Cerebral Intraparenchymal Hemorrhage

Abstract

pontaneous intraparenchymal hemorrhage (IPH) is relatively common and has devastating consequences. Recognition of risk factors (eg, hypertension), early distinction from an ischemic event, and identification of clinical features that can worsen IPH complications is important in optimizing outcomes from IPH. This review examines the pathophysiology of and management options for IPH, with the intent of helping clinicians better manage the condition. IPH accounts for 6.5% to 19.6% of cases of stroke 1,2 but is associated with the greatest rate of mortality; 1-year survival from IPH is approximately 40%, 3-5 and 10-year survival is 24%. 4 Across several studies, the rate of functional independence at follow-up varied from 12% to 39%. 5 A meta-analysis of 36 studies reported an incidence of IPH of 24.6 per 100 000 person-years (range, 1.8-129.6), and the rate was significantly higher in Asian and older populations. 5 MethodsThe PubMed database was searched on September 1, 2018, using the terms intracerebral hemorrhage and intraparenchymal hemorrhage, for English-language studies of the pathophysiology, epidemiology, and management of IPH published after January 1, 2015. Large population epidemiologic studies, randomized trials, and formal treatment guidelines were reviewed. Relevant references published before January 1, 2015, were extracted and also reviewed. Studies providing only aggregate data for all types of hemorrhagic stroke (including subarachnoid hemorrhage) were excluded. This review was based on 77 referenced articles, including 11 clinical trials, 10 meta-analyses, 41 observational studies, 2 guidelines, and 13 other reports.

Protective effects of medicinal plant breviscapine on postcerebral hemorrhage in rats

“…HE pathological experiments showed that breviscapine could inhibit the expressions of intercellular adhesion factors in inflammatory mediators and inflammation, reduce brain edema after cerebral hemorrhage, improve the ischemia and hypoxia of peripheral nerves of a cerebral hemorrhage, and promote the recovery of nerve function (Pengyue et al, 2017). The latest advances in molecular biology provide a new theoretical basis for us to understand the pathological mechanism of cerebral hemorrhage better (Gross et al, 2019). Molecular experiments showed that IL-6 and TNF-α levels are significantly increased after cerebral hemorrhage in rats (Jiang et al, 2017).…”

Combined Human Umbilical Cord-Derived Stem Cell and Hyperbaric Oxygen Therapy Effectively Preserved the Neurological Function and Brain Architecture in Rat After Acute Intracerebral Hemorrhage

“…It is well documented that the mechanical damage is always immediately elicited after ICH which commonly wrecks the brain tissue as it enlarges [2]. This, is frequently associated with the pressure created enough by blood and surrounding brain edema, resulting in a life-threatening situation [4]. The secondary damage is caused by cytotoxicity of blood [5,6], impaired calcium homeostasis [7], excitotoxicity from excitatory neurotransmitters/glial cells [8,9] and upregulation of oxidative stress and in ammation [6,[9][10][11][12][13][14].…”

“…In intracranial hemorrhage, the bleeding is usually derived from arterioles or small arteries directly into the brain, forming hematomas that spreads along white matter pathway. The hematoma frequently continues to grow until the pressure surrounding it increases enough to limit its spread or until the hemorrhage decompresses itself by emptying into the ventricular system or into the cerebrospinal uid [2,4]. Additionally, intracranial hemorrhage, always sabotages the brain tissue as it enlarges, i.e., rst primary injury to the brain is the mechanical damage [2].…”

“…Additionally, intracranial hemorrhage, always sabotages the brain tissue as it enlarges, i.e., rst primary injury to the brain is the mechanical damage [2]. The pressure created enough by blood and surrounding brain edema is life-threatening [4]. The secondary injuries result from cytotoxicity of blood [5,6], impaired calcium homeostasis [7], excitotoxicity from excitatory neurotransmitters (e.g.…”

Current approaches to diagnosing in intracerebral hemorrhage

“…Кроме того, ВМК развивается вторично на фоне структурных аномалий артерий (аневризмы, артериовенозные мальформации -АВМ, каверномы и дуральные артериовенозные фистулы -АВФ), других сосудистых заболеваний головного мозга (тромбоз венозных синусов, синдром обратимой церебральной вазоконстрикции, микотические аневризмы при инфекционном эндокардите, геморрагическая трансформация инфаркта мозга, васкулит), гипокоагуляции, а также опухолей (метастаза) головного мозга (см. таблицу) [2,7]. В первую очередь ВМК должно быть классифицировано анатомически, например на долевое/недолевое и супратенториальное/инфратенториальное, что возможно с использованием шкалы CHARTS.…”