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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute central nervous and cardiovascular effects of the local anesthetics ropivacaine and bupivacaine were compared in 12 volunteers in a randomized double-blind manner with use of intravenous infusions at a rate of 10 mg/min up to a maximal dose of 150 mg. The volunteers were all healthy men. They were familiarized with the central nervous system (CNS) toxic effects of local anesthetics by receiving a preliminary intravenous injection of lidocaine. The infusions of ropivacaine and bupivacaine were given not less than 7 days apart. CNS toxicity was identified by the CNS symptoms and the volunteers were told to request that the infusion be stopped when they felt definite but not severe symptoms of toxicity such as numbness of the mouth, lightheadedness, and tinnitus. In the absence of definite symptoms, the infusion was stopped after 150 mg had been given. Cardiovascular system (CVS) changes in conductivity and myocardial contractility were monitored using an interpretive electrocardiograph (which measured PR interval, QRS duration, and QT interval corrected for heart rate) and echocardiography (which measured left ventricular dimensions from which stroke volume and ejection fraction were calculated). Ropivacaine caused less CNS symptoms and was at least 25% less toxic than bupivacaine in regard to the dose tolerated. Both drugs increased heart rate and arterial pressure. Stroke volume and ejection fraction were reduced. There was no change in cardiac output. Although both drugs caused evidence of depression of conductivity and contractility, these appeared at lower dosage and lower plasma concentrations with bupivacaine than with ropivacaine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute toxicity of ropivacaine compared with that of bupivacaine. 267 30

Symptomatic common carotid artery occlusion (CCAO) is rare. We studied 17 patients with ischemic cerebrovascular symptoms and unilateral CCAO on angiography to help clarify clinical and radiologic features. Mean age was 62 years; 65% were women. Predominant symptoms and signs included visual-ipsilateral monocular or retrochiasmal symptoms (88%), motor weakness (88%), sensory disturbance (59%), dizziness/lightheadedness (53%), and syncope (24%). Dysarthria, headache, or involuntary limb shaking occurred less frequently. Positionally related symptoms occurred in approximately two-thirds of the patients. TIAs were often multiple and preceded a stroke or occurred without subsequent stroke in 82%. Hemispheric TIAs contralateral to the CCAO occurred in 41%. Ten patients (59%) suffered stroke, seven (70%) of which were ipsilateral to the CCAO. Vascular risk factors included cigarette use (76%), hypertension (71%), diabetes mellitus (41%), and hyperlipidemia (41%); 82% had two or more risk factors. Known cardiac disease was present in 59%. CCAO was present at the origin of the vessel in most patients. Most had atherosclerotic narrowing of multiple extracranial large vessels. During follow-up, none of the patients had a spontaneous second infarct; five had TIAs, including two with amaurosis fugax, all in the CCAO territory. More restricted external carotid collaterals may, in part, explain the higher frequency of ipsilateral stroke and contralateral TIAs than reported for internal carotid occlusion.
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PMID:Common carotid artery occlusion. 279 68

Embolic and thrombotic infarction in the territory of the posterior cerebral artery (PCA) is described with emphasis on the stroke and cerebrovascular features rather than special neurological syndromes. Of 47 cases of obstruction at the distal bifurcation of the basilar artery, 43 (95%) were consistent with embolism. The clinical categories and pathological findings are presented. Local embolism, vertebral distal-stump embolism, the dynamics of hemorrhagic infarction and embolus-in-transit are briefly described. The prodromal manifestations of PCA thrombotic occlusion include photopsias, hemianopic blackouts, headache, transient episodes of numbness, episodic lightheadedness, spells of bewilderment and rarely tinnitus. Recognition of these may allow prevention of a stroke. Prodromal photopsias did not closely resemble the scintillating displays of migraineurs. When the stroke occurred, visual complaints usually predominated. A sensory deficit occurred in one-third of cases. In 25 cases of memory impairment the dominant hemisphere was involved in 24. The kinds of visual hallucinations, simple and formed, are described.
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PMID:The posterior cerebral artery syndrome. 374 39

Operative intervention remains controversial for patients with transient nonhemispheric symptoms with occlusive disease of both the anterior and posterior cerebral circulations. In addition to the standard evaluation of these patients, we have used stable xenon-enhanced computed tomographic mapping of cerebral blood flow (Xe/CT CBF). This relatively new and potentially widely available CBF methodology, by measuring approximately 30,000 CBF values within each of three CT levels, provides a readily interpretable means of evaluating extremes of hemodynamic compromise within any or all vascular territories. In the past 30 months, Xe/CT CBF studies in 300 patients with occlusive vascular disease have identified nine patients with global low flow and nonhemispheric symptoms (vertigo, lightheadedness, and/or blurred vision). Blood pressures determined by ocular pneumoplethysmography of Gee were markedly abnormal with reduced ocular/brachial ratios. Each patient had a combination of both segmental carotid and vertebrobasilar occlusive disease. Each patient had a flow-augmenting procedure performed on the anterior circulation in an attempt to improve global flow: carotid endarterectomy (two patients), subclavian-external carotid bypass (one patient), and superficial temporal artery-middle cerebral artery bypass (six patients). In each case disabling transient symptoms were relieved. There were no operative deaths, but one stroke occurred, probably as a result of a brief period of postoperative hypotension. Postoperative Xe/CT CBF studies show a long-term improved global CBF in all patients.
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PMID:Relief of nonhemispheric symptoms in low flow states by anterior circulation revascularization: a physiologic approach. 382 Apr 2

NPS 1506 is a moderate affinity, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. NPS 1506 is neuroprotective in rodent models of ischemic stroke, hemorrhagic stroke, and head trauma, with a 2-hr window of opportunity. Neuroprotectant doses of NPS 1506 ranged from approximately 0.1-1.0 mg/kg, with peak plasma concentrations ranging from 8-80 ng/mL. Even at doses producing behavioral toxicity, NPS 1506 did not elicit MK-801-like behaviors, did not generalize to phencyclidine (PCP), and did not elicit neuronal vacuolization. In a Phase I study, intravenous (i.v.) doses of NPS 1506 from 5-100 mg were well tolerated and provided plasma concentrations in excess of those required for neuroprotection in rodents. Adverse events at the 100-mg dose included mild dizziness and lightheadedness, and mild to moderate ataxia. Neither PCP-like psychotomimetic effects nor cardiovascular effects were noted. The long plasma half-life of NPS 1506 (approximately 60 hr) suggests that a single i.v. dose will provide prolonged neuroprotection in humans.
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PMID:NPS 1506, a novel NMDA receptor antagonist and neuroprotectant. Review of preclinical and clinical studies. 1066 49

A 27-year old female had one episode of transient loss of consciousness and several of near-unconsciousness during strenuous exercise and sexual activity. Episodes started with abdominal discomfort or nausea and light headedness. Unconsciousness never exceeded one minute. When trying to stand up, she felt she would lose consciousness again. We performed a bicycle ergometer exercise test, continuously monitoring blood pressure via non-invasive finger photoplethysmography (Finometer, FMS, The Netherlands). Beat-to-beat changes in stroke volume, cardiac output and total peripheral resistance were calculated using Modelflow (FMS, The Netherlands). At a power of 140 W, the patient reported being near exhaustion; shortly after this she reported nausea. She stopped cycling 30 s later, then saw "black spots" and felt an oncoming loss of consciousness. Dismounting the ergometer and squatting provided immediate relief from symptoms. Symptoms during the test were similar to those during previous episodes. The diagnosis was exercise-induced vasovagal reactions. This is the first report that documents the beat-to-beat changes in blood pressure, stroke volume and total peripheral resistance during exercise-induced vasovagal syncope. It illustrates the usefulness of combining exercise testing with continuous non-invasive blood pressure monitoring in the diagnostic work-up of exercise-induced syncope, and shows the therapeutic value of squatting to prevent loss of consciousness in exercise-related vasovagal syncope.
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PMID:Syncope during exercise, documented with continuous blood pressure monitoring during ergometer testing. 1576 6

Atrial fibrillation (AF) is the most common chronic arrhythmia and the most serious heart rhythm irregularity in individuals older than 70. It is usually not life threatening in and of itself, but it can lead to serious medical problems, including stroke, additional heart rhythm problems, and heart failure. Symptoms of AF vary considerably. Some patients are asymptomatic and have a self-limiting arrhythmia of short duration that converts to normal sinus without any intervention. Symptomatic patients may experience minor palpitations, severe palpitations, or even more vague symptoms such as lightheadedness, shortness of breath, or fatigue. More serious symptoms, such as syncope, new or worsening heart failure, or a cerebral vascular accident, may occur. The initial goals of treatment include controlling ventricular rate and addressing anticoagulation status. New guidelines help clinicians effectively manage anticoagulant therapy for older adults newly diagnosed with AF.
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PMID:Anticoagulation therapy in older adults newly diagnosed with atrial fibrillation. 2191 22

Exercise-associated collapse (EAC) commonly occurs after the completion of endurance running events. EAC is a collapse in conscious athletes who are unable to stand or walk unaided as a result of light headedness, faintness and dizziness or syncope causing a collapse that occurs after completion of an exertional event. Although EAC is perhaps the most common aetiology confronted by the medical provider attending to collapsed athletes in a finish-line tent, providers must first maintain vigilance for other potential life-threatening aetiologies that cause collapse, such as cardiac arrest, exertional heat stroke or exercise-associated hyponatraemia. Previously, it has been believed that dehydration and hyperthermia were primary causes of EAC. On review of the evidence, EAC is now believed to be principally the result of transient postural hypotension caused by lower extremity pooling of blood once the athlete stops running and the resultant impairment of cardiac baroreflexes. Once life-threatening aetiologies are ruled out, treatment of EAC is symptomatic and involves oral hydration and a Trendelenburg position - total body cooling, intravenous hydration or advanced therapies is generally not needed.
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PMID:Exercise-associated collapse: an evidence-based review and primer for clinicians. 2194 22

A 72-year-old man with diabetes mellitus and hypertension was admitted to our hospital with lightheadedness. The patient showed lateropulsion to the right side, but his neurological findings were otherwise normal. Brain magnetic resonance images showed a fresh ischemic infarct in the left dorsal part of the lower pons. Body lateropulsion is characterized by an irresistible falling to one side and has been reported in lesions in several brain regions. However, it has rarely been reported in pontine lesions. We suggest that physicians should be aware that pontine lesions can cause isolated body lateropulsion without other neurological deficits.
J Stroke Cerebrovasc Dis 2013 Oct
PMID:Isolated body lateropulsion in a patient with pontine infarction. 2326 82

Swift diagnosis and treatment are critical for good outcomes in patients with nontraumatic subarachnoid hemorrhage, which is usually caused by a ruptured aneurysm. This type of stroke often results in death or disability. Rates of misdiagnosis and treatment delays for subarachnoid hemorrhage have improved over the years, but these are still common occurrences. Subarachnoid hemorrhage can be more easily diagnosed in patients who present with severe symptoms, unconsciousness, or with thunderclap headache, which is often accompanied by vomiting. The diagnosis is more elusive in patients who present in good condition, yet these patients have the best chance for good outcome if they are correctly diagnosed at the time of presentation. Physicians should be alert for warning headaches, which are often severe, and headaches that feel different to the patient. Other symptoms may include nausea, vomiting, impaired consciousness, nuchal rigidity, orbital pain, focal neurologic deficits, dysphasia, lightheadedness, and dizziness. The most important risk factors for subarachnoid hemorrhage include cigarette smoking, hypertension, heavy alcohol use, and personal or family history of aneurysm or hemorrhagic stroke. The first step in the diagnostic workup is noncontrast computed tomography of the head. If computed tomography is negative or equivocal, a lumbar puncture should be performed. Subsequent imaging may include computed tomographic angiography, catheter angiography, and magnetic resonance angiography.
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PMID:Recognition and evaluation of nontraumatic subarachnoid hemorrhage and ruptured cerebral aneurysm. 2413 85


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