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Journal articles on the topic 'Intracerebral haemorrhage'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2023

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1

Svensson, Edith H., Kasim Abul-Kasim, Gunnar Engström, and Martin Söderholm. "Risk factors for intracerebral haemorrhage – Results from a prospective population-based study." European Stroke Journal 5, no. 3 (June 12, 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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2

Grysiewicz, Rebbeca, and Philip B. Gorelick. "Update on Amyloid-associated Intracerebral Haemorrhage." European Neurological Review 7, no. 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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3

MacKenzie, J. M. "Intracerebral haemorrhage." Journal of Clinical Pathology 49, no. 5 (May 1, 1996): 360–64. http://dx.doi.org/10.1136/jcp.49.5.360.

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4

Sandercock, P. A. G. "Intracerebral haemorrhage." Neuromuscular Disorders 6, no. 1 (January 1996): 83–84. http://dx.doi.org/10.1016/s0960-8966(96)90015-2.

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5

Allen, C. "Intracerebral Haemorrhage." Journal of Neurology, Neurosurgery & Psychiatry 59, no. 3 (September 1, 1995): 346. http://dx.doi.org/10.1136/jnnp.59.3.346-a.

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6

Qureshi, Adnan I., A. David Mendelow, and Daniel F. Hanley. "Intracerebral haemorrhage." Lancet 373, no. 9675 (May 2009): 1632–44. http://dx.doi.org/10.1016/s0140-6736(09)60371-8.

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7

Caplan, L. R. "Intracerebral haemorrhage." Lancet 339, no. 8794 (March 1992): 656–58. http://dx.doi.org/10.1016/0140-6736(92)90804-c.

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8

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, no. 252 (August 1, 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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9

Dickinson, C. J. "Intracerebral haemorrhage revisited." QJM 100, no. 11 (September 19, 2007): 715–19. http://dx.doi.org/10.1093/qjmed/hcm093.

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10

Mendelow, A. D. "Spontaneous intracerebral haemorrhage." Journal of Neurology, Neurosurgery & Psychiatry 54, no. 3 (March 1, 1991): 193–95. http://dx.doi.org/10.1136/jnnp.54.3.193.

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11

Shakir, R. A. "Spontaneous intracerebral haemorrhage." Journal of Neurology, Neurosurgery & Psychiatry 55, no. 1 (January 1, 1992): 84. http://dx.doi.org/10.1136/jnnp.55.1.84-a.

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12

Wilson, D., M. E. Adams, F. Robertson, M. Murphy, and D. J. Werring. "Investigating intracerebral haemorrhage." BMJ 350, may20 10 (May 20, 2015): h2484. http://dx.doi.org/10.1136/bmj.h2484.

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13

Salman, R. A. S., D. L. Labovitz, and C. Stapf. "Spontaneous intracerebral haemorrhage." BMJ 339, jul24 1 (July 24, 2009): b2586. http://dx.doi.org/10.1136/bmj.b2586.

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14

Lorman-Carbó, Blanca, Josep Lluis Clua-Espuny, Eulalia Muria-Subirats, Juan Ballesta-Ors, Maria Antònia González-Henares, Meritxell Pallejà-Millán, and Francisco M. Martín-Luján. "Adjusted Morbidity Groups and Intracerebral Haemorrhage: A Retrospective Primary Care Cohort Study." International Journal of Environmental Research and Public Health 18, no. 24 (December 17, 2021): 13320. http://dx.doi.org/10.3390/ijerph182413320.

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Background: Intracerebral haemorrhage rates are increasing among highly complex, elderly patients. The main objective of this study was to identify modifiable risk factors of intracerebral haemorrhage. Methods: Multicentre, retrospective, community-based cohort study was conducted, including patients in the Adjusted Morbidity Group 4 with no history of intracerebral haemorrhage. Cases were obtained from electronic clinical records of the Catalan Institute of Health and were followed up for five years. The primary outcome was the occurrence of intracerebral haemorrhage during the study period. Demographic, clinical and pharmacological variables were included. Logistic regression analyses were carried out to detect prognostic variables for intracerebral haemorrhage. Results: 4686 subjects were included; 170 (3.6%) suffered an intracerebral haemorrhage (85.8/10,000 person–year [95% CI 85.4 to 86.2]). The HAS-BLED score for intracerebral haemorrhage risk detection obtained the best AUC (0.7) when used in the highest complexity level (cut-off point ≥3). Associated independent risk factors were age ≥80 years, high complexity and use of antiplatelet agents. Conclusions: The Adjusted Morbidity Group 4 is associated with a high risk of intracerebral haemorrhage, particularly for highly complex patients and the use of antiplatelet agents. The risk of bleeding in these patients must be closely monitored.

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15

Larsen, Kristin Tveitan, Elisabeth Forfang, Johanna Pennlert, Eva-Lotta Glader, Christina Kruuse, Per Wester, Hege Ihle-Hansen, et al. "STudy of Antithrombotic Treatment after IntraCerebral Haemorrhage: Protocol for a randomised controlled trial." European Stroke Journal 5, no. 4 (September 3, 2020): 414–22. http://dx.doi.org/10.1177/2396987320954671.

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Background and aims Many patients with prior intracerebral haemorrhage have indications for antithrombotic treatment with antiplatelet or anticoagulant drugs for prevention of ischaemic events, but it is uncertain whether such treatment is beneficial after intracerebral haemorrhage. STudy of Antithrombotic Treatment after IntraCerebral Haemorrhage will assess (i) the effects of long-term antithrombotic treatment on the risk of recurrent intracerebral haemorrhage and occlusive vascular events after intracerebral haemorrhage and (ii) whether imaging findings, like cerebral microbleeds, modify these effects. Methods STudy of Antithrombotic Treatment after IntraCerebral Haemorrhage is a multicentre, randomised controlled, open trial of starting versus avoiding antithrombotic treatment after non-traumatic intracerebral haemorrhage, in patients with an indication for antithrombotic treatment. Participants with vascular disease as an indication for antiplatelet treatment are randomly allocated to antiplatelet treatment or no antithrombotic treatment. Participants with atrial fibrillation as an indication for anticoagulant treatment are randomly allocated to anticoagulant treatment or no anticoagulant treatment. Cerebral CT or MRI is performed before randomisation. Duration of follow-up is at least two years. The primary outcome is recurrent intracerebral haemorrhage. Secondary outcomes include occlusive vascular events and death. Assessment of clinical outcomes is performed blinded to treatment allocation. Target recruitment is 500 participants. Trial status: Recruitment to STudy of Antithrombotic Treatment after IntraCerebral Haemorrhage is on-going. On 30 April 2020, 44 participants had been enrolled in 31 participating hospitals. An individual patient–data meta-analysis is planned with similar randomised trials.

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Seyfried, D. M., Y. Han, D. Yang, J. Ding, and M. Chopp. "Erythropoietin Promotes Neurological Recovery after Intracerebral Haemorrhage in Rats." International Journal of Stroke 4, no. 4 (August 2009): 250–56. http://dx.doi.org/10.1111/j.1747-4949.2009.00292.x.

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Background Attention has turned to neurorestorative therapies, including erythropoietin, for experimental ischaemic stroke and head injury. Treatments for intracerebral haemorrhage need to be developed, as this represents a particularly devastating and common form of neurological injury. Aim The aim of this study is to investigate the therapeutic potential of erythropoietin after intracerebral haemorrhage in rats and to measure its effects on mechanisms of recovery and neurogenesis. Methods Intracerebral haemorrhage was induced in 24 Wistar male rats by intrastriatal infusion of autologous blood. Recombinant human erythropoietin (5000 or 10000 U/kg BW/day) or saline was administered starting 1 day after intracerebral haemorrhage and continued daily for 1 week ( n = 8 for each group). To label proliferating cells, 5‘-bromo-2’ deoxyuridine was injected daily for 13 days after intracerebral haemorrhage. All animals survived for 2 weeks after intracerebral haemorrhage. Functional outcome, area of tissue loss and immunohistochemical staining were measured at 14 days after intracerebral haemorrhage. Global test or anova was used to test the erythropoietin dose effect. Results Rats receiving recombinant human erythropoietin after intracerebral haemorrhage exhibited significant improvement in modified neurological severity score and corner test at 14 days ( P<0·05). Increased expression of phenotypes of synaptogenesis and proliferating immature neurons were shown by immunohistochemical staining. Only the group receiving a lower dose of recombinant human erythropoietin had significantly less tissue loss compared with the control group ( P<0·05). In rats treated with recombinant human erythropoietin, double staining for 5‘-bromo-2’ deoxyuridine and TUJ1 revealed a subpopulation of cells that express an immature neuronal marker while still dividing. Conclusions Erythropoietin improves neurological outcome and increases histochemical parameters of neurogenesis when given after intracerebral haemorrhage in rats. Intriguingly, only the lower dose of recombinant human erythropoietin was effective in reducing tissue loss in the region of intracerebral haemorrhage.

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17

Ramsay, D. A., J. L. Penswick, and D. M. Robertson. "Fatal Streptokinase-Induced Intracerebral Haemorrhage in Cerebral Amyloid Angiopathy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 3 (August 1990): 336–41. http://dx.doi.org/10.1017/s0317167100030705.

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ABSTRACT:A fatal intracerebral haemorrhage (ICH) associated with streptokinase (SK) treatment of an acute myocardial infarction is described. Autopsy examination showed a lobar ICH and severe cerebral amyloid angiopathy (CAA). The close temporal relationship between SK administration and intracranial haemorrhage, the absence of pretreatment risk factors for ICH, and the presence of CAA suggests that these are related phenomena. Accordingly: 1. There may be a synergistic relationship between CAA and intracranial haemorrhage induced by fibrinolytic agents; 2. Thrombolytic agents may induce more frequent than expected intracranial haemorrhage in conditions associated with a high incidence of CAA, notably old age and Alzheimer's disease; 3. A regional defect in haemostasis other than vessel fragility may contribute to the intracranial haemorrhagic predisposition of CAA; 4. Autopsy examination of cases of ICH is an essential part of the audit of clinical trials of fibrinolytic agents.

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Bai, Qian, Mengzhou Xue, and V. Wee Yong. "Microglia and macrophage phenotypes in intracerebral haemorrhage injury: therapeutic opportunities." Brain 143, no. 5 (January 9, 2020): 1297–314. http://dx.doi.org/10.1093/brain/awz393.

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Abstract The prognosis of intracerebral haemorrhage continues to be devastating despite much research into this condition. A prominent feature of intracerebral haemorrhage is neuroinflammation, particularly the excessive representation of pro-inflammatory CNS-intrinsic microglia and monocyte-derived macrophages that infiltrate from the circulation. The pro-inflammatory microglia/macrophages produce injury-enhancing factors, including inflammatory cytokines, matrix metalloproteinases and reactive oxygen species. Conversely, the regulatory microglia/macrophages with potential reparative and anti-inflammatory roles are outcompeted in the early stages after intracerebral haemorrhage, and their beneficial roles appear to be overwhelmed by pro-inflammatory microglia/macrophages. In this review, we describe the activation of microglia/macrophages following intracerebral haemorrhage in animal models and clinical subjects, and consider their multiple mechanisms of cellular injury after haemorrhage. We review strategies and medications aimed at suppressing the pro-inflammatory activities of microglia/macrophages, and those directed at elevating the regulatory properties of these myeloid cells after intracerebral haemorrhage. We consider the translational potential of these medications from preclinical models to clinical use after intracerebral haemorrhage injury, and suggest that several approaches still lack the experimental support necessary for use in humans. Nonetheless, the preclinical data support the use of deactivator or inhibitor of pro-inflammatory microglia/macrophages, whilst enhancing the regulatory phenotype, as part of the therapeutic approach to improve the prognosis of intracerebral haemorrhage.

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19

Patrick Mitchell, Dipayan Mitra, Barbara A. Gregson, and A. David Mendelow. "Prevention of Intracerebral Haemorrhage." Current Drug Targets 8, no. 7 (July 1, 2007): 832–38. http://dx.doi.org/10.2174/138945007781077328.

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Kamboj, Ankita, Dr Paramjit Singh, and Dr Jagdish Kaur. "Antioxidants and intracerebral haemorrhage." Pharma Innovation 9, no. 11 (November 1, 2020): 75–78. http://dx.doi.org/10.22271/tpi.2020.v9.i11b.5312.

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21

Harries, D. P., and R. De Silva. "‘Ecstasy’ and Intracerebral Haemorrhage." Scottish Medical Journal 37, no. 5 (October 1992): 150–52. http://dx.doi.org/10.1177/003693309203700508.

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22

Mayer, Stephan A., and Fred Rincon. "Treatment of intracerebral haemorrhage." Lancet Neurology 4, no. 10 (October 2005): 662–72. http://dx.doi.org/10.1016/s1474-4422(05)70195-2.

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23

Balami, Joyce S., and Alastair M. Buchan. "Complications of intracerebral haemorrhage." Lancet Neurology 11, no. 1 (January 2012): 101–18. http://dx.doi.org/10.1016/s1474-4422(11)70264-2.

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Kolias, Angelos G., Hani J. Marcus, Marike L. Broekman, Peter J. Hutchinson, and Peter McCulloch. "Surgery for intracerebral haemorrhage." Lancet 394, no. 10199 (August 2019): e21. http://dx.doi.org/10.1016/s0140-6736(19)31410-2.

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Engrand, Nicolas, Mikael Mazighi, Caroline Le Guerinel, Matthieu Dorison, and Vera Dinkelacker. "Surgery for intracerebral haemorrhage." Lancet 394, no. 10199 (August 2019): e20. http://dx.doi.org/10.1016/s0140-6736(19)31625-3.

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Butcher, Kenneth, and John Laidlaw. "Current intracerebral haemorrhage management." Journal of Clinical Neuroscience 10, no. 2 (March 2003): 158–67. http://dx.doi.org/10.1016/s0967-5868(02)00324-7.

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27

Ferro, José M. "Update on intracerebral haemorrhage." Journal of Neurology 253, no. 8 (May 6, 2006): 985–99. http://dx.doi.org/10.1007/s00415-006-0201-4.

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Ragoschke-Schumm, A. "Intracerebral haemorrhage in CADASIL." Journal of Neurology, Neurosurgery & Psychiatry 76, no. 11 (November 1, 2005): 1606–7. http://dx.doi.org/10.1136/jnnp.2004.059212.

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Roquer, Jaume, Ernest Palomeras, Hernando Knobel, and Adolf Pou. "Intracerebral Haemorrhage in AIDS." Cerebrovascular Diseases 8, no. 4 (1998): 222–27. http://dx.doi.org/10.1159/000015855.

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Kelly, James. "New horizons: managing antithrombotic dilemmas in patients with cerebral amyloid angiopathy." Age and Ageing 50, no. 2 (January 22, 2021): 347–55. http://dx.doi.org/10.1093/ageing/afaa275.

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Abstract Cerebral amyloid angiopathy (CAA) most commonly presents with lobar intracerebral haemorrhage, though also with transient focal neurological episodes, cognitive impairment, as an incidental finding and rarely acutely or subacutely in patients developing an immune response to amyloid. Convexity subarachnoid haemorrhage, cortical superficial siderosis and lobar cerebral microbleeds are the other signature imaging features. The main implications of a diagnosis are the risk of intracerebral haemorrhage and frequent co-existence of antithrombotic indications. The risk of intracerebral haemorrhage varies by phenotype, being highest in patients with transient focal neurological episodes and lowest in patients with isolated microbleeds. There is only one relevant randomised controlled trial to CAA patients with antithrombotic indications: RESTART showed that in patients presenting with intracerebral haemorrhage while taking antiplatelets, restarting treatment appeared to reduce recurrent intracerebral haemorrhage and improve outcomes. Observational and indirect data are reviewed relevant to other scenarios where there are antithrombotic indications. In patients with a microbleed-only phenotype, the risk of ischaemic stroke exceeds the risk of intracerebral haemorrhage at all cerebral microbleed burdens. In patients with atrial fibrillation (AF), left atrial appendage occlusion, where device closure excludes the left atrial appendage from the circulation, can be considered where the risk of anticoagulation seems prohibitive. Ongoing trials are testing the role of direct oral anticoagulant (DOACs) and left atrial appendage occlusion in patients with intracerebral haemorrhage/AF but in the interim, treatment decisions will need to be individualised and remain difficult.

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Connor, Sophia, Omar Azzam, and David Prentice. "Intracerebral haemorrhage and Guillain-Barré syndrome: an exploration of potential pathophysiology." BMJ Case Reports 14, no. 8 (August 2021): e243245. http://dx.doi.org/10.1136/bcr-2021-243245.

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Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy classically thought to be caused by infections through the process of molecular mimicry. We report a case of GBS caused by intracerebral haemorrhage and postulate potential theories for the development of GBS following intracerebral haemorrhage and other non-infectious aetiologies by association. We highlight that GBS is an important differential diagnosis in patients developing generalised paresis following intracerebral haemorrhage.

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Wicaksono, Mohammad Arianto Satrio, Cep Juli, Chandra Calista, Uni Gamayani, Aih Cahyani, and Paulus Anam Ong. "Comparison of Cognitive Function between Intracerebral Haemorrhage Stroke Patients with and without Hypertensive Crisis." Althea Medical Journal 9, no. 1 (March 2022): 24–29. http://dx.doi.org/10.15850/amj.v9n1.2368.

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Background: Intracerebral haemorrhage (ICH) stroke is characterized by neurological dysfunction, caused by focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma. Hypertension is one of the main risk factors for intracerebral haemorrhage. Hypertensive crisis, which is a more severe type of uncontrolled hypertension may aggravate the cognitive outcomes. The aim of this study was to compare cognitive function between intracerebral haemorrhage stroke patients with and without hypertensive crisis. Methods: This study was a retrospective comparative analytic study, combined with a case-control study from August to November 2020. All medical records of patients with intracerebral haemorrhage, who were admitted to Dr. Hasan Sadikin General Hospital Bandung in 2019, were collected. The total score of mini-mental state examination (MMSE) which was recorded in the medical record was taken and compared between groups using the Mann-Whitney test. The MMSE was conducted on the day of discharge, and the minimum education level of the patients was elementary school. Results: We found a total of 109 medical records with ICH, 67 of which were with hypertensive crisis. The median MMSE score in the hypertensive crisis group was slightly higher than in the non-hypertensive crisis group. Furthermore, there was no statistical difference in MMSE scores between intracerebral haemorrhage patients with and without hypertensive crisis (p-value=0.439). Conclusion: There is no difference in cognitive function between intracerebral haemorrhage patients with and without hypertensive crisis. Further study is of great value to explore the relation between intracerebral haemorrhage patients with and without hypertensive crisis.

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Haas, Kirsten, Jan C. Purrucker, Timolaos Rizos, Peter U. Heuschmann, and Roland Veltkamp. "Rationale and design of the Registry of Acute Stroke Under Novel Oral Anticoagulants-prime (RASUNOA-prime)." European Stroke Journal 4, no. 2 (December 17, 2018): 181–88. http://dx.doi.org/10.1177/2396987318812644.

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Background Anticoagulation with vitamin K antagonists and non-vitamin K antagonists oral anticoagulants (NOAC) is effective in stroke prevention in patients with atrial fibrillation. However, anticoagulation also poses a major challenge for emergency treatment of patients suffering ischaemic stroke or intracerebral haemorrhage. Aim The registry RASUNOA-prime is designed to describe current patterns of emergency management, clinical course and outcome of patients with atrial fibrillation experiencing an acute ischaemic stroke or intracerebral haemorrhage under different anticoagulation schemes prior to stroke (NOAC, vitamin K antagonists or no anticoagulation). Methods and design RASUNOA-prime (ClinicalTrials.gov, NCT02533960) is a prospective, investigator-initiated, multicentre, observational cohort study aiming to recruit 3000 patients with acute ischaemic stroke and atrial fibrillation, and 1000 patients with acute intracerebral haemorrhage and atrial fibrillation with different anticoagulation schemes pre-stroke. It is a non-interventional triple-armed study aiming at a balanced inclusion of ischaemic stroke and intracerebral haemorrhage patients according to the different anticoagulation schemes. Patients will be followed up for clinical course, management and outcome up to three months after the event. Findings in ischaemic stroke and intracerebral haemorrhage patients on NOAC will be compared with patients taking vitamin K antagonists or no anticoagulant pre-stroke. Study outcomes Primary endpoint for ischaemic stroke patients: occurrence of symptomatic intracerebral haemorrhage, for intracerebral haemorrhage patients: occurrence of secondary haematoma expansion. Secondary endpoints include assessment of coagulation, use of thrombolysis and/or mechanical thrombectomy, occurrence of complications, implementation of secondary prevention. Summary Describing the current patterns of early management as well as outcome of stroke patients with atrial fibrillation will help guide physicians to develop recommendations for emergency treatment of stroke patients under different anticoagulation schemes.

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Law, Zhe Kang, Timothy J. England, Amit K. Mistri, Lisa J. Woodhouse, Lesley Cala, Rob Dineen, Serefnur Ozturk, et al. "Incidence and predictors of early seizures in intracerebral haemorrhage and the effect of tranexamic acid." European Stroke Journal 5, no. 2 (January 24, 2020): 123–29. http://dx.doi.org/10.1177/2396987320901391.

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Introduction Seizures are common after intracerebral haemorrhage. Tranexamic acid increases the risk of seizures in non-intracerebral haemorrhage population but its effect on post-intracerebral haemorrhage seizures is unknown. We explored the risk factors and outcomes of seizures after intracerebral haemorrhage and if tranexamic acid increased the risk of seizures in the Tranexamic acid for IntraCerebral Haemorrhage-2 trial. Patients and methods Seizures were reported prospectively up to day 90. Cox regression analyses were used to determine the predictors of seizures within 90 days and early seizures (≤7 days). We explored the effect of early seizures on day 90 outcomes. Results Of 2325 patients recruited, 193 (8.3%) had seizures including 163 (84.5%) early seizures and 30 (15.5%) late seizures (>7 days). Younger age (adjusted hazard ratio (aHR) 0.98 per year increase, 95% confidence interval (CI) 0.97–0.99; p = 0.008), lobar haematoma (aHR 5.84, 95%CI 3.58–9.52; p < 0.001), higher National Institute of Health Stroke Scale (aHR 1.03, 95%CI 1.01–1.06; p = 0.014) and previous stroke (aHR 1.66, 95%CI 1.11–2.47; p = 0.013) were associated with early seizures. Tranexamic acid did not increase the risk of seizure within 90 days. Early seizures were associated with worse modified Rankin Scale (adjusted odds ratio (aOR) 1.79, 95%CI 1.12–2.86, p = 0.015) and increased risk of death (aOR 3.26, 95%CI 1.98–5.39; p < 0.001) at day 90. Discussion and conclusion: Lobar haematoma was the strongest independent predictor of early seizures after intracerebral haemorrhage. Tranexamic acid did not increase the risk of post-intracerebral haemorrhage seizures in the first 90 days. Early seizures resulted in worse functional outcome and increased risk of death.

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Berwaerts, J., O. J. Robb, T. A. Jeffers, and J. Webster. "Intracerebral Haemorrhages and Oral Anticoagulation in the North of Scotland." Scottish Medical Journal 45, no. 4 (August 2000): 101–4. http://dx.doi.org/10.1177/003693300004500402.

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The aim of this study has been twofold: 1 - to examine the impact of oral anticoagulant (OAC) use on a possible recent rise in the admission rate of intracerebral haemorrhages to Aberdeen Royal Infirmary (ARI), and 2 - to estimate the absolute risk of intracranial haemorrhage for outpatients followed up in the OAC Clinic at AR1. The number of patients admitted to ARI with intracerebral bleedings increased by 60% between 1993 and 1998. A corresponding increase in the proportion of patients with concurrent OAC use (4.7% vs 15.7%, p=0.055) cannot sufficiently explain the increase in the total number of intracerebral haemorrhages. The average annual incidence of intracranial haemorrhages for the OAC Clinic at ARI is found to be acceptably low at 0.33% per year. Further audit of the large number of patients receiving warfarin outwith the supervision of the clinic is urgently required.

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Liu, Jingyi, Ximing Nie, Hongqiu Gu, Qi Zhou, Haixin Sun, Ying Tan, Dacheng Liu, et al. "Tranexamic acid for acute intracerebral haemorrhage growth based on imaging assessment (TRAIGE): a multicentre, randomised, placebo-controlled trial." Stroke and Vascular Neurology 6, no. 2 (April 1, 2021): 160–69. http://dx.doi.org/10.1136/svn-2021-000942.

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BackgroundStudies show tranexamic acid can reduce the risk of death and early neurological deterioration after intracranial haemorrhage. We aimed to assess whether tranexamic acid reduces haematoma expansion and improves outcome in intracerebral haemorrhage patients susceptible to haemorrhage expansion.MethodsWe did a prospective, double-blind, randomised, placebo-controlled trial at 10 stroke centres in China. Acute supratentorial intracerebral haemorrhage patients were eligible if they had indication of haemorrhage expansion on admission imaging (eg, spot sign, black hole sign or blend sign), and were treatable within 8 hours of symptom onset. Patients were randomly assigned (1:1) to receive either tranexamic acid or a matching placebo. The primary outcome was intracerebral haematoma growth (>33% relative or >6 mL absolute) at 24 hours. Clinical outcomes were assessed at 90 days.ResultsOf the 171 included patients, 124 (72.5%) were male, and the mean age was 55.9±11.6 years. 89 patients received tranexamic acid and 82 received placebo. The primary outcome did not differ significantly between the groups: 36 (40.4%) patients in the tranexamic acid group and 34 (41.5%) patients in the placebo group had intracranial haemorrhage growth (OR 0.96, 95% CI 0.52 to 1.77, p=0.89). The proportion of death was lower in the tranexamic acid treatment group than placebo group (8.1% vs 10.0%), but there were no significant differences in secondary outcomes including absolute intracranial haemorrhage growth, death and dependency.ConclusionsAmong patients susceptible to haemorrhage expansion treated within 8 hours of stroke onset, tranexamic acid did not significantly prevent intracerebral haemorrhage growth. Larger studies are needed to assess safety and efficacy of tranexamic acid in intracerebral haemorrhage patients.

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Masotti, Luca, Sandro Filippi, Serenella Acciai, Maria Teresa Mechi, Sandra Gori, Annalisa Mannucci, Anna Maria Bellizzi, et al. "Epidemiology of intracerebral haemorrhage in Livorno district." Reviews in Health Care 2, no. 1S (June 10, 2011): 5. http://dx.doi.org/10.7175/rhc.4321s5-13.

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BACKGROUND: Intracranial haemorrhage represents the most feared stroke subtype. AIM: To evaluate the burden of intracranial haemorrhage in Tuscany hospitals with special reference to Livorno district. MATERIALS AND METHODS: Data of patients discharged in 2009 from Tuscan and Livorno hospitals with codes ICD-9-CM related to any type of spontaneous intracranial haemorrhage were selected and analyzed. RESULTS: 3,472 patients were discharged from Tuscan hospitals with these diagnoses. Overall mortality was 24.3%. 50% of patients were admitted in Internal Medicine wards. Incidence of intracranial haemorrhage and intracerebral haemorrhage (ICH) in population of Livorno district was 64 and 45/100,000 inhabitants/year with related mortality of 36.5% and 39.4%respectively. Intra-hospital mortality of patients admitted in Livorno hospitals for intracranial haemorrhage were 36.7%. 40% of deaths occurred in the first 48 hours. 69.6% of intracranial haemorrhage were ICHs, 16.8% subaracnoideal. Intra-hospital mortality, admissions for intracranial haemorrhage in respect of total admissions and mortality for intracranial haemorrhage in respect to total mortality increased in the last decade. 23% of patients with intracranial haemorrhage and 16% of patients with ICH underwent to surgical procedures. ICHs related to antithrombotic treatment significantly increased in the last years. Mortality in patients on antithrombotic drugs was three times over compared to that in patients not undergone these drugs (43.7% vs 12.8%, p < 0.01). CONCLUSION: There is an increasing trend in frequency, mortality and hospital burden of intracranial haemorrhage and ICH. Efforts aimed at reducing the burden and consequences of this devasting disease are warranted.

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Masotti, Luca, Sandro Filippi, Serenella Acciai, Maria Teresa Mechi, Sandra Gori, Annalisa Mannucci, Anna Maria Bellizzi, et al. "Epidemiology of intracerebral haemorrhage in Livorno district." Reviews in Health Care 2, no. 1S (June 10, 2011): 5–13. http://dx.doi.org/10.7175/rhc.v2i1s.43.

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BACKGROUND: Intracranial haemorrhage represents the most feared stroke subtype. AIM: To evaluate the burden of intracranial haemorrhage in Tuscany hospitals with special reference to Livorno district. MATERIALS AND METHODS: Data of patients discharged in 2009 from Tuscan and Livorno hospitals with codes ICD-9-CM related to any type of spontaneous intracranial haemorrhage were selected and analyzed. RESULTS: 3,472 patients were discharged from Tuscan hospitals with these diagnoses. Overall mortality was 24.3%. 50% of patients were admitted in Internal Medicine wards. Incidence of intracranial haemorrhage and intracerebral haemorrhage (ICH) in population of Livorno district was 64 and 45/100,000 inhabitants/year with related mortality of 36.5% and 39.4%respectively. Intra-hospital mortality of patients admitted in Livorno hospitals for intracranial haemorrhage were 36.7%. 40% of deaths occurred in the first 48 hours. 69.6% of intracranial haemorrhage were ICHs, 16.8% subaracnoideal. Intra-hospital mortality, admissions for intracranial haemorrhage in respect of total admissions and mortality for intracranial haemorrhage in respect to total mortality increased in the last decade. 23% of patients with intracranial haemorrhage and 16% of patients with ICH underwent to surgical procedures. ICHs related to antithrombotic treatment significantly increased in the last years. Mortality in patients on antithrombotic drugs was three times over compared to that in patients not undergone these drugs (43.7% vs 12.8%, p < 0.01). CONCLUSION: There is an increasing trend in frequency, mortality and hospital burden of intracranial haemorrhage and ICH. Efforts aimed at reducing the burden and consequences of this devasting disease are warranted.

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Joy, AK, Annada Sankar Mohes, Th Bidyarani, L. Dorendrojit Singh, and Aten Jongky. "A Rare Case of Bilateral Spontaneous Intracerebral Haemorrhage Presenting With Left Hemiplegia: A Case Report." Indian Journal of Physical Medicine and Rehabilitation 26, no. 4 (2015): 109–10. http://dx.doi.org/10.5005/ijopmr-26-4-109.

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Abstract Haemorrhage is responsible for around 11% of stroke syndrome. Haemorrhage usually occurs at a single site. However, it can be at multiple sites in some specific conditions i.e. coagulopathy, vascular malformation, malignancy etc. A 56-year-old male with left sided hemiplegia was admitted in the rehabilitation ward of RIMS, Imphal. He was hypertensive and was on irregular medication for that. He was also an alcoholic and chronic smoker for last 20 years. Patient was conscious and clinical examination revealed left 7th and 12th cranial nerve involvement with left hemiplegia. Non-contrast CT scan of brain revealed right thalamus and left basal ganglia haemorrhages. Thorough history and investigations did not reveal any aetiology for bilateral haemorrhage. Patient was treated with conservative management and improvement was noticed in serial follow-ups. There are very few case reports about bilateral spontaneous intracerebral haemorrhage associated with other diseases like migraine, Japanese encephalitis etc. Cause of bilateral haemorrhage in our case is doubtful.

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Páscoa Pinheiro, João, Diogo Reis Carneiro, Daniela Matos, and Ricardo Pereira. "Primary intraventricular haemorrhage: the role of frontal minicraniotomy and external ventricular drainage." BMJ Case Reports 14, no. 2 (February 2021): e239448. http://dx.doi.org/10.1136/bcr-2020-239448.

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Primary intraventricular haemorrhage (PIVH) is an uncommon type of intracerebral haemorrhage, accounting for only 0.31% of all strokes and 3.1% of all intracerebral haemorrhages. Due to the low incidence of PIVH, little is known about its clinical characteristics, risk factors, aetiologies, prognosis and treatment. Acute hydrocephalus is common and is associated with a poor prognosis. External ventricular drainage (EVD) could promptly reduce intracranial pressure by diverting cerebrospinal fluid and intraventricular blood; however, the incidence of complications such as central nervous system infection, catheter occlusion and rebleeding are relatively common. Despite being an invasive procedure, frontal minicraniotomy is an available therapeutic option to avoid complications of EVD. The authors report a case of a PIVH managed with frontal minicraniotomy and perform a literature review about epidemiological data, clinical features and treatment of PIVH.

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Prats-Sánchez, Luis, Marina Guasch-Jiménez, Ignasi Gich, Elba Pascual-Goñi, Noelia Flores, Pol Camps-Renom, Daniel Guisado-Alonso, et al. "Influence of time to admission to a comprehensive stroke centre on the outcome of patients with intracerebral haemorrhage." European Stroke Journal 5, no. 2 (January 29, 2020): 115–22. http://dx.doi.org/10.1177/2396987320901616.

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Introduction In patients with spontaneous intracerebral haemorrhage, it is uncertain if diagnostic and therapeutic measures are time-sensitive on their impact on the outcome. We sought to determine the influence of the time to admission to a comprehensive stroke centre on the outcome of patients with acute intracerebral haemorrhage. Patients and methods We studied a prospective database of consecutive patients with intracerebral haemorrhage attended at two comprehensive stroke centres (2005–2017). We excluded patients with an unwitnessed time of onset of the intracerebral haemorrhage, or previous modified Rankin Scale >3 or in those in whom withdrawal of life-sustaining interventions were decided <24 h from admission. We recorded the time from the intracerebral haemorrhage onset to admission, demographic, clinical, radiological data, the functional outcome (favourable when modified Rankin Scale ≤3) and mortality at 90 days. We conducted a propensity score-matching analysis to evaluate functional outcome and mortality. Results We included 487 patients (mean age 72.3 ± 13.9 years), and 53.2% were men. Compared to patients with an admission >110 min, patients who were admitted ≤110 min were significantly younger, and had higher National Institutes of Health Stroke Scale scores. Moreover, patients admitted ≤110 min were more likely to have basal ganglia intracerebral haemorrhage, and to show neurological deterioration. The propensity score groups were well matched. We did not find an association between time to admission and the favourable outcome (OR: 1.42 (95% CI: 0.93–2.16)) or mortality (OR: 0.64 (0.41–0.99)) at 90 days. Conclusions Our results suggest that in patients with intracerebral haemorrhage and known symptom onset who are admitted to a comprehensive stroke centre, an early admission (≤110 min) does not influence the outcome at 90 days.

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Sweidan, Alexander Jacob, Navneet Kaur Singh, Joseph Luke Conovaloff, Matthew Bower, Leonid I. Groysman, Mohammad Shafie, and Wengui Yu. "Coagulopathy reversal in intracerebral haemorrhage." Stroke and Vascular Neurology 5, no. 1 (February 20, 2020): 29–33. http://dx.doi.org/10.1136/svn-2019-000274.

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As intracerebral hemorrahge becomes more frequent as a result of an aging population with greater comorbidities, rapid identification and reversal of precipitators becomes increasingly paramount. The aformentioned population will ever more likely be on some form of anticoagulant therapy. Understanding the mechanisms of these agents and means by which to reverse them early on is critical in managing the acute intracerebral hemorrhage.

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Prasad, Kameshwar. "Antiplatelet therapy after intracerebral haemorrhage." National Medical Journal of India 33, no. 4 (2020): 232. http://dx.doi.org/10.4103/0970-258x.316255.

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Paroutoglou, Kyriaki, and Adrian R. Parry-Jones. "Hyperacute management of intracerebral haemorrhage." Clinical Medicine 18, Suppl 2 (April 1, 2018): s9—s12. http://dx.doi.org/10.7861/clinmedicine.18-2-s9.

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Siddique, S. M., and A. D. Mendelow. "Surgical treatment of intracerebral haemorrhage." British Medical Bulletin 56, no. 2 (January 1, 2000): 444–56. http://dx.doi.org/10.1258/0007142001903085.

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Biffi, Alessandro, Abbas Rattani, Christopher D. Anderson, Alison M. Ayres, Edip M. Gurol, Steven M. Greenberg, Jonathan Rosand, and Anand Viswanathan. "Delayed seizures after intracerebral haemorrhage." Brain 139, no. 10 (August 6, 2016): 2694–705. http://dx.doi.org/10.1093/brain/aww199.

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Sung, C. Y., and N. S. Chu. "Epileptic seizures in intracerebral haemorrhage." Journal of Neurology, Neurosurgery & Psychiatry 52, no. 11 (November 1, 1989): 1273–76. http://dx.doi.org/10.1136/jnnp.52.11.1273.

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Mendelow, A. David, and Andreas Unterberg. "Surgical treatment of intracerebral haemorrhage." Current Opinion in Critical Care 13, no. 2 (April 2007): 169–74. http://dx.doi.org/10.1097/mcc.0b013e3280a9e5c2.

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Burrage, Daniel Richard. "Drug causes of intracerebral haemorrhage." Adverse Drug Reaction Bulletin 318, no. 1 (October 2019): 1231–34. http://dx.doi.org/10.1097/fad.0000000000000043.

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Schreuder, Floris H. B. M., Shoichiro Sato, Catharina J. M. Klijn, and Craig S. Anderson. "Medical management of intracerebral haemorrhage." Journal of Neurology, Neurosurgery & Psychiatry 88, no. 1 (November 16, 2016): 76–84. http://dx.doi.org/10.1136/jnnp-2016-314386.

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