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Littérature scientifique sur le sujet « Intracerebral haemorrhage »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 25 janvier 2023

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Articles de revues sur le sujet "Intracerebral haemorrhage"

Svensson, Edith H., Kasim Abul-Kasim, Gunnar Engström et Martin Söderholm. « Risk factors for intracerebral haemorrhage – Results from a prospective population-based study ». European Stroke Journal 5, n^o 3 (12 juin 2020) : 278–85. http://dx.doi.org/10.1177/2396987320932069.

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Introduction While the relationship between hypertension and incident intracerebral haemorrhage is well established, other risk factors are less clear. This study examined risk factors for primary intracerebral haemorrhage, separately for lobar and non-lobar intracerebral haemorrhage. Patients and methods Incidence of intracerebral haemorrhage was studied among 28,416 individuals from the population-based Malmö Diet and Cancer cohort. Intracerebral haemorrhage cases were ascertained using the Swedish Hospital Discharge Register and the Stroke Register of Malmö, validated by review of hospital records and images, and classified by location by a neuroradiologist. Multivariable Cox regression was used. Results Three hundred and thirty-three intracerebral haemorrhages occurred, mean follow-up time was 18.4 years. Systolic blood pressure (hazard ratio per 10 mmHg 1.19 [95% confidence interval 1.13–1.26], diastolic blood pressure (hazard ratio 1.42 [1.27–1.59]), oral anticoagulants (hazard ratio 4.26 [2.17–8.38]), smoking (hazard ratio 1.45 [1.14–1.87]), living alone (hazard ratio 1.32 [1.04–1.69]) and low apolipoprotein B (hazard ratio per 10 mg/dL: 0.94 [0.90–0.99]) were significantly associated with incident intracerebral haemorrhage after multivariable adjustment. Systolic blood pressure, smoking and oral anticoagulants were associated with lobar intracerebral haemorrhage. Systolic blood pressure, diastolic blood pressure, living alone and diabetes were associated with non-lobar intracerebral haemorrhage. Diabetes and diastolic blood pressure showed significantly different relationships with lobar and non-lobar intracerebral haemorrhage. Alcohol, apolipoprotein A1, body mass index, waist circumference, physical activity and education were not independently associated with intracerebral haemorrhage. Discussion and conclusions: Blood pressure, smoking, low apolipoprotein B, oral anticoagulants and living alone were associated with intracerebral haemorrhage. Diabetes was associated with non-lobar intracerebral haemorrhage only. Further research is required on differences between lobar and non-lobar intracerebral haemorrhage.

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Grysiewicz, Rebbeca, et Philip B. Gorelick. « Update on Amyloid-associated Intracerebral Haemorrhage ». European Neurological Review 7, n^o 1 (2012) : 22. http://dx.doi.org/10.17925/enr.2012.07.01.22.

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Cerebral congophilic or amyloid angiopathy (CAA) is a clinicopathological entity that is considered a common cause of primary non-traumatic brain haemorrhage in the elderly. CAA is frequently associated with Alzheimer’s disease (AD) and has become a primary focus of scientific inquiry. The spectrum of intracerebral haemorrhage (ICH) that may occur in CAA includes: cerebral lobar haemorrhages, deep haemorrhages, purely subarachnoid and subdural haemorrhages and cerebral microbleeds. CAA is also associated with microinfarcts, leukoencephalopathy and superficial siderosis. This brief article will provide an update on the advances in our understanding of CAA-associated ICH with a focus on the following topics: neuropathology and mechanism of CAA-related haemorrhage; epidemiology, including genetic and other possible risk factors; clinical presentation; diagnosis, including newer imaging modalities; and prospects for prevention and treatment.

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MacKenzie, J. M. « Intracerebral haemorrhage. » Journal of Clinical Pathology 49, n^o 5 (1 mai 1996) : 360–64. http://dx.doi.org/10.1136/jcp.49.5.360.

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Sandercock, P. A. G. « Intracerebral haemorrhage ». Neuromuscular Disorders 6, n^o 1 (janvier 1996) : 83–84. http://dx.doi.org/10.1016/s0960-8966(96)90015-2.

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Allen, C. « Intracerebral Haemorrhage ». Journal of Neurology, Neurosurgery & ; Psychiatry 59, n^o 3 (1 septembre 1995) : 346. http://dx.doi.org/10.1136/jnnp.59.3.346-a.

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Qureshi, Adnan I., A. David Mendelow et Daniel F. Hanley. « Intracerebral haemorrhage ». Lancet 373, n^o 9675 (mai 2009) : 1632–44. http://dx.doi.org/10.1016/s0140-6736(09)60371-8.

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Caplan, L. R. « Intracerebral haemorrhage ». Lancet 339, n^o 8794 (mars 1992) : 656–58. http://dx.doi.org/10.1016/0140-6736(92)90804-c.

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Shrestha, Dinuj, Upama Sharma, Janam Shrestha, Gopi Nepal, Bishal Shrestha, Pranaya Shrestha, Samir Acharya et al. « Surgical Management among Patients with Spontaneous Supratentorial Intracerebral Haemorrhage Admitted in a Tertiary Care Centre : A Descriptive Cross-sectional Study ». Journal of Nepal Medical Association 60, n^o 252 (1 août 2022) : 697–701. http://dx.doi.org/10.31729/jnma.7178.

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Introduction: Spontaneous intracerebral haemorrhage is the second most common form of stroke and the most deadly one. An understanding of changing trends in the epidemiology of intracerebral haemorrhage prevalence, its risk factors, current practice in management, case fatality, and long-term outcome is essential to measure the effectiveness of stroke prevention and various treatment efforts. The objective of this study was to find out the prevalence of surgical management among patients with spontaneous supratentorial intracerebral haemorrhage in a tertiary centre. Methods: A descriptive cross-sectional study was conducted in the Department of Neurosurgery from January 2017 to December 2019. Ethical approval was obtained from the Institutional Review Committee (Reference number: 06/2020/IRC-ANIAS). A convenience sampling method was used. Data of the patients were retrieved from online medical records. Point estimate and 95% Confidence Interval were calculated. Results: Among 221 patients with spontaneous supratentorial intracerebral haemorrhage, 115 (52.04%) (45.45-58.63, 95% Confidence Interval) underwent surgical management. In-hospital mortality was seen in 23 (20%) and survivors at 3 months were 78 (67.82%) patients. Conclusions: The prevalence of surgical management among spontaneous supratentorial intracerebral haemorrhages was higher than in other studies done in a similar setting.

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Dickinson, C. J. « Intracerebral haemorrhage revisited ». QJM 100, n^o 11 (19 septembre 2007) : 715–19. http://dx.doi.org/10.1093/qjmed/hcm093.

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Mendelow, A. D. « Spontaneous intracerebral haemorrhage. » Journal of Neurology, Neurosurgery & ; Psychiatry 54, n^o 3 (1 mars 1991) : 193–95. http://dx.doi.org/10.1136/jnnp.54.3.193.

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Thèses sur le sujet "Intracerebral haemorrhage"

Samarasekera, Neshika Erangi. « Does lobar intracerebral haemorrhage differ from non-lobar intracerebral haemorrhage ? » Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15836.

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Spontaneous (non-traumatic) intracerebral haemorrhage accounts for ~10% of all strokes in Western populations. Investigations may identify intracerebral haemorrhage (ICH) as ‘secondary’ to underlying causes such as tumours or aneurysms, but ~80% of ICHs which have no apparent underlying cause (so-called ‘primary’ ICH) tend to be attributed to small vessel vasculopathies such as arteriolosclerosis or cerebral amyloid angiopathy (CAA), on the basis of an adult’s risk factors and clinical and radiographic features of the ICH. The commonly accepted hypothesis is that CAA contributes to lobar ICH and arteriolosclerosis causes non-lobar ICH. In the following thesis, I set out to explore whether (a) the baseline demographic, clinical features and apolipoprotein E genotype of adults with lobar and non-lobar ICH differ, (b) the prognosis of adults with lobar and non-lobar ICH differ and (c) the neuroimaging correlates of small vessel disease in adults with lobar and non-lobar ICH differ since this might provide clues to the vasculopathies underlying lobar and non-lobar ICH. I explored (d) the strength of the association between CAA and ICH by systematically reviewing neuropathological case control studies and (e) the radiological and pathological features of lobar ICH to examine the nature of CAA in persons with lobar ICH and whether any computed tomography (CT) features of ICH are associated with CAA-related lobar ICH. I set up a prospective, community-based inception cohort study of adults with ICH in South East Scotland. Adults with spontaneous primary definite ICH had the opportunity to consent to participate in the Lothian Study of IntraCerebral Haemorrhage, Pathology, Imaging and Neurological Outcome (LINCHPIN), an ethically-approved, prospective community-based research study examining the causes of ICH using apolipoprotein E genotyping, brain MRI and research autopsy in case of death. Of 128 adults with first-ever spontaneous primary definite ICH diagnosed during 2010- 2011, age and pre-morbid hypertension did not differ by ICH location but a history of dementia was more common in adults with lobar ICH. The proportion of adults with one or more non-lobar brain microbleed (BMB) was significantly higher in adults with non-lobar ICH but I did not find any other differences in the severity or distribution of other neuroimaging correlates of small vessel disease between lobar and non-lobar ICH. The apolipoprotein e4 allele was more common in participants with lobar ICH in comparison to those with non-lobar ICH but the frequency of the e2 allele did not differ by ICH location. Adults with lobar ICH were significantly more likely to survive one year after their ICH in comparison to those with non-lobar ICH after adjustment for other known predictors of outcome. From a systematic review of neuropathological case control studies of CAA and ICH, stratified by ICH location, I found a significant association between CAA and lobar ICH but not with ICH in other locations. I examined the radiological and pathological features of 33 adults with first-ever lobar ICH. The presence of CAA or vasculopathy and the severity of CAA in a lobe affected by ICH was concordant with that of the corresponding contralateral unaffected lobe. Capillary CAA was associated with severe CAA. Subarachnoid extension of the ICH tended to be more frequent in those with CAA-related strictly lobar ICH. Having explored the incidence, risk factors and prognosis of lobar and non-lobar ICH, in future work I would aim to establish the strength of the association between CAA and ICH in different brain locations in a neuropathological case control study. Future work should examine the radiopathological features of lobar ICH in a larger cohort and the coexistence of other small vessel diseases, in particular arteriolosclerosis in persons with ICH.

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Sobowale, Oluwaseun. « Intracerebral haemorrhage and inflammation ». Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/intracerebral-haemorrhage-and-inflammation(7139560f-bd3c-4ff0-b628-f86ffc6477d2).html.

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Intracerebral haemorrhage (ICH) is a significant healthcare concern worldwide. Following ICH, primary injury occurs due to physical injury to neurones and glia as a result of mass effect from the haematoma. Secondary mechanisms of injury include haematoma expansion, toxic effects of the products of coagulation and blood breakdown products and sterile inflammation. Perihaematomal oedema can exacerbate mass effect in the acute and sub-acute phase of ICH. At present, the pathophysiology behind the secondary mechanisms of injury following ICH is not fully understood and this has led to inability to translate new treatments from bench to bedside. Haematoma expansion is a significant contributor to neurological deterioration in the acute phase; however, understanding of the factors leading to a third of patients developing haematoma expansion is limited. This thesis presents the results of work aiming to develop a reproducible model of haematoma expansion in preclinical ICH. Using this model we found that a systemic inflammatory stimulus failed to induce haematoma expansion in spontaneously hypertensive rats or their healthy controls. We gained further insight into factors that may contribute to haematoma expansion in ICH by studying the proteomic profile of patients in clinical ICH. We demonstrate the feasibility of multi-modality brain imaging in sub-acute ICH, which we propose will be a useful tool to monitor neuro-inflammation in the acute stages if the disease. Finally, we investigated the association between peripheral markers of inflammation (white blood cell count and C-reactive protein) and perihaematomal oedema at baseline and clinical outcome (mortality at 30 days). Our findings suggest that acute inflammation may drive acute perihaematomal oedema and interestingly, we found a negative association between C-reactive protein at baseline and 30-day mortality. Our findings are significant in the field of clinical ICH, and suggest that the inflammatory response is important. We will take our findings forward in future work with the goal of understanding why haematoma expansion occurs, with the aim of developing a test to identify patients at highest risk and interventions to improve outcome after ICH.

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Krishnan, Kailash. « Outcomes after acute intracerebral haemorrhage ». Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/43228/.

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Primary Intracerebral haemorrhage is a severe form of stroke with poor prognosis attributed to haematoma characteristics. High blood pressure is present during the acute phase of intracerebral haemorrhage and associated with poor outcome in part through expansion of haematoma. Data from the ‘Efficacy of Nitric Oxide in Stroke trial’ (ENOS) was used to analyse the performance characteristics of qualitative and quantitative descriptors of intracerebral haematoma. The results showed that formal measurement of haemorrhage characteristics and visual estimates are reproducible. Intracerebral haemorrhage volumes measured using the modified ABC/2 formula were significantly lower compared to standard ABC/2 and computer assisted semi-automatic segmentation. In 629 patients with intracerebral haemorrhage presenting within 48 hours, the effect of blood pressure lowering with transdermal glyceryl trinitrate was assessed. Glyceryl trinitrate lowered blood pressure, was safe but did not improve functional outcome. In a small group of patients treated within 6 hours, glyceryl trinitrate improved functional outcome. Analysis of 246 patients with acute intracerebral haemorrhage from ENOS was undertaken to assess whether there were any differences in functional outcome among those who continued prior antihypertensive drugs during the immediate stroke period compared to those assigned to stop temporarily for 7 days. The results were neutral indicating that there was no benefit in those who continued treatment. Data of 1,011 patients with intracerebral haemorrhage in hyperacute trials from the VISTA collaboration showed differences in baseline characteristics and functional outcomes among patients from various ethnic backgrounds. A systematic review was updated to assess the effect of 26 randomised controlled trials that aimed to alter blood pressure within one week of acute stroke. The results showed that blood pressure reduction did not improve functional outcome irrespective of stroke type. When examined by time, treatment within 6 hours appeared to benefit but the number of patients were small and more studies are needed. The analysis also showed that continuing prestroke antihypertensive drugs in the immediate period after stroke did not benefit and might be harmful. In summary, this thesis provides new information on parameters used to estimate intracerebral haematoma, relationship between management of blood pressure and outcomes after haemorrhagic stroke. The work supports testing of whether very early blood pressure lowering after ictus is beneficial as is being undertaken in ongoing randomised controlled trials. Adjusting for ethnic differences may further identify patients in whom treatment may confer measurable advantage.

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Abid, Kamran. « Modulation of inflammation in intracerebral haemorrhage ». Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/modulation-of-inflammation-in-intracerebral-haemorrhage(1a1793e0-0013-4f6b-9e51-a5c15828a8a5).html.

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Intracerebral Haemorrhage (ICH) exhibits the worst mortality and morbidity of any stroke subtype. There are no efficacious treatments for this condition and little improvement in patient outcome has been noted despite advancements in medical science over the previous three decades. Furthermore, current available data is increasingly obsolete as the population suffering the disease burden rapidly ages and develops co-morbidities. It is thought that future therapies for this condition may be able to target neuroinflammatory response triggered by the formation of brain haemorrhage however there is little published evidence that has examined this aspect of ICH pathophysiology. This study therefore examines the current prognosis of a large cohort of patients with ICH to determine the key factors which result in mortality. We find that patients treated at a specialist centre have a surprising and significantly improved survival advantage. Since clinical practice in the United Kindgom is widely influential, the second part of the study focuses on whether the optimal cases are currently being transferred to these centres. The next part of the study then uses MRI/PET brain imaging for the first time in patients with ICH to establish an important link between the processes of neuroinflammation and Blood-Brain-Barrier breakdown. Finally, the concluding part of the thesis presents functional and radiological data from a rat model of ICH in which the inflammatory cascade has been modulated by the use of an antagonist against IL-1. The thesis thus presents a novel and important contribution in our present understanding of the preclinical and clinical disease process.

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Charidimou, A. « Applied clinical neuroimaging in cerebral amyloid angiopathy and spontaneous intracerebral haemorrhage ». Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1461023/.

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Sporadic cerebral amyloid angiopathy is a common small vessel disease that preferentially involves small cortical and leptomeningeal arteries due to progressive amyloid-β deposition in their walls. Cerebral amyloid angiopathy occurs frequently in elderly people, and is a common and important cause of symptomatic lobar intracerebral haemorrhage and cognitive impairment. There is currently a growing interest in cerebral amyloid angiopathy, at least partly thanks neuroimaging, which now allows an unprecedented ability to investigate the disease dynamics in vivo using MRI to reveal complex patterns of cerebral bleeding and ischaemia. The detection of CAA during life is becoming an increasingly important challenge, since approaches of prevention or treatment (disease-modification) are now emerging as realistic possibilities. Determining the most promising treatments requires development of reliable biomarkers, the goal of my research. The main objective of this PhD thesis is to provide new insights into potential clinical and applied clinical neuroimaging biomarkers in patients with cerebral amyloid angiopathy. This is accomplished by a portfolio of research studies investigating: (a) the clinical and radiological spectrum of transient focal neurological episodes as a potential clinical clue for cerebral amyloid angiopathy; (b) cortical superficial siderosis, a distinct pattern on bleeding in the brain, as both a diagnostic and a prognostic marker of cerebral amyloid angiopathy; (c) MRI-visible perivascular spaces topography, as a new marker of small vessel disease and cerebral amyloid angiopathy; (d) potential pathological, neuroimaging and genetic differences in patients with pathology-proven CAA with and without intracerebral haemorrhage and presents evidence for different disease phenotypes; (e) the evidence whether the presence and burden of cerebral microbleeds on MRI scans is associated with an increased risk of recurrent spontaneous ICH, and if this risk is different according to MRI-defined microangiopathy subtype, in a meta-analysis.

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Zarros, Apostolos. « Development and assessment of in vitro simulation approaches to intracerebral haemorrhage ». Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8119/.

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This current PhD Thesis in Neuropathology focuses on the development and assessment of in vitro simulation approaches to intracerebral haemorrhage. The PhD Thesis provides a clinical and experimental neuropathological overview of intracerebral haemorrhage as well as an account of the in vitro simulation approaches to the disease, before proceeding to the presentation of the experimental work designed and performed by the author. The development of the herein presented in vitro simulation approaches to intracerebral haemorrhage was based on the use of an immortalized embryonic murine hippocampal cell-line (mHippoE-14) and its response to oligomycin-A and ferrum or haemin under appropriately selected conditions (aiming to simulate the natural history of the disease in a more reliable manner). The PhD Thesis provides a characterization of the mHippoE-14 cell-line (through a real-time cellular response analysis and a cytomorphological characterization), before proceeding to the actual experimental justification of the conditions chosen for the development of the herein presented in vitro simulation approaches to intracerebral haemorrhage, and their assessment. The latter was performed through the undertaking of: (a) real-time cellular response analysis, (b) cytomorphological assessment, (c) profiling of neuronal markers’ expression, (d) neurochemical assessment, and (e) proteomic profiling. All experiments were performed at the University of Glasgow. The current PhD Thesis also provides a critical appraisal of: (a) the utility, novelty and limitations of the developed in vitro simulation approaches, and (b) the positioning of the developed in vitro simulation approaches within the neuropathopoietic context.

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Sun, Luanluan. « Major blood lipids and risk of ischaemic stroke and intracerebral haemorrhage in Chinese adults ». Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:ac3a2ece-6d63-4112-8b29-678e3b2cf78f.

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Background Stroke is the second most common cause of premature death worldwide, and the leading cause of death and disability in China. Stroke is a clinical syndrome that includes three distinct pathological types (i.e., ischaemic stroke [IS], intracerebral haemorrhage [ICH] and subarachnoid haemorrhage [SAH]) that have a different underlying pathophysiology. Previous observational studies and randomised trials have reported conflicting results on the associations of major blood lipids, including low-density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), and triglycerides with stroke pathological types. Moreover, the causal relevance of many of these associations is still not fully understood. Methods The China Kadoorie Biobank (CKB) prospective study collected questionnaire, physical measurement data, and blood samples on 512 891 adults from 10 diverse regions in China in 2004-2008. By 1st January 2016, over 32 000 incident IS, and 8000 ICH cases were recorded. A nested case-control study of stroke included 16 541 adults (5475 IS, 4776 ICH, and 6290 controls), with measurements of baseline plasma concentrations of LDL-C, HDL-C, and triglycerides, and genotyping of known lipid-related genetic variants. Repeat measurements of blood lipids were obtained in random samples of participants at resurveys (2008 and 2013-2014) to correct for regression dilution bias. The associations of major blood lipids with stroke pathological types were examined after adjustment for confounders and correction for regression dilution bias. The causal relevance of these associations was assessed by Mendelian randomisation (MR) using genetic risk scores (GRSs) involving lipid-related genetic variants identified in Western populations. Multivariable logistic and Cox regressions were used to yield odds ratios (ORs) and hazard ratios (HRs), respectively, relating major blood lipids or genetic variants with risks of stroke pathological types. Results Overall, the incidence rates of first IS and ICH were 761 and 187 cases per 100 000 person-years, respectively, with ~20% of the incident strokes attributable to ICH. The mean (SD) plasma concentrations of LDL-C, HDL-C, and triglycerides were 2.3 (0.8) mmol/L, 1.3 (0.3) mmol/L, and 1.6 (1.1) mmol/L, respectively. The regression dilution ratios at the mid-point of follow-up (around 3.7 years after baseline) were 0.68 for LDL-C, 0.72 for HDL-C, and 0.62 for triglycerides, respectively. Throughout the range of LDL-C examined (1.7-3.2 mmol/L), there was a positive log-linear association of usual LDL-C with risk of IS (HR 1.17; 95% CI 1.10-1.25 per 1 mmol/L higher LDL-C), and an inverse association with ICH (0.86; 0.80-0.92). Likewise, after adjusting for non-lipid vascular risk factors, usual plasma triglycerides were positively associated with risk of IS (1.02; 1.00-1.04 per 30% higher triglycerides), albeit weaker than for LDL-C, and were inversely associated with risk of ICH (0.94; 0.92-0.96), independent of LDL-C. HDL-C was inversely associated with risk of IS (0.93; 0.89-0.97 per 0.3 mmol/L higher HDL-C), but not with ICH. The proportional relevance of LDL-C, triglycerides, and HDL-C with IS differed significantly from those for ICH (p _{heterogeneity}: <0.00001, <0.00001, 0.0006, respectively). In the MR analyses, an externally weighted GRS of 8 known LDL-C related genetic variants was associated with plasma LDL-C (p=1.15x10^-272), but not associated with other lipid fractions or non-lipid major vascular risk factors. Each 1 mmol/L higher genetically-determined LDL-C was associated with an OR of 1.28 (1.05-1.56) for IS, similar to the risk estimates in both observational studies and randomised trials. There was no significant association of genetically-determined LDL-C with ICH (OR 1.04; 0.87-1.25), but the estimates did not differ significantly from those in the observational studies (p _{heterogeneity}=0.06), and randomised trials (p _{heterogeneity}=0.8). Neither genetically-determined HDL-C nor triglycerides were significantly associated with either IS or ICH. Conclusion The associations of major blood lipids with stroke differed qualitatively between pathological types. Lower LDL-C is causally associated with lower risk of IS, and probably, higher risk of ICH. Better genetic instruments are needed to assess the causal relevance, if any, of the observed associations of HDL-C, and of triglycerides for stroke pathological types presented in this thesis.

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Alkherayf, Fahad. « Restarting Oral Anticoagulant in Patients with Mechanical Heart Valve(s) and Intracranial Haemorrhage ». Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23577.

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Patients with mechanical heart valves who present with intracranial haemorrhage are initially treated by reversing their coagulopathy. However, these patients will ultimately require that their oral anticoagulant be restarted. The time at which oral anticoagulants are restarted is critical since restarting too early may increase the risk of recurrent bleeding, while withholding anticoagulants increases the patient’s risk of thromboembolic events. The ideal time to restart patients on their oral anticoagulant medication is defined as the time at which all these risks are minimized. This thesis includes a systematic review and meta-analysis of the literature. The main outcomes were recurrent haematoma, valve thrombosis, stroke and peripheral emboli. Results were stratified by types of intracranial haemorrhage. We also conducted a survey to gain insight into current practices of neurosurgeons and thrombosis experts in Canada and USA when they are faced with deciding on anticoagulant restart times in patients with ICH. Results were stratified by type of intracranial bleed and participants’ characteristics and demographics. The systematic review identified that the ideal time for restarting anticoagulant therapy in patients following an ICH is unknown. Meta-analysis was limited by the heterogeneity of the studies. The survey results indicated that physicians had a wide range of practice and that their practice was dependent on the patient’s clinical features, but many physicians would restart oral anticoagulants between 4 and 14 days after the haemorrhage. For this reason we have proposed a multi centre cohort study to investigate the safety and efficacy of restarting patients on anticoagulation therapy between day 5 and 9 post haemorrhage. A full study protocol is presented in this thesis.

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Rannikmäe, Kristiina. « Genetic associations with sporadic cerebral small vessel disease ». Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/23585.

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Background: Cerebral small vessel disease (SVD) causes substantial cognitive, psychiatric and physical disabilities. Despite its common nature, SVD pathogenesis and molecular mechanisms remain poorly understood, and prevention and treatment are probably suboptimal. Identifying the genetic determinants of SVD will improve understanding and may help identify novel treatment targets. The aim of this thesis is to better understand genetic associations with SVD through investigating its pathological, radiological and clinical phenotypes. Methods: To unravel the genetic associations with SVD, I used three complementary approaches. First, I performed a systematic review looking at existing intracerebral haemorrhage (ICH) classification systems and their reliability, to help inform future studies of ICH genetics. Second, I performed a series of systematic reviews and meta-analyses, investigating associations between genetic polymorphisms and histopathologically confirmed cerebral amyloid angiopathy (CAA). Third, I performed meta-analyses of existing genome-wide datasets to determine associations of >1000 common single nucleotide polymorphisms (SNP) in the COL4A1/COL4A2 genomic region with clinico-radiological SVD phenotypes: ICH and its subtypes, ischaemic stroke and its subtypes, and white matter hyperintensities. Results: The reliability of existing ICH classification systems appeared excellent in eight studies conducted in specialist centres with experienced raters, although these existing systems have several limitations. In my systematic evaluation of CAA genetics, meta-analyses of 24 studies including 3520 participants showed robust evidence for a dose-dependent association between APOE ɛ4 and histopathological CAA. There was, however, no convincing association between APOE ɛ2 and presence of CAA in a meta-analysis of 11 studies including 1640 participants. Meta-analyses of five studies including 497 participants showed, contrary to an existing popular hypothesis, that while APOE 4 may increase the risk of developing severe CAA vasculopathy, there is no clear evidence to support a role of ɛ2. There were few data about the role of APOE in hereditary CAA, but in the three studies that had looked at this, there was no evidence for an association between APOE ɛ4 and CAA severity. There were too few studies and participants to draw firm conclusions about the effect of non-APOE ε2/ε3/ε4 genetic polymorphisms on CAA, but there were positive associations with TGF-β1, TOMM40 and CR1 genes in four studies. Finally, in my meta-analyses of the COL4A1/COL4A2 genomic region, three intronic SNPs in COL4A2 were associated with SVD phenotypes: significantly with deep ICH, and suggestively with lacunar ischaemic stroke and WMH. Conclusions: I have shown that while existing ICH classification systems appear to have very good reliability, further research is needed to determine their performance in different settings. For large population-based prospective studies of ICH genetics, anatomical systems are likely to be more feasible, scalable and appropriate, although they have limitations and will need to be further developed. Using systematic reviews and meta-analyses, I have confirmed a dose-related association between APOE ɛ4 and histopathological CAA, but also demonstrated that, despite popular acceptance, there is insufficient data to draw firm conclusions about the association with APOE ɛ2. I found some positive associations with CAA in other genes, which merit replication in further larger studies, and showed that there is currently insufficient data about the role of APOE in hereditary CAA. Finally, I identified a novel association between a locus in a known hereditary SVD gene – COL4A2 – and sporadic SVD. This highlights a new and successful approach for selecting candidate genes and can be expanded in future studies to include other known hereditary SVD genes.

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Fernandes, Helen M. « Primary intracerebral haemorrhage : a study of its effects upon intracranial haemodynamics, current clinical practice and a trial of early surgery ». Thesis, University of Newcastle upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247837.

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Livres sur le sujet "Intracerebral haemorrhage"

Markus, Hugh, Anthony Pereira et Geoffrey Cloud. Cerebral haemorrhage. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0013.

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This chapter covers the several types of cerebral haemorrhage: extradural, subdural, subarachnoid, and intracerebral. Subarachnoid haemorrhage (SAH) is an important cause of neurological disability and mortality, although only occasionally present with focal stroke symptoms. Intracerebral haemorrhage usually presents with a stroke, which can only be reliably distinguished from ischaemic stroke by brain imaging. The chapter discusses the diagnosis, investigation, and management of both SAH and intracerebral haemorrhage.

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Delcourt, Candice, et Craig Anderson. Management of parenchymal haemorrhage. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0237.

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Parenchymal intracerebral haemorrhage (ICH) affects several million people in the world each year, most of whom reside in developing countries. ICH accounts for 10-40% of strokes and is the least treatable form of stroke with a 30-day mortality of 30-55%, with half of these deaths occurring within the first few days of onset. . High blood pressure is both a causal and prognostic factor for ICH, with early control of hypertension being the only medical treatment which may improve recovery and the level of residual functioning. The role of surgery remains controversial. Management is largely supportive and aimed at reducing further brain injury and preventing complications.

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Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson et David Ledingham. Cerebrovascular disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0004.

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This chapter on cerebrovascular disease discusses the evidence-based management of acute stroke, transient ischaemic attacks (TIAs), and secondary stroke prevention (antiplatelet therapy, risk factor modification, atrial fibrillation (AF), carotid and vertebral artery dissection, and symptomatic carotid artery disease). Drug treatment of intracerebral haemorrhage, subarachnoid haemorrhage, and cerebral venous sinus thrombosis are also discussed.

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Carton, James. Neuropathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0018.

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This chapter discusses neuropathology, including nervous system malformations, epilepsy, head injury, cerebral infarction, intracerebral haemorrhage, subarachnoid haemorrhage, meningitis, cerebral infections, multiple sclerosis, Guillain–Barré syndrome, myasthenia gravis, Alzheimer’s disease, vascular dementia, dementia with Lewy bodies, Parkinson’s disease, Huntington’s disease, motor neurone disease, Creutzfeldt–Jacob disease, astrocytomas (including glioblastoma), oligodendroglioma, ependymoma, meningioma, medulloblastoma, primary CNS lymphomas, and cerebral metastases.

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Griffiths, James, et Kate Drummond. Neurological disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0045.

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This chapter predominantly focuses on the provision of obstetric anaesthesia and analgesia for the parturient with neurological disease. Diseases of the central nervous system are an important cause of maternal morbidity and mortality. Maternal deaths may occur from such conditions as subarachnoid haemorrhage, intracerebral haemorrhage, thrombosis, and epilepsy. Neurological disease may impact on maternal well-being during pregnancy and pregnancy has the potential to exacerbate many neurological diseases. Many neurological conditions also have important implications for the safe conduct of neuraxial anaesthesia and analgesia, such as spina bifida and hydrocephalus. Management of these conditions may require care to be coordinated by a multidisciplinary team including the obstetrician, neurologist, neurosurgeon, and anaesthetist.

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McDonald, Vickie, et Marie Scully. Anticoagulants and antithrombotics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0051.

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Coagulation is best thought of using the cell-based model of coagulation. Patients commenced on heparin therapy should have their platelet count monitored early because of the risk of heparin-induced thrombocytopenia, which can occur on any type or dose of heparin. Emergency reversal of warfarin should be with prothrombin complex concentrate (containing factors II, VII, IX, and X) and not fresh frozen plasma. New oral anticoagulants have the advantage of predictable pharmacokinetics and do not require routine monitoring, but optimal reversal strategies for these agents are not clear. Thrombolytic agents lead to variable degrees of systemic lysis, which may cause haemorrhage, including intracerebral haemorrhage

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Stocchetti, Nino, et Andrew I. R. Maas. Causes and management of intracranial hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0233.

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Intracranial hypertension may damage the brain in two ways—it causes tissue distortion and herniation, and reduces cerebral perfusion. The many different pathologies that can result in intracranial hypertension include subarachnoid haemorrhage, spontaneous intra-parenchymal haemorrhage, malignant cerebral hemispheric infarction, and acute hydrocephalus. The pathophysiology and specific treatment of intracranial hypertension may be different and depend on aetiology. In patients with subarachnoid haemorrhage a specific focus is on treating secondary hydrocephalus and maintaining adequate cerebral perfusion pressure (CPP). Indications for surgery in patients with intracranial hypertension due to intracerebral haemorrhage (ICH) are not only related to the mass effect, but also to remove the toxic effect of extravasated blood on brain tissue. Decompressive surgery should be considered for patients with a malignant hemispheric infarction, but in order to benefit the patient this surgery should be performed within 48 hours of the onset of the stroke. Hydrocephalus may result from obstruction of cerebrospinal fluid (CSF) flow, from impaired CSF re-absorption and occasionally from overproduction of CSF. Emergency management of acute hydrocephalus can be accomplished by external ventricular drainage of CSF. More definitive treatment may be either by third ventriculostomy or implantation of a CSF shunt diverting CSF to the abdominal cavity (a ventriculoperitoneal shunt) or to the right atrium of the heart (ventriculo-atrial shunt).

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Naidech, Andrew M., dir. Neurocritical Care. Cambridge University Press, 2022. http://dx.doi.org/10.1017/9781108907682.

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Events in a neurological intensive care unit are not always predictable and patients can often be unstable. This practical manual is a clear and concise guide for recognising and managing neurological emergencies. Each chapter covers a crucial topic in neurocritical care, from understanding the pathophysiology of various neurological diseases, to neuroradiology used in diagnosis, and best practice for difficult decision making in the ICU. A variety of conditions are described such as haemorrhage (intracerebral, subdural, and subarachnoid), seizures, trauma and temperature dysregulation. An international team of experts have contributed chapters, providing a breadth of experience and knowledge for readers. This is an invaluable guide for clinicians on the front line of caring for patients with neurological emergencies who need life-saving answers quickly.

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Forsyth, Rob, et Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.

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This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life; non-epileptic paroxysmal phenomena; functional illness, illness behaviour; headache; hydrocephalus; spina bifida and related disorders; idiopathic intracranial hypertension; infection of the CNS; congenital infection; mitochondrial disease; movement disorders; neuromuscular disease which covers neuropathy, anterior horn cell disease, and myasthenic syndromes; neurocutaneous syndromes; neurodegenerative conditions; late presentations of metabolic disease; neurotransmitter disorders; sleep disorders; stroke and intracerebral haemorrhage; tumours of the CNS; and vitamin-responsive disorders.

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Munshi, Sunil K., et Rowan Harwood, dir. Stroke in the Older Person. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198747499.001.0001.

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Stroke in the Older Person will inform the readers about every aspect of stroke disease and traverses the entire stroke pathway. It explores all aspects of stroke and in particular those singular features of stroke that afflict older people. Nearly three-quarters of all strokes occur in people over the age of sixty-five. Each chapter is a synthesis of up-to-date work and practical approaches, relevant to stroke physicians, geriatricians, neurologists, researchers, doctors of all grades, physiotherapists, occupational therapists, speech and language therapists, advanced nurse practitioners, and neuropsychologists. The important themes addressed are the patient’s perspective, epidemiology, aetiopathogenesis, clinical presentations, diagnostic work-up including imaging, primary and secondary prevention, thrombolysis, mechanical thrombectomy, and all aspects of rehabilitation. It addresses transient ischaemic attack (TIA), atrial fibrillation, intracerebral haemorrhage, carotid revascularization, nutrition, and stroke mimics, dysphagia, the burden of cerebrovascular disease in the community, cognitive impairment, ethical and moral dilemmas including do not attempt resuscitation (DNAR), advanced directives, and end-of-life care. Stroke predominantly affects older people but there is a great shortage of literature in this age group. The editors have put together an excellent collection of chapters written by frontline clinicians or well-known academicians in their field. Special attention has been paid to make the book very readable, with plenty of practical tips. Only through a greater awareness of every aspect of stroke in older people can we make progress and treat our older people with the excellent care and dignity that they deserve.

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Chapitres de livres sur le sujet "Intracerebral haemorrhage"

Bhatia, Rohit, N. Shobha, Pablo Garcia Bermejo et Dar Dowlatshahi. « Intracerebral Haemorrhage ». Dans Emergencies in Neurology, 239–62. Singapore : Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-5866-1_12.

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Best, Jonathan G., et David J. Werring. « Intracerebral Haemorrhage ». Dans Precision Medicine in Stroke, 127–59. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70761-3_7.

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Davies, Eryl. « Intracerebral Haemorrhage ». Dans The Final FFICM Structured Oral Examination Study Guide, 275–78. Boca Raton : CRC Press, 2022. http://dx.doi.org/10.1201/9781003243694-93.

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Ganesh, Aravind, et Michael D. Hill. « Special Systems of Care Considerations in Intracerebral Haemorrhage ». Dans Intracerebral Hemorrhage Therapeutics, 139–59. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77063-5_10.

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Gill, Sumanjit K., et David J. Werring. « Intracerebral Haemorrhage and Oral Anticoagulants ». Dans Stroke Medicine, 249–53. London : Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6705-1_39.

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Mendelow, A. D. « Surgical Trial in Intracerebral Haemorrhage (S.T.I.C.H) ». Dans Brain Edema XI, 521–22. Vienna : Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_109.

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Mendelow, A. D. « The international surgical trial in intracerebral haemorrhage (ISTICH) ». Dans Brain Edema XII, 441–43. Vienna : Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_90.

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Gasecki, Dariusz, Bartosz Karaszewski et Krzysztof Narkiewicz. « Management of High Blood Pressure in Intracerebral Haemorrhage ». Dans Updates in Hypertension and Cardiovascular Protection, 159–71. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32074-8_12.

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Wallenfang, Th, G. Fries, J. P. Jantzen, J. Bayer et F. Trautmann. « Pathomechanism of Brain Oedema in Experimental Intracerebral Mass Haemorrhage ». Dans Proceedings of the 8th European Congress of Neurosurgery, Barcelona, September 6–11, 1987, 182–85. Vienna : Springer Vienna, 1988. http://dx.doi.org/10.1007/978-3-7091-8978-8_39.

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Mendelow, A. D., R. Bullock, F. P. Nath, A. Jenkins, T. Kingman et G. M. Teasdale. « Experimental Intracerebral Haemorrhage : Intracranial Pressure Changes and Cerebral Blood Flow ». Dans Intracranial Pressure VI, 515–20. Berlin, Heidelberg : Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70971-5_97.

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Actes de conférences sur le sujet "Intracerebral haemorrhage"

Yang, Jinge, Dan Wu, Guang Zhang et Huabei Jiang. « Cross-sectional photoacoustic tomography of intracerebral haemorrhage in mice ». Dans International Conference on Photonics and Imaging in Biology and Medicine. Washington, D.C. : OSA, 2017. http://dx.doi.org/10.1364/pibm.2017.w3a.34.

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Shanbhag, S. S., G. R. Udupi, K. M. Patil et K. Ranganath. « Analysis of brain MRI images of intracerebral haemorrhage using frequency domain technique ». Dans 2011 IEEE International Conference on Image Information Processing (ICIIP). IEEE, 2011. http://dx.doi.org/10.1109/iciip.2011.6108887.

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Lee, Suk-Jun, et Seung-Man Yu. « Exercise Treatment Effect : The Brain Metabolite Change of Magnetic Resonance Spectroscopy in Intracerebral Haemorrhage Rat Model ». Dans The 2nd World Congress on New Technologies. Avestia Publishing, 2016. http://dx.doi.org/10.11159/icbb16.110.

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Ivany, Elena, Robyn R. Lotto, Gregory Lip et Deirdre A. Lane. « 77 Preventing stroke in patients with atrial fibrillation and intracerebral haemorrhage : a qualitative study of physicians’ decision-making ». Dans British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.77.

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Yang, Ye, Shanxiong Chen, Duo Tan, Rui Yao, Shiyu Zhu, Yuanyuan Jia, Wensong Yang et Yiqing Shen. « Fusion Branch Network with Class Learning Difficulty Loss Function for Recongnizition of Haematoma Expansion Signs in Intracerebral Haemorrhage ». Dans 2021 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2021. http://dx.doi.org/10.1109/bibm52615.2021.9669423.

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Aponte-Becerra, Laura, Rodrigo Quispe, Laura Mendez-Pino, Vera Novak, Magdy Selim et Vasileios-Arsenios Lioutas. « Continuous glucose monitoring in acute stroke ». Dans the 8th International Workshop on Innovative Simulation for Healthcare. CAL-TEK srl, 2019. http://dx.doi.org/10.46354/i3m.2019.iwish.016.

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"Hyperglycaemia upon admission is a pathophysiological response to acute brain ischemia that has been independently associated with high mortality rate and poor prognosis. Glycaemic variability (GV) has also shown association with poor clinical outcomes among stroke patients. GV is best assessed by continuous glucose monitoring (CGM), which enables consecutives glucose measurements every 5 minutes. This pilot study aimed: 1) To describe safety, feasibility and tolerability of CGM in the acute stroke setting; and 2) To compare CGM and conventional FS glucose-based monitoring regimen in terms of their relationship with GUA and the accuracy of hypoglycaemic episodes detection. Safety, feasibility and tolerability of CGM was excellent in our cohort of 23 patients with acute stroke (61% ischemic and 39% intracerebral haemorrhage) and there were no adverse events. CGM recorded ten hypoglycaemic episodes that were not detected by conventional FS monitoring. GUA was associated with coefficient of variation (CV) of CGM (p=0.03), CV of FS (p=0.01), standard deviation (SD) of CGM (p-value=0.01) and mean amplitude of glucose excursions (MAGE) (pvalue= 0.001)."

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