of an excess of cardiovascular events among patients on anagrelide. Among 809 patients who were also receiving aspirin as an antithrombotic (and who may not have met strict criteria for essential thrombocythaemia), arterial or venous thrombosis and haemorrhage were significantly more frequent with anagrelide, during a median follow-up of 39 months (55 versus 36 patients). (4) According to the results of 3 non comparative trials involving about 500 patients, and the European Medicines Agency report analysing these and other study populations, anagrelide reduces the platelet count to below 600 times 10 to the 9th power/litre in two-thirds of patients. No data are available on the clinical implications of this reduction in platelets. (5) Between 10% and 20% of patients treated with anagrelide experience cardiovascular adverse effects (palpitations, myocardial infarction, heart failure) or neurological adverse effects (headache, stroke, transient ischaemic attack). Gastrointestinal disturbances are also frequent (diarrhoea, nausea, abdominal pain, pancreatitis). Some of these adverse effects can be fatal. (6) Follow-up is too short to show whether anagrelide affects the risk of progression to cancer. (7) In practice, anagrelide has a less favourable risk-benefit balance than hydroxycarbamide, which remains the first-line cytotoxic agent in this setting. Anagrelide therapy can be considered if hydroxycarbamide fails or is poorly tolerated, provided patients are included in a long-term clinical trial.
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PMID:Anagrelide: new drug. Essential thrombocythaemia: further evaluation needed for this last-resort treatment. 1676 90

It is well known that the electroencephalographic finding in patients with moyamoya disease demonstrates the characteristic "re-build up" phenomenon a few minutes after hyperventilation. To evaluate the usefulness of an electroencephalogram (EEG) in the postoperative management of children with moyamoya disease, we studied the presence or absence of improvement in the clinical, single photon emission computed tomography (SPECT) and EEG findings, before and after surgery. Twenty-two patients, who underwent indirect revascularization surgery for moyamoya disease, were included in our study. Clinical improvement was assessed as the disappearance or decrease of a transient ischemic attack or headache. The findings on the EEG and SPECT were considered improved when the re-build up phenomenon was absent and when there was improvement in the cerebrovascular reserve as a result of the acetazolamide challenge test. The statistical correlation analysis for both clinical and EEG improvement were consistent (kappa value=0.409, p< 0.05). However, the result from the clinical and SPECT improvement as well as that from EEG and SPECT improvement were not statistically significant. Our results suggest that EEG can be used as a noninvasive and simple follow-up test for moyamoya disease after indirect revascularization surgery if the hyperventilation procedure is effectively performed during EEG recording.
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PMID:Postoperative electroencephalogram for follow up of pediatric Moyamoya disease. 1677 96

The importance of cerebral disease in patients with the Hughes syndrome is now becoming more widely recognized. The range of neuropsychiatric manifestations of APS is comprehensive, and includes focal symptoms attributable to lesions in a specific area of the brain as well as diffuse or global dysfunction. Patients with APS frequently present with strokes and TIA, but a wide spectrum of other neurologic features-also including non thrombotic neurologic syndromes-has been described in association with the presence of aPL. The recognition of APS has had a profound impact on the understanding and management of the treatment of CNS manifestations associated with connective tissue diseases, in particular, SLE. Many patients with focal neurologic manifestations and aPL, who a few years ago would have received high-dose corticosteroids or immunosuppression, are often successfully treated with anticoagulation. In our opinion, testing for aPL may have a major diagnostic and therapeutic impact not only in patients with autoimmune diseases and neuropsychiatric manifestations, but also in young individuals who develop cerebral ischemia, in those with atypical multiple sclerosis, transverse myelitis, and atypical seizures. We would also recommend testing for aPL for young individuals found with multiple hyperintensity lesions on brain MRI in the absence of other possible causes,especially when under the age of 40 years. It is our practice to anticoagulate patients with aPL suffering from cerebral ischemia with a target INR of 3.0 to prevent recurrences. Low-dose aspirin alone (with occasional exceptions)does not seem helpful to prevent recurrent thrombosis in these patients. Our recommendation, once the patient has had a proven thrombosis associated with aPL, is long-term (possibly life-long) warfarin therapy. Oral anti coagulation carries a risk of hemorrhage, but in our experience the risk of serious bleeding in patients with APS and previous thrombosis treated with oral anticoagulation to a target INR of 3.5 was similar to that in groups of patients treated with lower target ratios. Although a double-blind crossover trial comparing low molecular weight heparin with placebo in patients with aPL and chronic headaches did not show a significant difference in the beneficial effect of low molecular weight heparin versus placebo, in our experience selected patients with aPL and neuropsychiatric manifestations such as seizures, severe cognitive dys-function, and intractable headaches unresponsive to conventional treatment may respond to anticoagulant treatment. The neurologic ramifications of Hughes syndrome are extensive, and it behoves clinicians in all specialties to be aware of this syndrome because treatment with anticoagulation may profoundly change the outlook for these patients.
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PMID:Cerebral manifestations in the antiphospholipid (Hughes) syndrome. 1688 79

Traumatic cervical artery dissection (TCAD) is a complication of severe blunt head or neck trauma, the main cause being motor vehicle accidents. TCAD are increasingly recognized, and incidences of up to 0.86% for internal carotid and 0.53% for traumatic vertebral artery dissections (TVAD) among blunt trauma victims are reported. Diagnostic evaluation for TCAD is mandatory in the presence of (1) hemorrhage of potential arterial origin originating from the nose, ears, mouth, or a wound; (2) expanding cervical hematoma; (3) cervical bruit in a patient >50 years of age; (4) evidence of acute infarct at brain imaging; (5) unexplained central or lateralizing neurological deficit or transient ischemic attack, or (6) Horner syndrome, neck or head pain. In addition, a number of centers screen asymptomatic patients with blunt trauma for TCAD. Catheter angiography is the standard of reference for diagnosis of TCAD. Color duplex ultrasound, computed tomographic, and magnetic resonance angiography are noninvasive screening alternatives, but each method has its diagnostic limitations compared to catheter angiography. Anticoagulants and antiplatelet drugs may prevent ischemic stroke, but bleeding from traumatized tissues may offset the benefits of antithrombotic treatment. Endovascular therapy of dissected vessels, thrombarterectomy, direct suture of intimal tears, and extracranial-intracranial bypass should be considered in exceptional cases. Neurological outcome is probably worse in TCAD compared to spontaneous CAD, although it is unclear whether this is due to dissection-induced ischemic stroke or associated traumatic lesions.
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PMID:Traumatic cervical artery dissection. 1729 Jan 11

Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. Headache is observed in 65-68%, facial pain in 34-53%, and neck pain in 9-26%. Horner syndrome consisting essentially of miosis and ptosis is detected in 28-41%. Cranial nerve palsy is reported in 8-16%; the lower cranial nerves IX-XII are most commonly affected, in particular the hypoglossal nerve. The facial nerve may also be involved; dysgeusia results mainly from involvement of the chorda tympani (0.5-7.0%) or the glossopharyngeal nerve. Transient pareses of the ocular motor (III, IV and VI) and trigeminal nerves have been observed. Pulsatile tinnitus is reported in 16-27%. About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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PMID:Clinical manifestations of carotid dissection. 1729 Jan 13

The most frequent clinical manifestation of vertebral artery dissection is posterior headache or neck pain accompanied or followed by posterior circulation transient ischemic attack or stroke. Rarer clinical features include isolated headache or neck pain, cervical spinal cord ischemia and cervical root impairment. Asymptomatic vertebral artery dissections have been reported. In the case of primary intracranial vertebral artery dissection or intracranial extension of an extracranial dissection, subarachnoid hemorrhage and rarely rostral cervical spinal cord ischemia or posterior fossa mass effect may occur.
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PMID:Clinical manifestations of vertebral artery dissection. 1729 Jan 14

Stroke is a major public health burden worldwide and is responsible for a large proportion of disability; and ranks third in the causation of morbidity and mortality. This disease although regarded as a disease of old age, it is not uncommon in younger population in developing countries.. A retrospective study of cerebro-vascular accidents (stroke) managed at Department of Medicine, Nepal Medical College Teaching Hospital during the period of 1st April 2000 to 31st March 2005 was done to study demographics and risk factors. Cases of TIA were not included in the final analysis of the data due to uncertainty of diagnosis and lack of imaging (CT scan). The collected data was analyzed using data analysis software SPSS (version 12). We identified 72 cases of stroke excluding TIA. The mean age at which patients in this study experienced their first ever stroke was 61.7 yrs (SD 14.9 yrs). The commonest presenting complaints in our study population were weakness of limbs (90.3%), slurring of speech (33.3%), altered mental status (29.8%), deviation of angle of mouth and headache (22.2%) each and urinary incontinence (13.9%). Vomiting, dizziness, fever, personality changes, seizure, tingling sensation of limbs were uncommon clinical presentation and were present in 15.28% of cases. Risk factors were smoking (58.3%), hypertension (47.2%), alcohol (41.4%), atrial fibrillation (12.5%) and diabetes mellitus (11.1%). To conclude, stroke in countries like Nepal is a public health problem. The clinical presentations and risk factors are in agreement with other studies. The low mean age of stroke patient reflects demographic feature of this region.
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PMID:Retrospective analysis of stroke and its risk factors at Nepal Medical College Teaching Hospital. 1735 48

Patent foramen ovale (PFO) has been implicated in the pathogenesis of cryptogenic stroke, arterial desaturation, decompression illness, and migraine headache (MH). This study evaluated the safety of percutaneous transcatheter PFO closure in patients with cryptogenic stroke, transient ischemic attack, or arterial desaturation. Additionally, symptomatic reduction in MH was determined after interatrial shunt closure. Of the 252 patients referred to the University of California, Los Angeles, with PFO, 131 underwent closure of the interatrial communication with a CardioSEAL (n = 30) or Amplatzer (n = 101) device. PFO morphology was evaluated with transesophageal echocardiography. Follow-up was conducted at 1 to 2 months with echocardiography, with clinical assessment annually thereafter. At an average follow-up of 30 months, there was no recurrence of any thromboembolic event (transient ischemic attack, stroke, or peripheral). There was a reduction in MH, defined as the complete resolution of headache or a >50% reduction in the number of headache days, in 85% of patients after PFO closure. Temporary problems after device implantation, including chest discomfort and palpitations, were reported in 23% of patients and occurred more frequently in patients with nickel hypersensitivity (p <0.05). In conclusion, transcatheter PFO closure is an effective and safe therapeutic modality in the prevention of thromboembolic events and MH associated with interatrial shunting in patients who present with cryptogenic stroke. Pending randomized, controlled trials are necessary to determine if this invasive approach is preferable to medical therapy for the prevention of recurrent stroke or as primary treatment for patients with MH.
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PMID:Five-year experience with percutaneous closure of patent foramen ovale. 1747 65

Children with sickle cell disease, a chronic hemolytic anemia, present with a wide variety of neurological syndromes, including ischemic and hemorrhagic stroke, transient ischemic attacks, 'soft neurological signs', seizures, headache, coma, visual loss, altered mental status, cognitive difficulties, and covert or 'silent' infarction. Those with ischemic stroke usually have stenosis or occlusion of the distal internal carotid and proximal middle cerebral arteries. Indefinite transfusion prevents recurrence in most patients who have had a stroke, and can prevent first stroke in those with high transcranial Doppler velocities. High white cell count, low hemoglobin and oxyhemoglobin desaturation predict neurological complications. Other risk factors for overt ischemic stroke include hypertension, previous transient ischemic attack, covert infarction and chest crisis. For hemorrhagic stroke, aneurysms are common in adults but not children, who often present with hypertension after transfusion or corticosteroids. Seizures are particularly common in patients with cerebrovascular disease and covert infarction; the latter is also associated with hyposplenism and infrequent pain. Factors associated with cognitive difficulties include thrombocytosis, infarction, large-vessel disease, and perfusion abnormality on neuroimaging. As well as investigating the role of genes and the possibility that hydroxyurea or blood pressure control reduce neurological complications, we should explore the modifiable effects of poor nutrition, chronic infection, hemolysis and oxyhemoglobin desaturation on stroke risk.
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PMID:Therapy insight: stroke risk and its management in patients with sickle cell disease. 1747 74

The main symptoms of acute primary angle-closure glaucoma (PACG) include pain in the head and/or the eyes in addition to the characteristic halo and blurred vision. When loss of vision is accompanied by such pain, PACG is usually suspected. However, no information has been available regarding painless acute angle-closure glaucoma. Recently, we treated a patient with painless acute PACG mimicking amaurosis fugax as a type of transient ischemic attack. Generally, amaurosis fugax causes transient monocular loss of vision due to occlusion of the ophthalmic artery. The formation of microemboli derived from the heart or carotid artery and/or the occurrence of some hemodynamic abnormality due to arteriosclerosis is closely related to amaurosis fugax, and most cases are complicated by intracranial or extracranial arterial lesions. In the present case, we provisionally diagnosed transient amaurosis fugax which, however, was shown by additional ocular testing to be painless PACG. Herein we describe our diagnostic process and the outcome.
Headache
PMID:Painless transient monocular loss of vision resulting from angle-closure glaucoma. 1763 5


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