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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hereditary Haemorrhagic Teleangiectasia (HHT) is a vascular disorder of angiogenesis transmitted in an autosomal dominant pattern, characterised by heterogeneity in clinical manifestations. One of the most important organ involved is lung, including pulmonary arteriovenous malformations (PAVM). PAVM occur in 20 to 30% of the HHT population and recently are considered a marker of disease. PAVM are direct artery-to-vein connections with low pressure and without an interveining capillary bed. PAVM are classified as simple (supplied by one feeding artery) or complex (receiving blood supply from two or more feeding artery). According to the international reports, treatment it's recommendable for all PAVM with feeding vessels 3mm or larger, in order to reduce the risk of cerebral ischaemia and neurologic manifestations frequently attributed to paradoxical embolisation. Transcatheter embolotherapy of PAVM is a form of treatment based on occlusion of the feeding artery to a PAVM by using platinum coils or detachable balloons. The technique of coil embolisation involves the exact localisation of PAVM by pulmonary angiography followed by superselective percutaneous caheterisation of feeding artery obtained by using a dedicated 7F guiding catheter, which coaxially allocates a 5F hydrophilic catheter advanced in order to perform both superselective angiography of feeding artery and embolisation itself. Inside the 5F catheter the platinum coils are advanced using a .035'' guide-wire and released until an optimal occlusion of feeding artery is achieved. At the end of the procedure angiographic control is performed in order to verify the occlusion of feeding artery. The use of platinum coils is preferable over detachable balloons when feeding artery are greater than 7 mm in diameter and have irregular anatomical configuration. On the other hand, the principal advantage of using detachable balloons is that the balloon itself can be deflated and repositioned if necessary. Transcatheter embolotherapy is technically safe and clinically effective and may represent the primary choice of treatment in HHT patients. On the other hand the most common complications of this treatment (pleurisy and air embolism) can be prevented by using some tips during the embolisation procedure like "anchor technique," "scaffold technique" and "balloon assisted technique." Cerebral arteriovenous malformations (CAVM) are present in 10-20% of patients with HHT and multiple in 50% of cases. Cortical surface is the most frequent localisation. Angiography is needed to diagnose all CAVM and to clarify the angioarchitecture of the lesion. In HHT CAVM are usually either micro-AVM, with a nidus not bigger than 1 cm, or small AVM, with a nidus between 1 and 3 cm. Quite frequently there are lesions characterised by arteriovenous fistulas. In the three patterns of CAVM usually found in HHT, small AVM are the most risky for bleeding although the risk is lower than that associated with sporadic ones. It is estimated from 0.38 to 0.69% per year in spite of the general incidence of bleeding in sporadic CAVM that ranges from 2 to 4% per year. In HHT patients, at present, the precise indications and timing of treatment are not established. Trend is to treat small AVM and AVF and to follow-up micro-AVM with MRI and angiography. As for sporadic CAVM, treatment of small AVM is usually referred to stereotactic radiosurgery. Endovascular embolisation is proposable if the lesion is easily reachable by microcatheterism and the position of the microcatheter is safe. Glue is used for embolisation and the technique is briefly discussed.
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PMID:Endovascular treatment of pulmonary and cerebral arteriovenous malformations in patients affected by hereditary haemorrhagic teleangiectasia. 1661 Nov 6

Vascular parkinsonism (VP) is a heterogeneous clinical entity. The idea of a relationship between cerebral vascular disease and parkinsonism may be traced back to the 1920s, when the diagnostic unit called "arteriosclerotic parkinsonism", a predecessor of VP, was established. This review is concerned with historical and contemporary views regarding the possible vascular genesis of parkinsonism. Confusion persists as a result of vaguely defined diagnostic criteria. The following types of simultaneous occurrence of parkinsonism and cerebral vascular disease (CVD) may be recognised: 1. gait disorders of the lower body parkinsonism type are caused mostly by white matter lesions in the frontal lobes; such disorders may require a diagnosis of vascular origin. We suggest replacing the term "lower body parkinsonism" with a more appropriate term not including the word "parkinsonism": an alternative term could be "cerebrovascular gait disorder"; 2. if the signs and symptoms are typical for idiopathic Parkinson's disease (IPD), the coincidence of IPD and CVD should be considered; 3. if the symptoms of parkinsonism are neither typical for IPD nor for VP, and there are clinical or MR signs of CVD, VP should be regarded as possible when alternative causes are excluded; 4. if the symptoms of parkinsonism and clinical and MR signs are typical for VP, VP should be regarded as probable; 5. if a stroke affecting the contralateral basal ganglia is followed by the occurrence of hemiparkinsonism, the diagnosis of VP is unambiguous. Vascular parkinsonism (VP) is probably one of the most frequently erroneous neurological diagnoses. The reason for this misdiagnosis is that both cerebral vascular disease (CVD) and parkinsonism usually occur at the same age. Due to the high incidence of CVD, it is possible for CVD and idiopathic Parkinson's disease (IPD) to coincide in some cases. Another reason for the misdiagnosis is that the concept of VP lacks clarity. This review aims to contribute to an improved understanding of VP in clinical practice. In this context, the term "CVD" is understood in the broad sense of a brain impairment caused by cerebral vessel pathology. It covers various concepts, as some authors use the term CVD to mean a manifestation of vascular lesions in pathologico-anatomical material or in the imaging techniques; others mean the history and clinical manifestation of cerebral ischaemia, or, more rarely, haemorrhage. The term CVD may cover large vessel disease as well as small vessel disease. This means that territorial and lacunar infarcts and white matter lesions (WML) are all considered as CVD.
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PMID:Vascular parkinsonism--an update. 1676 89

Findings from gene expression profiling studies are leading to new diagnostic and therapeutic strategies that can be applied in medical practice, especially in the field of oncology. Promising results of gene expression profiling of the peripheral blood in patients with ischaemic stroke have been obtained in recent pilot studies, demonstrating a partially reproducible gene signature of acute cerebral ischaemia. However, questions remain. Given that blood is at least in part a surrogate tissue for ischaemic stroke, the specificity of these signatures needs to be evaluated. Furthermore, it needs to be determined whether standardization of this methodology is required and whether clinical signatures can be identified that are improvements over the tools currently used in clinical practice. Clinically useful signatures would include those of haemorrhagic as well as ischaemic stroke, reclassification of stroke type and prognosis, and vascular disease risk. If these conditions are met, then it should be possible to develop cost-effective and rapid assays.
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PMID:Blood genomic profiling: novel diagnostic and therapeutic strategies for stroke? 1707 10

Cytidine 5'-diphosphocholine, CDP-choline, or citicoline is an essential intermediate in the biosynthetic pathway of structural phospholipids in cell membranes, particularly phosphatidylcholine. Following administration by both the oral and parenteral routes, citicoline releases its two main components, cytidine and choline. Absorption by the oral route is virtually complete, and bioavailability by the oral route is therefore approximately the same as by the intravenous route. Once absorbed, citicoline is widely distributed throughout the body, crosses the blood-brain barrier and reaches the central nervous system (CNS), where it is incorporated into the membrane and microsomal phospholipid fraction. Citicoline activates biosynthesis of structural phospholipids of neuronal membranes, increases brain metabolism, and acts upon the levels of different neurotransmitters. Thus, citicoline has been experimentally shown to increase norepinephrine and dopamine levels in the CNS. Owing to these pharmacological mechanisms, citicoline has a neuroprotective effect in hypoxic and ischemic conditions, decreasing the volume of ischemic lesion, and also improves learning and memory performance in animal models of brain aging. In addition, citicoline has been shown to restore the activity of mitochondrial ATPase and membrane Na+/K+ATPase, to inhibit activation of certain phospholipases, and to accelerate reabsorption of cerebral edema in various experimental models. Citicoline has also been shown to be able to inhibit mechanisms of apoptosis associated to cerebral ischemia and in certain neurodegeneration models, and to potentiate neuroplasticity mechanisms. Citicoline is a safe drug, as shown by the toxicological tests conducted, that has no significant systemic cholinergic effects and is a well tolerated product. These pharmacological characteristics and the action mechanisms of citicoline suggest that this product may be indicated for treatment of cerebral vascular disease, head trauma (HT) of varying severity, and cognitive disorders of different causes. In studies conducted in the treatment of patients with HT, citicoline was able to accelerate recovery from post-traumatic coma and neurological deficits, achieving an improved final functional outcome, and to shorten hospital stay in these patients. Citicoline also improved the mnesic and cognitive disorders seen after HT of minor severity that constitute the so-called post-concussional syndrome. In the treatment of patients with acute ischemic cerebral vascular disease, citicoline accelerates recovery of consciousness and motor deficit, achieves a better final outcome, and facilitates rehabilitation of these patients. The other major indication of citicoline is for treatment of senile cognitive impairment, either secondary to degenerative diseases (e.g. Alzheimer disease) or to chronic cerebral vascular disease. In patients with chronic cerebral ischemia, citicoline improves scores in cognitive rating scales, while in patients with senile dementia of the Alzheimer type it stops the course of disease, and neuroendocrine, neuroimmunomodulatory, and neurophysiological benefits have been reported. Citicoline has also been shown to be effective in Parkinson disease, drug addictions, and alcoholism, as well as in amblyopia and glaucoma. No serious side effects have occurred in any series of patients treated with citicoline, which attests to the safety of treatment with citicoline.
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PMID:Citicoline: pharmacological and clinical review, 2006 update. 1717 Nov 87

Reactive oxygen species (ROS) have been implicated in the pathogenesis of cerebral injury after ischemia-reperfusion (I/R). Fish n-3 essential fatty acids (EFA), contain eicosapentaenoic acids (EPA) and docosahexoenoic acids (DHA), exhibit antioxidant properties. DHA is an important component of brain membrane phospholipids and is necessary for the continuity of neuronal functions. EPA prevents platelet aggregation and inhibits the conversion of arachidonic acid into thromboxane A(2) and prostaglandins. They have been suggested to be protective agents against neurological and neuropsychiatric disorders. In this study, the neuroprotective effects of fish n-3 EFA on oxidant-antioxidant systems and number of apoptotic neurons of the hippocampal formation (HF) subjected to cerebral I/R injury was investigated in Sprague-Dawley rats. Six rats were used as control (Group I). Cerebral ischemia was produced by occlusion of both the common carotid arteries combined with hypotension for 45 min, followed by reperfusion for 30 min, in rats either on a standard diet (Group II) or a standard diet plus fish n-3 EFA (Marincap((R)), 0.4 g/kg/day, by gavage) for 14 days (Group III). At the end of procedures, the rats were sacrificed and their brains were removed immediately. The levels of malonedialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in left HF. In addition, the number of apoptotic neurons was counted by terminal transferase dUTP nick end labelling (TUNEL) assay in histological samples of the right HF. We found that SOD activities and MDA levels increased in Group III rats compared with Group II rats. On the other hand, CAT activities and NO levels were found to be decreased in Group III rats compared with Group II rats. Additionally, the number of apoptotic neurons was lower in Group III in comparison with Group II rats. The present findings suggest that fish n-3 EFA could decrease the oxidative status and apoptotic changes in ischemic rat hippocampal formation. Dietary supplementation of n-3 EFA may be beneficial to preserve or ameliorate ischemic cerebral vascular disease.
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PMID:The protective effect of fish n-3 fatty acids on cerebral ischemia in rat hippocampus. 1718 1

Homocysteine is a thiol aminoacid synthesized during the metabolism of methionine. Increased plasma levels of homocysteine can be the result of mutations in the enzymes responsible for homocysteine metabolism, particularly cystathionine-beta synthase (CBS) and 5,10-methylenetetrahydrofolate reductase (MTHFR). Additionally, nutritional deficiencies in B vitamin cofactors required for homocysteine metabolism, including folic acid, vitamin B6 (pyridoxal phosphate), and/or vitamin B12 (methylcobalamin), can induce hyperhomocysteinemia. Over the last decade, following in vitro and in vivo observations of a homocysteine-associated vascular pathology, convincing epidemiological evidence has been gathered on the relation between moderate elevation of plasma homocysteine and vascular disease, including cerebral ischemia. However, causality has yet to be established. The association between homocysteine and ischemic stroke might be a spurious epidemiological finding because of confounding or it might reflect reverse causality. If this is the case, elevated levels of plasma homocysteine should be interpreted as an epiphenomenon secondary to the vascular disease itself. Thus, whether lowering homocysteine concentration prevents cerebral ischemia remains to be determined. The only method to answer the question of the causal relation between homocysteine and ischemic stroke is by intervention trials in which patients at high vascular risk, such as those who have had a recent cerebral ischemic event are randomly allocated to placebo or homocysteine-lowering multivitamin therapy, and followed prospectively. Some of these randomized controlled trials are currently ongoing. Their results should hopefully resolve the issue in the next future.
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PMID:Homocysteine and cerebral ischemia: pathogenic and therapeutical implications. 1730 30

Schimke-immuno-osseous dysplasia is an autosomal-recessive multisystem disorder with the prominent clinical features disproportionate growth failure, progressive renal failure, and T-cell immunodeficiency. Neurological symptoms caused by transient ischemic attacks (TIAs) and strokes are a typical clinical finding in severe SIOD. Cerebral ischemia and white matter changes, moyamoya phenomena and absence of a cerebellar hemisphere and partial absence of the cerebellar vermis have been described in patients with severe SIOD. We present three SIOD patients with atrophy of the caudal parts of the cerebellar vermis (posterior lobule) and of the cerebellar hemispheres. We hypothesize that these cerebellar abnormalities are a continuum of the ongoing vascular disease in severe SIOD.
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PMID:Cerebellar atrophy in Schimke-immuno-osseous dysplasia. 1767 1

The temporary occlusion of cerebral vessels is being used with increased frequency in the surgical management of cerebral vascular disease, and this procedure places brain tissue at risk of infarction. Using a modified version of a well-established model of focal cerebral ischemia in the rabbit, we tested the protective effect of a combination of six agents; each agent was selected to temporarily block one or more neuronal functions, hence reducing their metabolic demands. The combination of six agents had been previously shown to protect neurological function against ischemia. Ten male adult New Zealand White rabbits were anesthetized with halothane, and physiological parameters were maintained within normal ranges. A branch of the left external carotid artery was catheterized and the vasculature supplying the left middle cerebral artery (MCA) territory was isolated. Mannitol was infused via the external carotid artery into the left internal carotid artery to open the blood-brain barrier in the territory of the MCA. This infusion was followed by either Ames' medium alone (control) or Ames' medium containing the combination of agents: tetrodotoxin (0.1 micromol/L), 2-amino-4-phosphonobutyric acid (20 mumol/L), 2-amino-5-phosphonovaleric acid (1 mmol/L), amiloride (1 mmol/L), magnesium (10 mmol/L), and lithium (10 mmol/L). Ischemia in the left MCA territory was then induced for 2 hours, followed by 4 hours of reperfusion. Animals pretreated with the combination of agents sustained infarctions that were markedly smaller (mean+/-SEM, 46+/-19.7 mm(3), n=5) than control animals (300+/-46.5 mm(3), n=5, P<.001). We conclude that the strategy of locally delivering a combination of agents designed to temporarily reduce neuronal metabolic demands by temporarily blocking several nonvital neuronal functions, can reduce the infarction induced by a focal reduction in cerebral blood flow in the rabbit.
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PMID:Avoiding stroke during cerebral arterial occlusion by temporarily blocking neuronal functions in the rabbit. 1789 3

With the development of molecular biology, genome science becomes an important subject currently. Characterized by high-throughput, high-integration, high-parallelism, miniaturization and automation, it is the integrated study of gene properties on a large scale. Stroke, an important cerebral vascular disease, is one of the threats to human health. The utilization of microarray study for the pathogenesis of stroke, not only reveals the essentials of the disease in the overall level of genes, but also contributes to the detection of therapeutic targets and the development of novel drugs for stroke. Referring to our own work, this discussion focuses on the progress of the mechanisms underlying experimental cerebral ischemia investigation in vivo as well as anti-cerebral ischemia agents by gene chip technology.
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PMID:[Advances in the study of gene chip technology for the investigation of the mechanisms underlying cerebral ischemia and anti-cerebral ischemia agents]. 1794 25

The metabolic syndrome (MS) is the combination of factors which, when occurring in an individual, can result in an increased risk of diabetes mellitus (DM) and of episodes of vascular disease. We present a systematic review of the diagnostic criteria, pathology, prevalence and risk of vascular disease (including stroke) associated with the MS and, if the patients have already suffered cerebral ischemia and have the MS and/or DM, the appropriate therapies from which they could benefit.
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PMID:The metabolic syndrome and cerebrovascular disease: suspicion and evidence. 1797 40


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