Primary intracerebral hemorrhage.

This article reviews the epidemiology, pathophysiology and management of primary intracerebral hemorrhage. In North American and European populations, 15% of strokes are due to intracerebral hemorrhage. Pathologically in hypertension, early arteriolar proliferation of smooth muscle is followed later by smooth muscle cell death and collagen deposition. This eventually leads to occlusion or ectasia of arterioles. The latter leads to Charcôt-Bouchard aneurysm formation and possible intracerebral hemorrhage. Amyloid deposition in the tunica media causes similar brittle arterioles. Fibrin globes in concentric spheres attempt to seal off the site of bleeding. But vasculopathy (either amyloid or hypertensive) inhibits the contractile capability of arterioles. The size of the final sphere of blood at cessation of bleeding determines the clinical spectrum, from asymptomatic to fatal. Since arteriolar bleeding is slower than arterial bleeding, several hours exist where intervention may be useful. While medical intervention is controversial, guidelines for blood pressure, intracranial pressure, glucose and seizure management exist. Surgical trials have tended to show no benefit. Recombinant factor VIIa is undergoing investigation as hemostatic therapy for intracerebral hemorrhage, to limit clot expansion and possibly also as a hemostatic adjunct to surgery.     

Surgery for intracerebral hemorrhage

Neurological Sciences - The surgical treatment of intracerebral hemorrhage (ICH) is one of the most controversial areas of neurosurgery. Randomized trials are inconclusive due to the small number...     

Inflammation after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a devastating clinical event without effective therapies. Increasing evidence suggests that inflammatory mechanisms are involved in the progression of ICH-induced brain injury. Inflammation is mediated by cellular components, such as leukocytes and microglia, and molecular components, including prostaglandins, chemokines, cytokines, extracellular proteases, and reactive oxygen species. Better understanding of the role of the ICH-induced inflammatory response and its potential for modulation might have profound implications for patient treatment. In this review, a summary of the available literature on the inflammatory responses after ICH is presented along with discussion of some of the emerging opportunities for potential therapeutic strategies. In the near future, additional strategies that target inflammation could offer exciting new promise in the therapeutic approach to ICH.     

Autophagy after experimental intracerebral hemorrhage.

Autophagy contributes to ischemic brain injury, but it is not clear if autophagy occurs after intracerebral hemorrhage (ICH). This study examined whether ICH-induced cell death is partly autophagic. It then examined the role of iron in inducing this form of cell death after ICH. Male, adult Sprague-Dawley rats received an infusion of autologous whole blood or ferrous iron into the right basal ganglia. Control rats (sham) had a needle insertion. The rats were killed at 1, 3, 7, or 28 days later. Some rats were treated with either deferoxamine or vehicle after ICH. Microtubule-associated protein light chain-3 (LC3), a biomarker of autophagosome, and cathepsin D, a lysosomal biomarker, were measured by Western blot analysis and immunohistochemistry. Immunofluorescent double-labeling was used to identify the cell types expressing cathepsin D. Electron microscopy was performed to examine the cellular ultrastructure changes after ICH. We found that conversion of LC3-I to LC3-II, cathepsin D expression, and vacuole formation are increased in the ipsilateral basal ganglia after ICH. Intracerebral infusion of iron also resulted in enhanced conversion of LC3-I to LC3-II and increased cathepsin D levels. Deferoxamine (an iron chelator) treatment significantly reduced the conversion of LC3-I to LC3-II and cathepsin D levels after ICH. Our results demonstrated that autophagy occurs after ICH, and iron has a key role in ICH-induced autophagy. This also suggests that iron-induced autophagy may play a role in brain injury in other diseases associated with iron overload.     

Oral-anticoagulant-related intracerebral hemorrhage

BACKGROUND: The characteristics, management and outcomes of patients who suffer intracerebral hemorrhage (ICH) while taking oral anticoagulants (OAC) are relatively unreported. DESIGN: Retrospective cohort study of consecutive cases with ICH associated with OAC. SETTING: A university-affiliated tertiary care hospital in Ontario, Canada. PATIENTS/PARTICIPANTS: 368 charts of individuals with a discharge diagnosis of ICH (ICD-9 code 431) between January 1993 and May 1998 were reviewed. MAIN RESULTS: 20 (5.4%, 95% confidence interval (CI): 3.1-7.7%) of the 368 ICHs occurred in people taking OAC. The median age of patients on OAC was 74 years (S.D.+/-9.8), and 70% (95% CI: 49-91%) were female. The median INR at presentation was 3.4 (intraquartile (IQR) range 2.2-4.4). Nine of 20 (45%) patients had INR values which exceeded the target range. The case fatality rate was 45% (95% CI: 23-67%). Approximately 2.8 years after the initial ICH, 9 of the 11 patients who survived the initial ICH were still alive, and 6 had restarted OAC. CONCLUSIONS: ICH is a serious complication in patients taking OAC, and the case-fatality rate is high. Given the increasing use of OAC in patients with cardiovascular disease, the relative benefits and risks of this therapy must be weighed carefully.     

Spontaneous intracerebral hemorrhage

To determine the prognostic value of etiology and localization in spontaneous intracerebral hemorrhage, 896 patients with spontaneous intracerebral hemorrhage, as proven by CT, operation or autopsy, were retrospectively studied using univariate data analysis. Etiologies were hypertension in 63.5%, cerebrovascular malformations in 8.5% and abnormal hemostasis in 15% of the patients. In 23% no etiology was determined. Main localizations were cerebral lobes in 49.2%, basal ganglia in 34.4%, brain stem in 6.9%, cerebellum in 6.7% and primary intraventricular in 2.3% of the patients. Ventricular extension was present in 47.0%. A higher case fatality correlated with: 1) ventricular extension ( P <0.00001), 2) increasing age ( P =0.00005), 3) surgical treatment ( P =0.00010), 4) localization in basal ganglia ( P =0.0108) and 5) hypertension as only etiology ( P =0.01471). A lower case fatality was found in patients with cerebrovascular malformations ( P =0.00006) and when the hemorrhage was localized to the cerebral lobes ( P =0.0050). We conclude that etiology and localization are of prognostic value in spontaneous intracerebral hemorrhage.     

Anticoagulant-associated intracerebral hemorrhage

The incidence of anticoagulant-associated intracerebral hemorrhage (AAICH) quintupled during the 1990 s, probably due to increased warfarin use for the treatment of atrial fibrillation. Anticoagulant-associated intracerebral hemorrhage now accounts for nearly 20% of all intracranial hemorrhage (ICH). Among patients using warfarin for atrial fibrillation, the annual risk of ICH in trials is 0.3 to 1.0%. Predictors of potential anticoagulant-associated hemorrhage are increasing age, prior ischemic stroke, hypertension, leukoaraiosis, the early period of warfarin use, higher intensity anticoagulation, and antiplatelet use in addition to anticoagulation. Compared with other intracranial hemorrhage patients, anticoagulated patients have a greater risk of hematoma expansion, subsequent clinical deterioration and death, necessitating vigorous reversal of their coagulopathy. Recommended methods of warfarin reversal are administration of intravenous vitamin K and either prothrombin complex concentrates or fresh frozen plasma. Reversal of unfractionated heparin is accomplished with intravenous protamine sulfate. Surgical treatment of intracranial hemorrhage may be life saving in select cases, but has not reduced morbidity or mortality in large randomized trials.     

Recurrent intracerebral hemorrhage

Objective: In order to study the clinical manifestation and risk factor of recurrent intracerebral hemorrhage(ICH).Methods:The 256 patients were analysed who admitted to our hospital for intracerebral hemorrhage between 1995 and 1997.The 15(5 .86%)patients had a recurrent ICH.There were 9 men and 6 women and the mean age of the patients was 63.5 ± 6.4years at the first bleeding episode and 67.8± 8. 5 years at the second. The mean interval between the two bleeding episodes was 44.6 ± 12.5 months. The 73.3%patients were hypertensive .′The site of the first hemorrhage was ganglionic in 8 patients , ]ohar in six paients and brainstem in one .The recurrent hemorrhage occurred at a different location from the previous ICH.The most common pattern of recurrence was “ganglionic -ganglionic” (7 patients), lobar - ganglionic (3 patients), lobar-lobar(three patients), which was always observed in hypertensive patients. The outcome after the recurrent hemorrhage was usually poor. By comparison with 24 patients followed up to average 47.5± 18.7 months with isolated ICH without recurrence .Only lobar hematoma and a younger age were risk factors for recurrences whereas sex and previous hypertension were not. The mechanism of recurrence of ICH were multiple(hypertension, cerebral amyloid angiopathy).Contral of blood pressure and good living habit after the first hemorrhage may prevent ICH recurrences.     

Spontaneous intracerebral hemorrhage

Spontaneous intracerebral hemorrhage (sICH) is defined as bleeding within the brain parenchyma, and occurs twice as commonly as subarachnoid hemorrhage, but is equally as deadly. Risk factors for sICH include hypertension, advanced age, leukoaraiosis, prior ICH, renal failure, use of anticoagulant drugs, and cerebral amyloid angiopathy. When a patient is clinically suspected of having sICH, head computed tomography scan is the standard diagnostic tool. However, newer magnetic resonance neuroimaging techniques may aid in determining the underlying pathology and aid in prognosis. Supportive care and blood pressure management are important in the care of patients with sICH. Ongoing research is aimed at determining a safe blood pressure goal that may also prevent expansion of hemorrhage. Hemostatic medications and neuroprotectants have thus far not shown clinical improvement. Although several neurosurgical trials have failed to demonstrate benefit for surgical evacuation of sICH, multiple research trials are ongoing investigating acute blood pressure control, deep or basal ganglionic hemorrhage evacuation via minimally invasive approach (MISTIE; http://mistietrial.com/default.aspx), lobar ICH evacuation (STICH; II http://research.ncl.ac.uk/stich/), and intraventricular thrombolysis with tissue plasminogen activator (tPA) (CLEAR III; http://biosgroup-johnshopkinsmedicine.health.officelive.com/default.aspx).     

Warfarin-associated intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is the most serious complication of oral anticoagulant therapy (OAT), with mortality in excess of 50%. Major risk factors are advanced patient age, elevated systolic blood pressure, intensity of anticoagulation, and previous cerebral ischemia. A number of acute treatments are available, but all have significant side effects and no randomized clinical trials assessing clinical outcome have been performed. Future trials will have to address choice and dose of agent, the timing of its administration, and the risk of side effects.     

Anticoagulant-related intracerebral hemorrhage

Twenty-four patients had intracerebral hemorrhage while they were being treated with anticoagulants. Hypertension was present in 67% of the cases, head trauma was an uncommon preceding event, and simultaneous bleeding in other organs occurred in only one instance. Neurologic abnormalities progressed for several hours in 58%. Seizures occurred at onset in 12.5%. The location of the hemorrhage was as follows: cerebellum (nine cases), lobar white matter (six), basal ganglia (five), thalamus (two), and hemisphere, unspecified (two). In 61%, the hemorrhages occurred within 6 months of therapy. In 75%, the prothrombin time was beyond 1 1/2 times the control value. Mortality was 62.5%. Survivors had smaller hematomas than did patients with fatal hemorrhage.     

立体定向微创治疗高血压性脑出血

目的 探讨立体定向微创治疗高血压性脑出血的疗效及优越性。方法 对32例高血压性脑出血行立体定向血肿排空术或小骨窗开颅、显微镜辅助手术清除颅内血肿。结果本组32例术后立即复查头颅CT，血肿均清除70％以上，瞳孔散大者均有不同程度回缩。32例分刖住院12～31d，死亡4例。结论 立体定向微创治疗高血压性脑出血具有定位准确、创伤小、恢复快、病死率低等优点。     

高血压脑出血的手术治疗

我院自1998年至2001年手术治疗高血压脑出血24例。现总结报导如下。     

Therapy for spontaneous intracerebral haemorrhage

Spontaneous intracerebral haemorrhage (ICH) is a common and serious disease. It is responsible for 10-17% of all strokes, and mortality exceeds 50%. A variety of underlying causes exist for ICH, advancing age and hypertension being the most important risk factors. Other causes of ICH include vascular malformations, coagulation disorders, and use of anticoagulants and thrombolytic agents. Treatment options comprise conservative as well as surgical management. In addition, a recently published clinical trial evaluating the use of activated recombinant Factor VII allows specific haemostatic therapies to be used in ICH treatment. That and other studies have significantly added to the understanding of the disease. The European Stroke Initiative, which represents the European Stroke Council, European Neurological Society, and European Federation of Neurological Societies, will soon publish recommendations for the management of spontaneous intracerebral haemorrhages. Those recommendations form the basis of this article.