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

Symptomatic early neurosyphilis is a rare manifestation of syphilis that usually occurs within the first 12 months of infection. Most neurologic symptoms of early neurosyphilis result from acute or subacute meningitis, abnormalities in cranial nerve function, and inflammatory vasculitis leading to a cerebrovascular accident. Symptomatic early neurosyphilis essentially disappeared in the United States after the introduction of penicillin treatment for syphilis in the late 1940s but reappeared in the 1980s among persons with human immunodeficiency virus (HIV) infection. The disease burden from neurosyphilis is unknown because national reporting of this disease is incomplete. Because the increase in syphilis cases during the past 5 years has occurred primarily among MSM, many of whom were infected with HIV, CDC conducted a review of possible neurosyphilis cases to describe the clinical course of symptomatic early neurosyphilis and to better characterize the risk for this illness among HIV-infected MSM. The review included health department records from four U.S. cities (Los Angeles, California; San Diego, California; Chicago, Illinois; and New York, New York) for the period January 2002-June 2004. This report describes the results of that review, which identified 49 HIV-positive MSM with symptomatic early neurosyphilis during that 30-month period. Among HIV-positive MSM with early syphilis, the estimated risk for having symptomatic early neurosyphilis was 1.7%, and the risk for having early neurosyphilis with persistent symptoms 6 months after treatment was 0.5%. These findings emphasize the importance of preventing syphilis in HIV-infected persons. HIV-infected persons with cranial nerve dysfunction or other unexplained neurologic symptoms should be evaluated for early neurosyphilis.
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PMID:Symptomatic early neurosyphilis among HIV-positive men who have sex with men--four cities, United States, January 2002-June 2004. 1817 79

The impact of hepatitis C virus (HCV) and other comorbid conditions upon survival is not well quantified in patients on dialysis. We identified HCV-infected and uninfected persons in the USRDS using claims data in 1997-1998 and followed until September 22, 2002 or death. We used Gray's time-varying coefficients model to examine factors associated with survival. Subjects with a renal transplant were excluded. A total of 5737 HCV-infected and 11 228 HCV-uninfected persons were identified. HCV-infected subjects were younger (mean age 57.8 vs 65.3 years), more likely to be male (57.6%vs 49.6%) and black (54.0%vs 36.4%). They were more likely to have a diagnosis of drug (16.5%vs 4.6%) and alcohol use (14.0%vs 3.1%), and to be human immunodeficiency virus (HIV) co-infected (7.4%vs 1.8%) (all comparisons, P < 0.0005). In an adjusted Gray's time-varying coefficient model, HCV was associated with an increased risk of mortality (P < 0.0005). The hazards were highest at the time of HCV diagnosis and decreased to a stable level 2 years after diagnosis. Other factors associated with increased risk of mortality were (P < 0.0005 unless stated) HIV coinfection; diagnosis of drug use (P = 0.001); coronary artery disease (P = 0.006); stroke; diabetes as the primary cause for renal failure; peripheral vascular disease; depression and presence of anaemia. HCV was associated with higher risk of death in patients on dialysis, even after adjusting for concurrent comorbidities. The risk was highest at the time of HCV diagnosis and stabilized over time. Clinical trials of HCV screening and treatment to reduce mortality in this population are warranted.
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PMID:Impact of hepatitis C virus infection and other comorbidities on survival in patients on dialysis. 1787 3

This case illustrates surgical treatment of an arteriovenous malformation (AVM) in a patient with hemophilia A also infected with human immunodeficiency virus (HIV). A 31-year-old man was admitted to our hospital with right parietal intracerebral hemorrhage. He had previously been diagnosed with hemophilia A and HIV. Carotid angiography revealed an AVM. As the hematoma enlarged and clinical symptoms progressed, we resected the hematoma and the AVM while providing supplemental infusion of Factor VIII before, during, and after the operation. The patient did not experience abnormal postoperative bleeding, and he was discharged with mild motor weakness of the left lower extremity. We discuss the surgical indications, risk, and patient management in relation to hemophilia and HIV infection.
J Stroke Cerebrovasc Dis
PMID:Surgical treatment of arteriovenous malformation in a patient with human immunodeficiency virus infection and hemophilia a: case report. 1790 51

Protease-activated receptors (PARs) are G protein-coupled receptors that regulate the cellular response to extracellular serine proteases, like thrombin, trypsin, and tryptase. The PAR family consists of four members: PAR-1, -3, and -4 as thrombin receptors and PAR-2 as the trypsin/tryptase receptor, which are abundantly expressed in the brain throughout development. Recent evidence has supported the direct involvement of PARs in brain development and function. The expression of PARs in the brain is differentially upregulated or downregulated under pathological conditions in neurodegenerative disorders, like Parkinson's disease, Alzheimer's disease, multiple sclerosis, stroke, and human immunodeficiency virus-associated dementia. Activation of PARs mediates cell death or cell survival in the brain, depending on the amplitude and the duration of agonist stimulation. Interference or potentiation of PAR activation is beneficial in animal models of neurodegenerative diseases. Therefore, PARs mediate either neurodegeneration or neuroprotection in neurodegenerative diseases and represent attractive therapeutic targets for treatment of brain injuries. Here, we review the abnormal expression of PARs in the brain under pathological conditions, the functions of PARs in neurodegenerative disorders, and the molecular mechanisms involved.
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PMID:Protease-activated receptors in the brain: receptor expression, activation, and functions in neurodegeneration and neuroprotection. 1791 33

Chemokines and chemokine receptors, primarily found to play a role in leukocyte migration to the inflammatory sites or to second lymphoid organs, have recently been found expressed on the resident cells of the central nervous system (CNS). These proteins are important for the development of the CNS and are involved in normal brain functions such as synaptic transmission. Increasing lines of evidence have implicated an involvement for chemokines and their receptors in several neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), human immunodeficiency virus-associated dementia (HAD), multiple sclerosis (MS), and stroke. Specific inhibition of the biological activities of chemokine receptors could gain therapeutic benefit for these neurodegenerative disorders. In recent years, non-peptide antagonists of chemokine receptors have been disclosed and tested in relevant pharmacological models and some of these inhibitors have entered clinical trials. The aim of this review is to outline the recent progress regarding the role of chemokines and their receptors in neurodegenerative diseases and the advancements in the development of chemokine receptor inhibitors as potential therapeutic approaches for these neurodegenerative diseases.
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PMID:The many roles of chemokine receptors in neurodegenerative disorders: emerging new therapeutical strategies. 1797 99

Methamphetamine is a stimulant commonly abused in many parts of the United States. Most methamphetamine users are white men 18 to 25 years of age, but the highest usage rates have been found in native Hawaiians, persons of more than one race, Native Americans, and men who have sex with men. Methamphetamine use produces a rapid, pleasurable rush followed by euphoria, heightened attention, and increased energy. Possible adverse effects include myocardial infarction, stroke, seizures, rhabdomyolysis, cardiomyopathy, psychosis, and death. Chronic methamphetamine use is associated with neurologic and psychiatric symptoms and changes in physical appearance. High-risk sexual activity and transmission of human immunodeficiency virus are also associated with methamphetamine use. Use of methamphetamine in women who are pregnant can cause placental abruption, intrauterine growth retardation, and preterm birth, and there can be adverse consequences in children exposed to the drug. Treatment of methamphetamine intoxication is primarily supportive. Treatment of methamphetamine abuse is behavioral; cognitive behavior therapy, contingency management, and the Matrix Model may be effective. Pharmacologic treatments are under investigation.
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PMID:Methamphetamine abuse. 1799 Aug 40

Glutamate is an essential neurotransmitter regulating brain functions. Excitatory amino acid transporter (EAAT)-2 is one of the major glutamate transporters primarily expressed in astroglial cells. Dysfunction of EAAT2 is implicated in acute and chronic neurological disorders, including stroke/ischemia, temporal lobe epilepsy, amyotrophic lateral sclerosis, Alzheimer disease, human immunodeficiency virus 1-associated dementia, and growth of malignant gliomas. Ceftriaxone, one of the beta-lactam antibiotics, is a stimulator of EAAT2 expression with neuroprotective effects in both in vitro and in vivo models based in part on its ability to inhibit neuronal cell death by glutamate excitotoxicity. Based on this consideration and its lack of toxicity, ceftriaxone has potential to manipulate glutamate transmission and ameliorate neurotoxicity. We investigated the mechanism by which ceftriaxone enhances EAAT2 expression in primary human fetal astrocytes (PHFA). Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-kappaB (NF-kappaB) signaling pathway. The antibiotic promoted nuclear translocation of p65 and activation of NF-kappaB. The specific NF-kappaB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated EAAT2 induction. In addition, ceftriaxone increased glutamate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhibited ceftriaxone-induced glutamate uptake activity in PHFA. Taken together, our data indicate that ceftriaxone is a potent modulator of glutamate transport in PHFA through NF-kappaB-mediated EAAT2 promoter activation. These findings suggest a mechanism for ceftriaxone modulation of glutamate transport and for its potential effects on ameliorating specific neurodegenerative diseases through modulation of extracellular glutamate.
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PMID:Mechanism of ceftriaxone induction of excitatory amino acid transporter-2 expression and glutamate uptake in primary human astrocytes. 1832 97

The looming epidemic of stroke and other chronic non-communicable diseases associated with lifestyle and demographic transitions occurring all over the world is increasingly being acknowledged. However, the significance of these trends in the relatively young populations of the countries comprising Sub-Saharan Africa (SSA) is less certain and considerably overshadowed by attention given to the impact of human immunodeficiency virus and other infectious diseases. We undertook a literature review of the burden of stroke in SSA and provide recommendations for future research. Despite the paucity of high quality studies, the mostly hospital-based data and limited community surveys indicate there to be high and increasing rates of stroke affecting people at much younger ages in SSA than in developed countries. In general, awareness, diagnosis and management of stroke are poor, and the associated case fatality and residual disability are high. As elsewhere, elevated blood pressure is the major determinant of stroke but there are also high rates of strokes related to the complications of rheumatic heart disease and other infections. Given high attributable risks exposures in association with rapid ageing and urbanisation in SSA, the future is not bright. Population-based incidence studies are urgently needed to map the profile and outcome of stroke. Such data would provide the necessary evidence base to improve prevention and treatments for stroke alongside current efforts to bring infectious diseases under control in SSA.
Int J Stroke 2006 Nov
PMID:The neglected burden of stroke in Sub-Saharan Africa. 1870 15

The mechanism by which human immunodeficiency virus (HIV)-1 infection in humans leads to the erosion of lean body mass is poorly defined. Therefore, the purpose of the present study was to determine whether transgenic (Tg) rats that constitutively overexpress HIV-1 viral proteins exhibit muscle wasting and to elucidate putative mechanisms. Over 7 mo, Tg rats gained less body weight than pair-fed controls exclusively as a result of a proportional reduction in lean, not fat, mass. Fast- and slow-twitch muscle atrophy in Tg rats did not result from a reduction in the in vivo-determined rate of protein synthesis. In contrast, urinary excretion of 3-methylhistidine, as well as the content of atrogin-1 and the 14-kDa actin fragment, was elevated in gastrocnemius of Tg rats, suggesting increased muscle proteolysis. Similarly, Tg rats had reduced cardiac mass, which was independent of a change in protein synthesis. This decreased cardiac mass was associated with a reduction in stroke volume, but cardiac output was maintained by a compensatory increase in heart rate. The HIV-induced muscle atrophy was associated with increased whole body energy expenditure, which was not due to an elevated body temperature or secondary bacterial infection. Furthermore, the atrophic response could not be attributed to the development of insulin resistance, decreased levels of circulating amino acids, or increased tissue cytokines. However, skeletal muscle and, to a lesser extent, circulating insulin-like growth factor I was reduced in Tg rats. Although hepatic injury was implicated by increased plasma levels of aspartate and alanine aminotransferases, hepatic protein synthesis was not different between control and Tg rats. Hence, HIV-1 Tg rats develop atrophy of cardiac and skeletal muscle, the latter of which results primarily from an increased protein degradation and may be related to the marked reduction in muscle insulin-like growth factor I.
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PMID:Skeletal and cardiac myopathy in HIV-1 transgenic rats. 1871 59

Over 8.3 million people living in the Asia Pacific region are human immunodeficiency virus (HIV) positive and up to 40% of these individuals have had prior acquired immunodeficiency syndrome (AIDS) illnesses. Recently endeavors have been made to better characterize the burden of HIV-related neurological disease within the Asia Pacific region and, with this in mind, the NeuroAIDS in Asia and the Pacific Rim workshop was held in Sydney, Australia, as an affiliated event of the 4th IAS Conference on HIV Pathogenesis, Treatment and Prevention. The workshop was supported by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute of Mental Health (NIMH) of the United States National Institutes of Health and the Australian Government overseas AID program, AusAID. HIV neurologists, infectious disease physicians, pediatricians, psychiatrists, immunologists, virologists,and researchers from 12 countries of the Asia Pacific region (including Australia), the United States, and the United Kingdom attended the meeting. A broad range of topics were addressed, including common HIV neurological disorders, the lack of diagnostic, management, and research infrastructure, central nervous system (CNS) immune restoration disease, pediatric neuroAIDS, and current clinical and laboratory research projects being undertaken within the Asia Pacific region.
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PMID:NeuroAIDS in the Asia Pacific Region. 1903 Dec 89


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