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

Vascular cognitive impairment (VCI) was proposed as an umbrella term to include subjects affected with any degree of cognitive impairment resulting from cerebrovascular disease (CVD), ranging from mild cognitive impairment (MCI) to vascular dementia. VCI may or may not exclude the host of "focal" circumscribed impairments of specialized functions such as language (aphasia), intentional gesture (apraxia), or categorical recognition (agnosia), among others, that may result from a stroke. Therefore, there are no universally accepted diagnostic criteria for VCI. We conclude that this concept could be more useful if it were to be limited to cases of vascular MCI without dementia, by analogy with the concept of amnestic MCI, currently considered the earliest clinically diagnosable stage of Alzheimer disease (AD). In agreement with our view,the Canadian Study on Health and Aging successfully implemented a restricted definition of VCI, excluding cases of dementia (i.e., vascular cognitive impairment no dementia, VCI-ND). The Canadian definition and diagnostic criteria could be utilized for future studies of VCI. This definition excludes isolated impairments of specialized cognitive functions. Vascular dementia (VaD): The main problem of this diagnostic category stems from the currently accepted definition of dementia that requires memory loss as the sine qua non for the diagnosis. This may result in over-sampling of patients with AD worsened by stroke (AD+CVD). This problem was minimized in controlled clinical trials of VaD by excluding patients with a prior diagnosis of AD, those with pre-existing memory loss before the index stroke, and those with amnestic MCI. We propose a definition of dementia in VaD based on presence of abnormal executive control function, severe enough to interfere with social or occupational functioning. Vascular cognitive disorder (VCD): This term, proposed by Sachdev [P. Sachdev, Vascular cognitive disorder. Int J Geriat Psychiatry 14 (1999)402-403.] would become the global diagnostic category for cognitive impairment of vascular origin, ranging from VCI to VaD. It would include specific disease entities such as post-stroke VCI, post-stroke VaD, CADASIL, Binswanger disease, and AD plus CVD. This category explicitly excludes isolated cognitive dysfunctions such as those mentioned above.
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PMID:Vascular cognitive disorder: a new diagnostic category updating vascular cognitive impairment and vascular dementia. 1553 26

A number of clinical trials associated with the Women's Health Initiative (WHI) have assessed the potential benefits of hormone replacement therapy (HRT) for protection against the development of cardiovascular disease and memory loss in menopausal women. The results of the WHI Memory Study suggest that HRT increases the risk of stroke and dementia in menopausal women. This finding has called into question the results of hundreds of basic science studies that have suggested that estrogen could protect brain cells from damage and improve cognition. A number of researchers have argued that inappropriate formulation, improper dosing, a limited study population, and poor timing of administration likely contributed to the reported findings from the clinical trial. Regarding appropriate formulation, it has been suggested that interactions between estrogen and other hormones should be considered for further investigation. A review of the literature has led us to conclude that a thorough investigation into such hormonal interactions is warranted. We hypothesize that the increased risk of cerebrovascular disease observed in menopausal women may, in part, be due to changes in the circulating levels of melatonin and estrogen and their modulatory affects on many relevant endothelial cell biological activities, such as regulation of vascular tone, adhesion to leukocytes, and angiogenesis, among others. Our hypothesis is supported by numerous studies demonstrating the reciprocal inhibitory effects of melatonin and estrogen on vascular tone, neuroprotection, and receptor expression. We believe that a thorough analysis of the distribution, localization, expression, quantification, and characterization of hormonal receptor subtypes, as well as changes in structural morphology in diseased and normal, healthy cerebrovascular tissue, will substantially aid in our understanding of the effects of HRT on the cerebrovascular circulation. The application of new molecular biological techniques such as tissue microarray analysis, gene and protein arrays, and multi-photon confocal microscopy may be of tremendous benefit in this regard.
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PMID:Interactions between melatonin and estrogen may regulate cerebrovascular function in women: clinical implications for the effective use of HRT during menopause and aging. 1569 89

In response to concerns regarding the safety of ephedra-containing dietary supplements, manufacturers have marketed "ephedra-free" products. Many of these contain synephrine, a sympathomimetic amine from the plant Citrus aurantium. Synephrine is structurally similar to ephedrine and has vasoconstrictor properties. We describe a 38-year-old patient with ischemic stroke associated with an ephedra-free dietary supplement containing synephrine and caffeine. The patient presented with memory loss and unsteady gait after taking 1 or 2 capsules per day of a dietary supplement (Stacker 2 Ephedra-Free) for 1 week. He had no notable medical history or major atherosclerotic risk factors and took no other medications. Physical examination showed a mildly ataxic gait and substantial Impairment of both concentration and memory. Computed tomography and magnetic resonance Imaging of the brain showed subacute infarctions in the left thalamus and left cerebellum in the distribution of the vertebrobasilar circulation. Other causes of ischemic stroke were evaluated, and findings were unremarkable; a vasospastic origin was considered most likely. The patient was discharged with nearly complete resolution of symptoms. Synephrine, a sympathomimetic amine related to ephedrine, may be associated with Ischemic stroke. Consumers and clinicians need to be Informed about the potential risks of ephedra-free products.
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PMID:Ischemic stroke associated with use of an ephedra-free dietary supplement containing synephrine. 1581 93

The cessation of ovarian estrogen production occurring around the time of menopause has the potential to influence central nervous system function, as well as a number of neurological disorders that affect women during midlife and old age, including memory loss and mild cognitive impairment, ischemic stroke, Parkinson's disease, and Alzheimer's disease. During midlife, there is observational evidence that episodic memory is not substantially affected by natural menopause or by use of estrogen-containing hormone therapy, but short-term clinical trial evidence suggests hormone therapy might benefit verbal memory after surgical menopause. Clinical trial data indicate that hormone therapy does not reduce, and may increase, stroke incidence. Parkinson's disease and Alzheimer's disease are the 2 most common neurodegenerative illnesses. Estrogen influences dopaminergic pathways within the central nervous system. However, available observational evidence is limited and inconclusive regarding any role of hormone therapy in influencing risk or symptoms of Parkinson's disease, a disorder of dopaminergic neurons. Finally, clinical trial data indicate that hormone therapy should not be initiated in the late postmenopause with the goal of improving memory, preventing cognitive decline, reducing dementia risk, or improving Alzheimer's disease symptoms. An important priority for clinical investigation is to determine whether hormone therapy used during the menopausal transition and early postmenopause has long-term effects on cognition or dementia risk. The critical window hypothesis as applied to Alzheimer's disease conjectures that effects of early hormone therapy might differ from those of hormone therapy initiated in the late postmenopause, but convincing evidence is yet to be obtained.
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PMID:Menopause and disorders of the central nervous system. 1630 63

Adverse neurologic outcomes after cardiac surgery can have devastating consequences, among them increased mortality risk and, among survivors, loss of independence and a diminished quality of life. They also represent a burden on the health-care system, requiring prolonged hospitalizations and additional aftercare and, therefore, greater costs. Adverse outcomes are classified by their severity. Frank stroke is the most serious. This complication is associated with patient age; however, the presence of significant ascending aortic disease represents the greatest hazard. Multivariable analysis also indicates that prior neurologic events, diabetes, chronic obstructive pulmonary disease, preoperative status, and diffuse vascular disease are predictive. The second type of adverse cerebral outcome includes neurocognitive abnormalities such as memory loss and diminished emotional health. The strongest predictors of these abnormalities are hypertension and a history of alcohol use, as well as age. These predictive factors have been incorporated into the Multicenter Study of Perioperative Ischemia stroke-risk index, which clinicians can use to better assess the risk of adverse neurologic events. Clinical research examining the relationship between the predictive variables for neurologic adverse events and cerebral blood flow has suggested some surgical strategies for minimizing risk, such as limiting manipulation of the ascending aorta. The benefits of strategies such as using low or high mean arterial pressures and manipulating pump flow remain unclear. Off-pump coronary bypass surgery has been proposed as a means of reducing neurologic risk, but its effectiveness is unproved in this area. One pharmacologic strategy, the administration of aprotinin, has been shown to reduce the incidence of stroke in high-risk patients.
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PMID:Predicting and preventing adverse neurologic outcomes with cardiac surgery. 1649 92

Several types of mass lesions may occur in the third and lateral ventricles. Typically they arise from the lining of the ventricular cavity or from contiguous structures, by extension into the ventricle. The authors describe two patients, each of whom presented with a different rare lesion of the ventricular system. The first was a 53-year-old woman with a history of hypertension who sustained a blunt traumatic injury to the occipital region and subsequently developed a progressively worsening right-sided headache. Radiological examinations over the next 2 years revealed an enlarged right lateral ventricle and, ultimately, a choroid plexus cyst in its anterior and middle third, near the foramen of Monro, which is a rare location for these lesions. The cyst was removed en bloc, and follow-up examinations showed a significant improvement in her headache and a minimal differences in size between right and left ventricles. The authors also describe a 57-year-old man with hypertension, diabetes mellitus, and an old mycardial infarct, who presented to an outside institution with a progressively worsening headache, generalized malaise, and loss of olfactory sensation. Diagnostic imaging revealed a 1.5-cm oval lesion centered in the lamina terminalis region, an open craniotomy was performed, and evaluation of a biopsy sample demonstrated the mass to be a chordoid glioma of the third ventricle, a recently described glioma subtype. Two days after surgery, he suffered a left parietal stroke and an anterior mycardial infarction. After convalescing, he presented to The University of Texas M. D. Anderson Cancer Center for radiotherapy and follow up; 7 months later he was readmitted complaining of headache, short-term memory loss, and worsening confusion and disorientation. Neuroimaging revealed progression of the tumor (now 2 cm in diameter), which was removed by gross-total resection. His headache resolved immediately, and 2 months later his only complaint was of episodes of confusion. Three weeks later he died of a massive myocardial infarction. These two patients represent the sixth case of an adult with a choroid plexus cyst in the anterior lateral ventricle and the 19th case of an adult with a chordoid glioma of the third ventricle, respectively.
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PMID:Choroid plexus cyst and chordoid glioma. Report of two cases. 1672 23

Stroke is an important risk factor for dementia, but the exact mechanisms involved in cognitive decline remain unclear. In this study, we related baseline MRI brain measures with later cognitive decline. Seventy-nine stroke survivors aged 75+ years without dementia were recruited 3-month post-stroke. They underwent yearly neuropsychological assessments and had an MRI at baseline and 2 years. Medial temporal lobe atrophy (MTA) was scored and volume of white matter hyperintensities (WMH) was measured at baseline. The rate of ventricular enlargement was measured by comparing the baseline and repeat images. Linear regression indicated that memory loss was related to both baseline memory and MTA (p=0.001; standardized regression coefficient beta=-0.35) but not WMH volume. The only independent predictor of ventricular enlargement was MTA (p=0.003; beta=0.47). However, no baseline MRI variable differed between those who did (18%) and did not (82%) develop dementia. The association of MTA but not WMH with subsequent cognitive decline and increasing brain atrophy suggests a greater role for Alzheimer type than vascular pathology in delayed cognitive impairment after stroke.
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PMID:Medial temporal atrophy rather than white matter hyperintensities predict cognitive decline in stroke survivors. 1693 70

Studies involving animal models of acute central nervous system (CNS) stroke and trauma strongly indicate that sex and/or hormonal status are important determinants of outcome after brain injury. The present study was undertaken to examine the ability of estradiol to protect hippocampal neurons from lateral fluid percussion brain injury. Sprague-Dawley female rats (211-285 g; n = 119) were ovariectomized, and a subset (n = 66) were implanted with 17beta-estradiol pellets to provide near physiological levels of estradiol. Animals were subjected to lateral fluid percussion brain injury or sham injury 1 week later. Activation of caspase-3 (n = 26) and TUNEL staining (n = 21) were assessed at 3 and 12 h after injury, respectively, in surviving control and estradiol-treated animals. Memory retention was examined using a Morris water maze test in a separate subset of animals (n = 43) at 8 days after injury. Activated caspase-3 and TUNEL staining were observed in the dentate hilus, granule cell layer, and CA3 regions in all injured rats, indicative of selective hippocampal cell apoptosis in the acute posttraumatic period. Estradiol did not significantly alter the number of hippocampal neurons exhibiting caspase-3 activity or TUNEL staining. Brain injury impaired cognitive ability, assessed at 1 week post-injury (p < 0.001). However, estradiol at physiological levels did not significantly alter injury-induced loss of memory. These data indicate that estradiol at physiological levels does not ameliorate trauma-induced hippocampal injury or cognitive deficits in ovariectomized female rats.
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PMID:Effects of estradiol on cognition and hippocampal pathology after lateral fluid percussion brain injury in female rats. 1718 91

In 1983, a detailed clinical description of a new syndrome was published. This prothrombotic syndrome was initially called the anticardiolipin syndrome and subsequently the antiphospholipid syndrome (APS), or Hughes Syndrome. Almost uniquely, it results in arterial as well as venous thrombosis and is marked by the presence of circulating antiphospholipid antibodies. Clinical features are protean, ranging from peripheral deep vein thrombosis (DVT) to involvement of internal organs such as the liver, kidneys, and adrenals. Likewise, arterial thrombosis can result in life-threatening infarction of organs such as the heart. The nervous system is frequently affected, with migraine, memory loss, balance disorders, stroke, and atypical multiple sclerosis being prominent. Other features include recurrent miscarriage, thrombocytopenia, and livedo reticularis. More recent observations have included ischemic bone fractures, renal and celiac artery stenosis, and a possible tendency toward accelerated atherosclerosis. The condition is seen in patients with lupus, but, significantly, occurs without associated lupus ("primary" APS)-indeed, increasing clinical recognition of Hughes Syndrome suggests that this condition will overtake lupus in prevalence. Treatment at present is by anticoagulation. The mechanisms for thrombosis are being worked out; it has been suggested that in some situations (e.g., pregnancy loss), an inflammatory component as well as thrombosis may play a part.
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PMID:Hughes Syndrome: the antiphospholipid syndrome--a clinical overview. 1742 56

Transient Global Amnesia (TGA) is a benign and temporary loss of anterograde memory with the preservation of remote memories and immediate recall. TGA was first described in 1956 and since then epilepsy, transient ischaemic attacks (TIA), migraine and now intracranial venous stasis have been implicated in its aetiology. Precipitants of TGA include physical exertion and valsalva-like manoeuvres. In order to diagnose TGA the criteria created by Hodge and Warlow in 1990 can be used. This requires the episode of memory loss to be witnessed and involve anterograde amnesia. The patient must not have any evidence of neurological signs or deficits, features of epilepsy, active epilepsy or recent head injury. Finally the episode must have resolved within 24 h. In this case study the patient's symptoms are mistakenly attributed to a TIA. There is no increased risk of TIA or CVA in patients who have had TGA and there are no increased levels of mortality amongst these patients. In this article we aim to help doctors working in the emergency department to diagnose and manage TGA.
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PMID:The diagnosis and management of transient global amnesia in the emergency department. 1751 54


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