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Cerebral Hemorrhage (cerebral + hemorrhage)
Kinds of Cerebral Hemorrhage Selected AbstractsStroke in renal transplant recipients: epidemiology, predictive risk factors and outcomeCLINICAL TRANSPLANTATION, Issue 1 2003Anna Oliveras Abstract: Background:, Cerebrovascular and cardiovascular diseases are the most important causes of increased morbidity and mortality in patients with end-stage renal disease. Stroke has been widely reported in chronic dialysis patients, but there is scarce information about stroke in renal transplant recipients (RTR), although cerebrovascular events are the most common and potentially life-threatening neurological complications in them. Our aim is to analyze the prevalence, risk factors, etiopathogenia, clinical aspects and outcome of stroke in RTR. Methods:, We analyzed 403 patients who received one or more renal grafts between 1979 and 2000: group A = patients who had stroke (n = 19); group B = those who did not (n = 384). Medical records and pertinent data were compiled. The risk of stroke was studied using univariate and multivariate Cox regression models. Results:, prevalence of stroke in RTR was 7.97% at 10 yr. Time elapsed between renal transplantation (RT) and stroke: 49.3 months. Possible risk factors based on the univariate analyses were: diabetic nephropathy (DN) (p <,0.001) and autosomal-dominant-polycystic-kidney-disease (p =,0.049) as original nephropathies, peripheral vascular disease (PVD) (p <,0.001), diabetes mellitus prior to RT (p =,0.005), age older than 40 yr (p =,0.037) and hypertension (p =,0.049). Other analysed risk factors such as gender, renal function, cytomegalovirus infection, hyperlipidemia, hyperuricemia, erythrocytosis or hypertensive donor failed to show any significant predictive value for stroke in these patients. When multivariate analyses were carried out, we found that DN (OR = 4.8; p = 0.010), PVD (OR = 8.2; p < 0.001) and age > 40 yr (OR = 3.3; p = 0.019) were predictive risk factors for stroke. For group A, hypertension was present in all patients, 68.4% had hyperlipidemia and 42.1% reported previous stroke. Cerebral hemorrhage occurred in seven of 19 (36.84%) of the stroke patients, but no subarachnoid hemorrhage occurred in them. Seven of 12 ischemic strokes were atherotrombotic. Considering all strokes, basal ganglia was the predominant localization. The outcome was poor, as nearly half of the patients died in the 3 months following stroke. Conclusions:, Prevalence of stroke in our RTR population was 7.97%. Cerebral hemorrhage appears to be more prevalent in RTR than in general population. More than that, the cerebral hemorrhage rate we found is higher than that reported elsewhere in RTR. The main predictors of stroke were DN, PVD and age. No patient with interstitial nephropathy suffered stroke. Mortality is high in RTR with stroke. [source] An ischemic stroke during intravenous recombinant tissue plasminogen activator infusion for evolving myocardial infarctionEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2001Gregory Youngnam Chang A 56-year-old man without a previous history of stroke received intravenous recombinant tissue plasminogen activator (tPA) for an evolving myocardial infarction. During the infusion, the patient developed aphasia and right hemiparesis. The CT and MRI confirmed an ischemic stroke without evidence of hemorrhage. Although the cerebral hemorrhage after tPA infusion is relatively more common, in rare cases, tPA infusion may result in fragmentation of a cardiac thrombus resulting in an ischemic cerebral stroke. [source] Coarctation of the Aorta: A Secondary Cause of HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 6 2004L. Michael Prisant MD Coarctation of the aorta is a constriction of the aorta located near the ligamentum arteriosum and the origins of the left subclavian artery. This condition may be associated with other congenital disease. The mean age of death for persons with this condition is 34 years if untreated, and is usually due to heart failure, aortic dissection or rupture, endocarditis, endarteritis, cerebral hemorrhage, ischemic heart disease, or concomitant aortic valve disease in uncomplicated cases. Symptoms may not be present in adults. Diminished and delayed pulses in the right femoral artery compared with the right radial or brachial artery are an important clue to the presence of a coarctation of the aorta, as are the presence of a systolic murmur over the anterior chest, bruits over the back, and visible notching of the posterior ribs on a chest x-ray. In many cases a diagnosis can be made with these findings. Two-dimensional echocardiography with Doppler interrogation is used to confirm the diagnosis. Surgical repair and percutaneous intervention are used to repair the coarctation; however, hypertension may not abate. Because late complications including recoarctation, hypertension, aortic aneurysm formation and rupture, sudden death, ischemic heart disease, heart failure, and cerebrovascular accidents may occur, careful follow-up is required. [source] Cerebral vascular accumulation of Dutch-type A,42, but not wild-type A,42, in hereditary cerebral hemorrhage with amyloidosis, Dutch typeJOURNAL OF NEUROSCIENCE RESEARCH, Issue 13 2007Kazuchika Nishitsuji Abstract Hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D), is an autosomal dominant disorder caused by the Dutch mutation (E693Q) in the ,-amyloid precursor protein. This mutation produces an aberrant amyloid , (A,) species (A,E22Q) and causes severe meningocortical vascular A, deposition. We analyzed the A, composition of the vascular amyloid in the brains of HCHWA-D patients. Immunohistochemistry demonstrated that the vascular amyloid contained both A,40 and A,42, with a high A,40/A,42 ratio. In Western blotting of cerebral microvessel fractions isolated from the brains, both wild-type and Dutch-type A,40 were observed as major species. Reverse-phase HPLC-mass spectrometric analysis of the fractions revealed both wild-type and Dutch-type A,38 as the other main components of the vascular amyloid. Moreover, we detected peaks corresponding to Dutch-type A,42 but not to wild-type A,42. These results suggest a pathogenic role for the mutant A,42 in addition to the mutant A,40 in the cerebral amyloid angiopathy of HCHWA-D. © 2007 Wiley-Liss, Inc. [source] Hereditary cerebral hemorrhage with amyloidosis-Dutch typeNEUROPATHOLOGY, Issue 4 2005Marion Maat-Schieman The amyloid ,-protein (A,) E22Q mutation of the rare disorder hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) causes severe cerebral amyloid angiopathy (CAA) with hemorrhagic strokes of mid-life onset and dementia. The mutation does not affect total A, production but may alter the A,1,42:A,1,40 ratio, and affect the proteolytic degradation of A, and its transport across the blood,brain barrier. A, E22Q aggregates faster into more stable amyloid-like fibrils than wild-type A,. Non-fibrillar A,(x-42) deposits precede the appearance of fibrils and the deposition of A,(x-40) in the vascular basement membrane. CAA severity tends to increase with age but may vary greatly among patients of comparable ages. Lumenal narrowing of affected blood vessels, leukoencephalopathy, CAA-associated vasculopathies, and perivascular astrocytosis, microgliosis, and neuritic degeneration complicate the development of HCHWA-D CAA. Parenchymal A, deposition is also enhanced in the HCHWA-D brain with non-fibrillar membrane-bound A,(x-42) deposits evolving into relatively fibrillar diffuse plaques variously associated with reactive astrocytes, activated microglia, and degenerating neurites. Plaque density tends ,to ,decrease ,with ,age. ,Neurofibrillary ,degeneration is absent or limited. HCHWA-D dementia is associated with CAA severity independently of Braak stage, age, and plaque density. Particularly, microaneurysms may contribute to the development of (small) hemorrhages/infarcts and the latter to cognitive decline in affected subjects. However, the relative importance of cerebral hemorrhages/infarcts, white matter damage and/or other CAA- or A,-related factors for cognitive deterioration in HCHWA-D remains to be determined. [source] Cerebral amyloid angiopathy: An overviewNEUROPATHOLOGY, Issue 1 2000Masahito Yamada Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels. Several cerebrovascular amyloid proteins (amyloid ,-protein (A,), cystatin C (ACys), prion protein (AScr), transthyretin (ATTR), gelsolin (AGel), and ABri (or A-WD)) have been identified, leading to the classification of several types of CAA. Sporadic CAA of A, type is commonly found in elderly individuals and patients with Alzheimer's disease. Cerebral amyloid angiopathy is an important cause of cerebrovascular disorders including lobar cerebral hemorrhage, leukoencephalopathy, and small cortical hemorrhage and infarction. We review the clinicopathological and molecular aspects of CAA and discuss the pathogenesis of CAA with future perspectives. [source] Familial amyloidotic polyneuropathy (ATTR Val30Met) with widespread cerebral amyloid angiopathy and lethal cerebral hemorrhagePATHOLOGY INTERNATIONAL, Issue 6 2001Naomi Sakashita We report an autopsy case of familial amyloidotic polyneuropathy (FAP) with cerebral hemorrhage. A 38-year-old woman with a typical FAP pedigree started developing severe diarrhea and sensori-motor polyneuropathy at the age of 28 years; autonomic nervous system, heart and renal dysfunction manifested themselves in the following years. Genetic analysis revealed a single amino acid substitution at codon 30 of transthyretin (ATTR Val30Met). Ten years after her initial symptoms, the patient died of a sudden convulsive attack and respiratory failure. Autopsy revealed lethal cerebral hemorrhages and uremic lungs. Histochemical and immunohistochemical analyses revealed TTR-derived amyloid protein in every tissue examined, particularly in glomeruli and peripheral vessels. Severe meningo-cerebrovascular amyloidosis was also detected. Because uremia causes oxidative damage to the vascular system and amyloid formation is closely associated with oxidative stress, it is possible that uremic endothelial damage facilitated an unusual cerebral amyloid deposition. In typical FAP (ATTR Val30Met), cerebral amyloid angiopathy does not usually have clinical manifestations. However, cerebral amyloid angiopathy should be considered to explain FAP symptoms when some risk factors such as uremic vascular damage are accompanying features. [source] Biopsy-Diagnosed Renal Disease in Patients After Transplantation of Other Organs and TissuesAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2010A. Schwarz Renal function deteriorates in about half of patients undergoing other transplants. We report the results of 105 renal biopsies from 101 nonrenal transplant recipients (bone marrow 14, liver 41, lung 30, heart 20). Biopsy indications were protracted acute renal failure (9%), creatinine increases (83%), heavy proteinuria (22%), or renal insufficiency before re-transplantation (9%). Histological findings other than nonspecific chronic changes, hypertension-related damage, and signs of chronic CNI toxicity included primary glomerular disease (17%), mostly after liver transplantation (21%) or after bone marrow transplantation (29%), and thrombotic microangiopathy (TMA) namely (10%). TMA had the most serious impact on the clinical course. Besides severe hypertension, one TMA patient died of cerebral hemorrhage, 5 had hemolytic-uremic syndrome, and 6 rapidly developed end-stage renal failure. TMA patients had the shortest kidney survival post-biopsy and, together with patients with acute tubular injury, the shortest kidney and patient survival since transplantation. Nine TMA patients had received CNI, 3 of them concomitantly received an mTOR-inhibitor. CNI toxicity is implicated in most patients with renal failure after transplant of other organs and may play a role in the development of TMA, the most serious complication. However, decreased renal function should not be routinely ascribed to CNI. [source] Central facial palsy revisited: A clinical-radiological study,ANNALS OF NEUROLOGY, Issue 3 2010Luigi Cattaneo MD We investigated the pattern of volitional facial motor deficits in acute stroke patients. We assessed the strength of single facial movements and correlated it to the site of infarct classified on computed tomography scans. Exclusion criteria were previous stroke, cerebral hemorrhage, and subcortical stroke. Results showed that weakness in eyelid closure was associated with anterior cerebral artery (ACA) stroke. Weakness in lip opening was associated with middle cerebral artery (MCA) stroke. We suggest that sparing of upper facial movements in MCA stroke is due to the presence of an upper face motor representation in both the MCA and ACA territories. ANN NEUROL 2010;68:404,408 [source] Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is independent of plaques and neurofibrillary tanglesANNALS OF NEUROLOGY, Issue 6 2001Remco Natté MD Cerebral amyloid angiopathy is frequently found in demented and nondemented elderly persons, but its contribution to the causation of dementia is unknown. Therefore, we investigated the relation between the amount of cerebral amyloid angiopathy and the presence of dementia in 19 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type. The advantage of studying hereditary cerebral hemorrhage in amyloidosis-Dutch type is that patients with this disease consistently have severe cerebral amyloid angiopathy with minimal neurofibrillary pathology. The amount of cerebral amyloid angiopathy, as quantified by computerized morphometry, was strongly associated with the presence of dementia independent of neurofibrillary pathology, plaque density, or age. The number of cortical amyloid ,-laden severely stenotic vessels, vessel-within-vessel configurations, and cerebral amyloid angiopathy-associated microvasculopathies was associated with the amount of cerebral amyloid angiopathy and dementia. A semiquantitative score, based on the number of amyloid ,-laden severely stenotic vessels, completely separated demented from nondemented patients. These results suggest that extensive (more than 15 amyloid ,-laden severely stenotic vessels in five frontal cortical sections) cerebral amyloid angiopathy alone is sufficient to cause dementia in hereditary cerebral hemorrhage with amyloidosis,Dutch type. This may have implications for clinicopathological correlations in Alzheimer's disease and other dementias with cerebral amyloid angiopathy. [source] Programmed cell death-10 enhances proliferation and protects malignant T cells from apoptosisAPMIS, Issue 10 2010BRITT LAUENBORG Lauenborg B, Kopp K, Krejsgaard T, Eriksen KW, Geisler C, Dabelsteen S, Gniadecki R, Zhang Q, Wasik MA, Woetmann A, Odum N. Programmed cell death-10 enhances proliferation and protects malignant T cells from apoptosis. APMIS 2010; 118: 719,28. The programmed cell death-10 (PDCD10; also known as cerebral cavernous malformation-3 or CCM3) gene encodes an evolutionarily conserved protein associated with cell apoptosis. Mutations in PDCD10 result in cerebral cavernous malformations, an important cause of cerebral hemorrhage. PDCD10 is associated with serine/threonine kinases and phosphatases and modulates the extracellular signal-regulated kinase pathway suggesting a role in the regulation of cellular growth. Here we provide evidence of a constitutive expression of PDCD10 in malignant T cells and cell lines from peripheral blood of cutaneous T-cell lymphoma (Sezary syndrome) patients. PDCD10 is associated with protein phosphatase-2A, a regulator of mitogenesis and apoptosis in malignant T cells. Inhibition of oncogenic signal pathways [Jak3, Notch1, and nuclear factor-,B (NF-,B)] partly inhibits the constitutive PDCD10 expression, whereas an activator of Jak3 and NF-,B, interleukin-2 (IL-2), enhances PDCD10 expression. Functional data show that PDCD10 depletion by small interfering RNA induces apoptosis and decreases proliferation of the sensitive cells. To our knowledge, these data provide the first functional link between PDCD10 and cancer. [source] Mortality in the catastrophic antiphospholipid syndrome: Causes of death and prognostic factors in a series of 250 patientsARTHRITIS & RHEUMATISM, Issue 8 2006Silvia Bucciarelli Objective To assess the main causes of death and the prognostic factors that influence mortality in patients with the catastrophic antiphospholipid syndrome (CAPS). Methods We analyzed the case reports of 250 patients included in the CAPS Registry up to February 2005. To identify prognostic factors for CAPS, we compared the main clinical and immunologic features and the types of treatment in the patients who died with those features in the patients who survived. Results Recovery occurred in 56% of the episodes of CAPS and death occurred in 44%. Cerebral involvement, consisting mainly of stroke, cerebral hemorrhage, and encephalopathy, was considered the main cause of death, being present in 27.2% of patients, followed by cardiac involvement (19.8%) and infection (19.8%). The only factor we identified that was prognostic of a higher mortality rate was the presence of systemic lupus erythematosus (SLE). A higher recovery rate was associated with combined treatment with anticoagulants (ACs) plus corticosteroids (CS) plus plasma exchange (PE) (77.8%), followed by ACs plus CS plus PE and/or intravenous immunoglobulins (69%). In contrast, concomitant treatment with cyclophosphamide did not demonstrate additional benefit. Conclusion Cerebral involvement (mainly consisting of stroke), cardiac involvement, and infections were considered the main causes of death in patients with CAPS. The presence of SLE was related to a higher mortality rate. According to the results of the present study, ACs plus CS plus PE should be the first line of therapy in patients with CAPS. [source] The Role of Cystatin C in Cerebral Amyloid Angiopathy and Stroke: Cell Biology and Animal ModelsBRAIN PATHOLOGY, Issue 1 2006Efrat Levy A variant of the cysteine protease inhibitor, cystatin c, forms amyloid deposited in the cerebral vasculature of patients with hereditary cerebral hemorrhage with amyloidosis, icelandic type (hchwa-i), leading to cerebral hemorrhages early in life. however, cystatin c is also implicated in neuronal degenerative diseases in which it does not form the amyloid protein, such as alzheimer disease (ad). accumulating data suggest involvement of cystatin c in the pathogenic processes leading to amyloid deposition in cerebral vasculature and most significantly to cerebral hemorrhage in patients with cerebral amyloid angiopathy (caa). This review focuses on cell culture and animal models used to study the role of cystatin c in these processes. [source] Untreated or uncontrolled cardiovascular risk factors are associated with an increased risk of cerebral hemorrhage during colder periodsACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010T. C. Turin No abstract is available for this article. [source] Familial amyloidotic polyneuropathy (ATTR Val30Met) with widespread cerebral amyloid angiopathy and lethal cerebral hemorrhagePATHOLOGY INTERNATIONAL, Issue 6 2001Naomi Sakashita We report an autopsy case of familial amyloidotic polyneuropathy (FAP) with cerebral hemorrhage. A 38-year-old woman with a typical FAP pedigree started developing severe diarrhea and sensori-motor polyneuropathy at the age of 28 years; autonomic nervous system, heart and renal dysfunction manifested themselves in the following years. Genetic analysis revealed a single amino acid substitution at codon 30 of transthyretin (ATTR Val30Met). Ten years after her initial symptoms, the patient died of a sudden convulsive attack and respiratory failure. Autopsy revealed lethal cerebral hemorrhages and uremic lungs. Histochemical and immunohistochemical analyses revealed TTR-derived amyloid protein in every tissue examined, particularly in glomeruli and peripheral vessels. Severe meningo-cerebrovascular amyloidosis was also detected. Because uremia causes oxidative damage to the vascular system and amyloid formation is closely associated with oxidative stress, it is possible that uremic endothelial damage facilitated an unusual cerebral amyloid deposition. In typical FAP (ATTR Val30Met), cerebral amyloid angiopathy does not usually have clinical manifestations. However, cerebral amyloid angiopathy should be considered to explain FAP symptoms when some risk factors such as uremic vascular damage are accompanying features. [source] | |||||||||||||||||||||||||