Deep Intracerebral Hemorrhage Research Articles

Frameless Stereotactic Aspiration and Thrombolysis of Deep Intracerebral Hemorrhage is Associated With Reduction of Hemorrhage Volume and Neurological Improvement

This is a phase-2 safety trial to demonstrate the ability of frameless stereotactic aspiration and thrombolysis of ICH to safely remove blood. Patients with ICH in the deep basal ganglia and internal capsule of > 5 cc volume were consented to undergo computed tomographic imaging for frameless stereotactic guidance registration. Using the frameless stereotactic (CT) guidance, a 4-mm diameter catheter was inserted into the body of the hematoma using a frontal burr hole approach. The catheter was aspirated and then flushed with saline and aspirated to remove unclotted blood. After a confirmatory CT scan to localize the catheter, 1 mg of recombinant tissue plasminogen activator (t-PA) was infused into the clot, permitted to bathe the clot for 30 minutes, and then drained into a closed circuit collection system. t-PA was infused every 8 hours for 48 hours. A follow up CT scan was obtained at 48 hours. 28 patients with ICH (mean age 67.1) were admitted and underwent the procedure. Mean initial ICH volume was 54.6 cc +/-6 37.8. Mean time from onset to aspiration was 44 hours (range 7-180). Mean initial NIH Stroke scale (NIHSS) score was 24 (range 15-33). Compared with initial CT scan, there was a mean reduction of ICH volume by 77 +/-6 13% on final CT scan (p < 0.0002). Compared with initial NIHSS, the discharge mean NIHSS (16 +/- 6) was significantly improved (p < 0.001). There were no infectious, hemodynamic or neurologic complications. There were no episodes of symptomatic hemorrhagic enlargement and one case of asymptomatic bleeding along the catheter tract. Frameless stereotactic aspiration and thrombolysis (FAST) of deep spontaneous intracerebral hemorrhage is a safe therapy that is associated with reduction in ICH volume, early improvement in NIHSS and potentially could be used to improve outcome.

Dotlike hemosiderin spots on T2*-weighted magnetic resonance imaging as a predictor of stroke recurrence: a prospective study

Microangiopathy associated with hypertension is a notable cause of cerebral small vessel disease (SVD), including deep intracerebral hemorrhage (ICH) and lacunar infarct. Dotlike low-intensity spots (dotlike hemosiderin spots: dotHSs) on T2*-weighted magnetic resonance (MR) images have been histologically diagnosed as old cerebral microbleeds associated with lipohyalinosis, amyloid angiopathy, or other microangiopathies and located in deep or subcortical regions. The aim of this study was to determine whether dotHSs indicate the severity of microangiopathy, and if so, whether large numbers of deep dotHSs are associated with SVD recurrence. The authors prospectively analyzed the number of dotHSs in 337 patients-191 men and 146 women with a mean age of 66 +/- 10.4 years (range 37-94 years)-with SVD (199 ICHs and 138 lacunar infarcts) who had been consecutively admitted to Hakodate Municipal Hospital. The follow-up period was 3.5 to 42 months (22.5 +/- 13.1 months). Patients were divided into two groups based on the recurrence. The hazard ratio (HR) for recurrence was estimated based on the Cox proportional hazard model by using the number of deep and subcortical dotHSs as well as other factors. Of 337 patients, 20 were readmitted with recurrence. Results of a multivariate analysis revealed an elevated rate of recurrence in patients with many subcortical dotHSs (> or = 5, HR 4.36, p = 0.0019) or a history of ICH (HR 3.82, p = 0.014). A trend toward a positive correlation (Pearson correlation coefficient 0.548, p < 0.0001) was found between the number of deep and subcortical dotHSs. Although a small sample size limited the power of analyses, the findings indicate that a large number of subcortical dotHSs may predict SVD recurrence.

Temporal profile of matrix metalloproteinases and their inhibitors after spontaneous intracerebral hemorrhage: relationship to clinical and radiological outcome.

Matrix metalloproteinases (MMPs) are related to blood-brain barrier disruption, and some members of this family have been recently involved in brain bleedings. We aimed to investigate the temporal profile of MMPs and their natural inhibitors (TIMPs) after acute intracerebral hemorrhage (ICH) and to study its influence on neuroimaging and clinical outcome. MMP-2, MMP-9, and MMP-3, as well as TIMP-1 and TIMP-2, were serially determined by enzyme-linked immunosorbent assay on admission (<12 hours), and at 24 hours, 48 hours, 7 days, and 3 months in 21 ICH patients. ICH and perihematomal edema (PE) volumes were serially measured on baseline and follow-up computed tomography (48 hours, 7 days, and 3 months), just at the time of neurological assessment. Deep ICH was found in 62% patients. Baseline ICH volume did not influence MMP-TIMP level. Highest levels of MMP-2 and TIMP-2 were found at baseline, for MMP-9 and TIMP-1 at 24 hours, and for MMP-3 at 24 to 48 hours. Baseline MMP-9 was positively correlated to PE volume (r=0.67, P=0.004) and, conversely, its inhibitor TIMP-1 was negatively correlated to PE (r=-0.51, P=0.04). Mortality reached 35% and MMP-3 was the only MMP/TIMP related to mortality (7.5 versus 2.4 ng/mL; P=0.035) and its most powerful baseline predictor (odds ratio = 22, confidence interval: 1.5 to 314.2). Both MMP-9 and MMP-3 correlated to the residual scar volume at 3 months (r=0.68, P=0.01 for baseline MMP-9, and r=0.86, P<0.001 for 24-hour MMP-3). A characteristic temporal profile of MMP/TIMP release exists in ICH. Increased MMP-9 is associated with PE, and increased MMP-3 is associated with mortality. Both molecules are related to residual cavity volume.

Antithrombotic Therapy After Cerebral Hemorrhages

To the Editor: Oral anticoagulation (OAC) generally increases the likelihood of intracerebral hemorrhage (ICH). When there is an indication for OAC in a patient with a history of ICH, the clinician is in the difficult situation of assessing risks and benefits of OAC. In the absence of data from clinical trials, Eckman et al1 have used a decision-analysis model to compare the expected values of 3 treatment strategies—OAC, aspirin, and no antithrombotic therapy—in patients with ICH and atrial fibrillation (AF).1 They conclude that all survivors of lobar ICH and most survivors of deep hemispheric ICH with AF should not be offered OAC. Only patients with deep hemispheric ICH at high risk for stroke or embolism or low risk of ICH recurrence might benefit from OAC.1 Before these recommendations are integrated into clinical practice, several assumptions in the decision-analysis model have to be clarified: 1. The origin of ICH is multifactorial. Some underlying pathologies such as vascular malformations or vasculitis are treatable. For others, no causal treatment is available. Cause and treatment influence the recurrence rate of ICH. Thus, in a patient with ICH and indication for OAC, the ICH origin has to be assessed, as does whether there was any kind of treatment. We miss this kind of evaluation in the model assumptions. Possibly, the assumption is that all “secondary” causes of ICH like vascular malformations, tumors, hemorrhagic infarcts, trauma, and vasculitis have been definitively excluded. If this is the case, it should be stated. 2. For patients with lobar ICH, a high annual recurrence rate of 15% is assumed on the basis of 1 study with 71 patients that also included patients with a previous ICH before the index ICH.2 This rate is much higher than the 0.0% to 5.7% reported by other studies.3 …

Matrix metalloproteinase-9 concentration after spontaneous intracerebral hemorrhage.

Matrix metalloproteinases (MMPs) are overexpressed in the presence of some neurological diseases in which blood-brain barrier disruption exists. The authors investigated the MMP-9 concentration in patients after acute intracerebral hemorrhage (ICH) and its relation to perihematomal edema (PHE). Concentrations of MMP-9 and related proteins were determined in plasma by performing an enzyme-linked immunosorbent assay of samples drawn after hospital admission (< 24 hours after stroke) from 57 patients with ICH. The diagnosis of ICH was made on the basis of findings on computerized tomography (CT) scans. The volumes of ICH and PHE were measured on baseline and follow-up CT scans at the same time that the patient's neurological status was assessed using the Canadian Stroke Scale and the Glasgow Coma Scale. Increased expression of MMP-9 was found among patients with ICH. In cases of deep ICH, MMP-9 was significantly associated with PHE volume (r = 0.53; p = 0.01) and neurological worsening (237.4 compared with 111.3 ng/ml MMP-9; p = 0.04). A logistic regression model focusing on the study of absolute PHE volume showed ICH volume as an independent predictor (odds ratio [OR] 3.37; 95% confidence interval [CI] 1.1-10.3; p = 0.03). A second analysis of relative PHE volume (absolute PHE volume/ICH volume) in patients with deep ICH demonstrated that the only factor related to it was MMP-9 concentration (OR 11.6; 95% CI 1.5-89.1; p = 0.018). Expression of MMP-9 is raised after acute spontaneous ICH. Among patients with deep ICH this increase is associated with PHE and the development of neurological worsening within the acute stage.

A mysterious temporal penetrating head wound without fracture

Unwitnessed head injuries are often diagnostic and management dilemmas. Low-velocity penetrating head wounds are rare. This paper describes a case of an accidental low-velocity penetrating head wound through the soft tissue of the temporal region. This lesion resulted in a deep intra-cerebral haemorrhage, after the initial assessment revealed no evidence of skull fracture, missile or missile track. The diagnostic evaluation and medical course of this case are presented. This is the first case in the medical literature of a brain injury by an object that penetrated the calvarium at low velocity but which did not produce a fracture of the skull. The evolving diagnostic dilemma is outlined to its conclusion, through 3 years of follow-up observation.

Predictors of Early Seizures after Stroke

Prevalence and Predictors of Early Seizure and Status Epilepticus after First StrokeLabovitz DL, Allen Hauser W, Sacco RLNeurology 2001;57:200–206BackgroundEarly seizure (ES) has been reported in 2 to 6% of strokes and is a predictor of recurrent seizures. Acute stroke has been reported to cause 22% of all cases of status epilepticus (SE) in adults. The determinants of ES and SE after stroke, however, are not well understood.MethodsAn incidence study was conducted to identify all cases of first stroke in adult residents of northern Manhattan. Cases of ES and SE within 7 days of stroke were identified through medical record review. Statistical analyses were performed by using univariate and multivariate logistic regression models.ResultsThe cohort consisted of 904 patients; ES occurred in 37 (4.1%). The frequency of ES by stroke subtype and location was deep infarct in two (0.6%) of 356, lobar infarct in 20 (5.9%) of 341, deep intracerebral hemorrhage (ICH) in four (4.0%) of 101, lobar ICH in seven (14.3%)...

Predictors of Early Seizures after Stroke

Prevalence and Predictors of Early Seizure and Status Epilepticus after First Stroke Labovitz DL, Allen Hauser W, Sacco RL Neurology 2001;57:200–206 Background Early seizure (ES) has been reported in 2 to 6% of strokes and is a predictor of recurrent seizures. Acute stroke has been reported to cause 22% of all cases of status epilepticus (SE) in adults. The determinants of ES and SE after stroke, however, are not well understood. Methods An incidence study was conducted to identify all cases of first stroke in adult residents of northern Manhattan. Cases of ES and SE within 7 days of stroke were identified through medical record review. Statistical analyses were performed by using univariate and multivariate logistic regression models. Results The cohort consisted of 904 patients; ES occurred in 37 (4.1%). The frequency of ES by stroke subtype and location was deep infarct in two (0.6%) of 356, lobar infarct in 20 (5.9%) of 341, deep intracerebral hemorrhage (ICH) in four (4.0%) of 101, lobar ICH in seven (14.3%) of 49, and subarachnoid hemorrhage in four (8.0%) of 50. SE occurred in 10 (1.1%) patients, representing 27.0% of patients with ES. Diabetes, hypertension, current smoking, alcohol use, age, gender, and race/ethnicity were not significant determinants of ES. In a subgroup of patients who had a National Institutes of Health (NIH) stroke scale (NIHSS) score recorded, NIHSS score was not an independent predictor of ES in multivariate analysis. After accounting for stroke severity, ES was not a predictor of 30-day case fatality. Conclusions Lesion location and stroke subtype are strong determinants of ES risk, even after adjusting for stroke severity. ES does not predict 30-day mortality. SE occurs in more than one fourth of patients with ES.

Molecular signatures of brain injury after intracerebral hemorrhage

The mechanisms of cellular death in the tissue surrounding an intracerebral hemorrhage (ICH) are not defined. To investigate the relationship of markers of excitotoxicity and inflammation to brain injury after ICH. A total of 124 consecutive patients with spontaneous ICH admitted within 24 hours of stroke onset were prospectively investigated. The volumes of the initial ICH, peripheral edema on days 3 to 4, and the residual cavity at 3 months were measured on CT scan. Glutamate, cytokines, and adhesion molecules were measured in blood samples obtained on admission. Stroke severity and neurologic outcome were evaluated with the Canadian Stroke Scale. Poor neurologic outcome at 3 months (Canadian Stroke Scale < 7) was observed in 53 patients (43%). Stroke severity and glutamate concentrations (by each increment of 10 micromol/L, odds ratio 1.23; 95% CI 1.09 to 1.41), but not the initial volume of ICH, were independent predictors of poor outcome. In the multiple linear regression analyses, tumor necrosis factor-alpha concentration was correlated (r = 0.83, p < 0.0001) with the volume of perihematoma edema, and glutamate concentrations were correlated (r = 0.78, p < 0.0001) with the volume of the residual cavity. These same results were observed when lobar (n = 58) and deep (n = 66) ICH were analyzed separately. High plasma levels of proinflammatory molecules within 24 hours of intracerebral hemorrhage onset are correlated with the magnitude of the subsequent perihematoma brain edema, whereas poor neurologic outcome and the volume of the residual cavity are related to increased plasma glutamate concentrations.

Prevalence and predictors of early seizure and status epilepticus after first stroke.

Early seizure (ES) has been reported in 2% to 6% of strokes and is a predictor of recurrent seizures. Acute stroke has been reported to cause 22% of all cases of status epilepticus in adults. The determinants of ES and status epilepticus (SE) after stroke, however, are not well understood. An incidence study was conducted to identify all cases of first stroke in adult residents of northern Manhattan. Cases of ES and SE within 7 days of stroke were identified through medical record review. Statistical analyses were performed using univariate and multivariate logistic regression models. The cohort consisted of 904 patients; ES occurred in 37 (4.1%). The frequency of ES by stroke subtype and location was deep infarct 0.6% (2/356), lobar infarct 5.9% (20/341), deep intracerebral hemorrhage (ICH) 4.0% (4/101), lobar ICH 14.3% (7/49), and subarachnoid hemorrhage 8.0% (4/50). SE occurred in 10 patients (1.1%), representing 27.0% of patients with ES. Diabetes, hypertension, current smoking, alcohol use, age, gender, and race/ethnicity were not significant determinants of ES. In a subgroup of patients who had an NIH stroke scale (NIHSS) score recorded, NIHSS score was not an independent predictor of ES in multivariate analysis. After accounting for stroke severity, ES was not a predictor of 30-day case fatality. Lesion location and stroke subtype are strong determinants of ES risk, even after adjusting for stroke severity. ES does not predict 30-day mortality. SE occurs in more than one-quarter of patients with ES.

Intracerebral hemorrhage: update.

The present review focuses on evolving concepts in the pathogenesis and management of deep and lobar intracerebral hemorrhage subtypes, with particular focus on the relationship between lobar intracerebral hemorrhage, apolipoprotein E subtypes and cerebral amyloid angiopathy; deep intracerebral hemorrhage and the potential interaction between hypertension and low cholesterol; and new concepts in medical and surgical therapy for acute intracerebral hemorrhage.

Does Leukoaraiosis Have Any Significance in TPA Treated Patients?

P56 Background: Leukoaraiosis (LA) has been associated with increased risk of hemorrhage in patients treated with anticoagulants in the SPIRIT, and has been associated with a higher incidence of deep intracerebral hemorrhages (ICH). Individuals with LA have a higher risk of death, and dependency 3 months after cerebral ischemia, recurrent strokes, MI, vascular deaths, and post-stroke dementia. Given the frequency of LA on CT, and its association with increased risk for hemorrhage with anticoagulants, this could represent a predictable risk for stroke patients about to receive TPA. We examined the correlation of LA with stroke severity, risk of hemorrhage, short-term outcome after TPA and associated stroke risk factors. Methods: We evaluated pre-treatment, non-contrast CT scans in patients with Middle Cerebral Artery (MCA) strokes, for the presence and extent of LA using the van Swieten rating system. The NIHSS scores were obtained at baseline and 24 hours. Lesion volumes were determined on a follow-up scan using the (A*B*C)/2 method. Admission systolic BP and glucose were also obtained. Results: A total of 54 TPA-treated patients were studied, aged (mean ±SD) 68 years ±14.9, and baseline NIHSS 16.5 ±6.1 (n=45). Leukoaraiosis was found in 37%(20/54) of all patients on pre-treatment CT scans. No relationship was found between LA presence on pre-treatment CT scans and hemorrhagic transformation, NIHSS scores at baseline and 24 hrs, age, gender, serum glucose, and ASPECT scores. There was, however, a negative correlation between LA scores and ASPECT scores (r=-0.32 p=0.05). Systolic blood pressure correlated significantly (r=0.38, p=0.01) with LA score. There was a non-significant trend towards higher LA scores and increasing age.

Does Leukoaraiosis Have Any Significance in TPA Treated Patients

P56 Background: Leukoaraiosis (LA) has been associated with increased risk of hemorrhage in patients treated with anticoagulants in the SPIRIT, and has been associated with a higher incidence of deep intracerebral hemorrhages (ICH). Individuals with LA have a higher risk of death, and dependency 3 months after cerebral ischemia, recurrent strokes, MI, vascular deaths, and post-stroke dementia. Given the frequency of LA on CT, and its association with increased risk for hemorrhage with anticoagulants, this could represent a predictable risk for stroke patients about to receive TPA. We examined the correlation of LA with stroke severity, risk of hemorrhage, short-term outcome after TPA and associated stroke risk factors. Methods: We evaluated pre-treatment, non-contrast CT scans in patients with Middle Cerebral Artery (MCA) strokes, for the presence and extent of LA using the van Swieten rating system. The NIHSS scores were obtained at baseline and 24 hours. Lesion volumes were determined on a follow-up scan using the (A*B*C)/2 method. Admission systolic BP and glucose were also obtained. Results: A total of 54 TPA-treated patients were studied, aged (mean ±SD) 68 years ±14.9, and baseline NIHSS 16.5 ±6.1 (n=45). Leukoaraiosis was found in 37%(20/54) of all patients on pre-treatment CT scans. No relationship was found between LA presence on pre-treatment CT scans and hemorrhagic transformation, NIHSS scores at baseline and 24 hrs, age, gender, serum glucose, and ASPECT scores. There was, however, a negative correlation between LA scores and ASPECT scores (r=-0.32 p=0.05). Systolic blood pressure correlated significantly (r=0.38, p=0.01) with LA score. There was a non-significant trend towards higher LA scores and increasing age.

Utility of magnetic resonance imaging in acute intracerebral hemorrhage.

The authors determine whether magnetic resonance imaging (MRI) during acute hospitalization for spontaneous intracerebral hemorrhage (ICH) provides new diagnostic information. ICD-9 codes were used to identify consecutive patients with spontaneous ICH at Hermann Hospital, Houston, Texas, between January 1995 and August, 1997. Two investigators employed rigorous criteria to determine whether the MRI findings led to a specific new diagnosis. Two hundred ninety-one patients met inclusion and exclusion criteria. Sixty-seven (23%) patients underwent brain MRI during the acute hospitalization. MRI provided a new diagnosis in 15 of these 67 patients (22%). Amyloid angiopathy and vascular malformation (four each) were the most frequently identified etiologies. The yield of MRI was low in basal ganglia and thalamic hemorrhage. Two of 23 (9%) patients with deep ICH and 13 of 44 (30%) patients with lobar and infratentorial hemorrhage had etiology determined by MRI. Timing of MRI did not affect yield.

Diffusion-weighted magnetic resonance imaging in the early evaluation of corticospinal tract injury to predict functional motor outcome in patients with deep intracerebral hemorrhage.

Diffusion-weighted (DW) magnetic resonance imaging was used to visualize corticospinal tract injury in patients with deep intracerebral hemorrhage (ICH), and the results were used to predict motor impairment of the extremities. Twenty-eight patients with deep ICH (17 men and 11 women, mean age 58+/-14 years) were examined. The volume of the ICH was assessed on initial computerized tomography scans. Twelve patients had ICH volumes of 40 ml or more and were treated surgically, and 16 patients who had an ICH volume of less than 40 ml were treated medically. Initial corticospinal tract injury was classified into four grades according to the anatomical relationship between the corticospinal tract and the ICH on DW images. Motor impairment of both the upper and lower extremities was assessed at admission and 1 month poststroke by using the National Institutes of Health Stroke Scale. The extent of correlation was determined between motor impairment and corticospinal tract injury. Initial corticospinal tract injury was not correlated with the impairment of extremities at admission but was closely correlated with motor impairment of the upper (r = 0.843, p < 0.001) and lower (r = 0.868, p < 0.001) extremities at 1 month poststroke. Impairment of the upper extremities correlated better with anterior than with posterior corticospinal tract injury (r = 0.911 compared with r = 0.600), and impairment of the lower extremities correlated better with posterior than with anterior injury (r = 0.890 compared with r = 0.787). Early evaluation of corticospinal tract injury based on DW imaging can provide predictive value for motor functional outcome in patients with deep ICH.

Alcohol and Stroke: A Community Case-Control Study in Asturias, Spain

The relationship between alcohol consumption and stroke is uncertain. Heavy alcohol consumption has been associated with an increased risk of stroke, while light drinking appears to be protective. However, the evidence is not uniform. We sought to examine the relationship between alcohol consumption and stroke, according to stroke type. We performed a population-based case-control study from September 1990 to December 1991. The study comprised 467 incident cases of stroke and 477 controls aged between 40 and 85. Case was defined following WHO criteria and control was randomly selected from the study base population. Alcohol exposure was obtained by medical interview. We found that consumption of less than 30 g./day of alcohol was protective against all stroke types combined, the multivariated adjusted odds ratio (OR) was 0.58 (95% confidence interval [CI], 0.41–0.83). Moderate alcohol drinking is also protective against all cerebral infarction combined (OR = 0.53; 95% CI, 0.35–0.80) and cortical infarction (OR = 0.40; 95% CI, 0.18–0.86). Drinking up to 30 g/day of alcohol has a borderline protective effect on deep cerebral infarction (OR = 0.40; 95% CI, 0.16–1.02) and has no effect on intracerebral hemorrhage (OR = 0.88; 95% CI, 0.44–1.74). Heavy alcohol drinking, over 140 g/day, is a risk factor for all stroke types combined (OR = 3.2; 95% CI, 1.1–9.7), all cerebral infarction combined (OR = 5.0; 95% CI, 1.5–16.3), small deep cerebral infarction (OR = 9.7; 95% CI, 2.6–36.7), intracerebral hemorrhage (OR = 6.2; 95% CI, 1.3–24.0), and is marginally associated with superficial cerebral infarction (OR = 4.6; 95% CI, 1.0–20.6). The relationship between alcohol and stroke depends on the alcohol dose and the pathology of the disease. Atherosclerosis of the large and medium cerebral arteries is found mainly in superficial cerebral infarction, and this type of stroke shows a J-shaped relationship with alcohol similar to that found in coronary heart disease, suggesting that they are similar diseases. On the other hand, arteriosclerosis of the penetrating arteries has been found in deep cerebral infarction and intracerebral hemorrhage, while atherosclerosis is not prominent. This may explain why alcohol does not have a protective effect on cerebral hemorrhage whereas heavy drinking is a strong risk factor in these two types of stroke.

Intracerebral Hemorrhage in the Rat: Effects of Hematoma Aspiration

Deep intracerebral hemorrhage is associated with considerable mortality and morbidity, but the value of surgical therapy is debatable. The purpose of this study was to evaluate whether aspiration of the hematoma in a rodent model of intracerebral hemorrhage could improve final neurological outcome. Intracerebral hemorrhage was induced in 2 groups of rats by injection of bacterial collagenase into the caudate nucleus. In 1 group of rats, streptokinase was used to lyse the hematoma 4 hours after hemorrhage induction, and the clot was then aspirated. Behavioral function was evaluated repeatedly until the rats were killed 7 weeks after collagenase injection. Histology was used to assess neuronal loss, astroglial proliferation, and overall brain morphology. In a second experiment, brain water was measured at 24 hours. The treated rats performed significantly better than controls on a motor-behavior evaluation on days 1, 2, and 28 after aspiration. Skilled forelimb testing performed for 3 weeks after the global behavior evaluations showed a significant deficit of contralateral forelimb function in both groups, but there was no significant difference between the 2 groups. Neuronal loss in the perihematoma striatum was significantly greater in untreated compared with treated rats. In most rats, structural damage extended into the internal capsule and thalamus. Aspiration of the hematoma after collagenase-induced hemorrhage slightly improved acute functional outcome and reduced neuronal loss from the striatum. Further studies are required to delineate the mechanism of the effect.

High frequency of apolipoprotein E ϵ2 allele is specific for patients with cerebral amyloid angiopathy-related haemorrhage

The apolipoprotein E (APOE) ϵ2 allele is a putative risk factor for cerebral amyloid angiopathy-related haemorrhage. We explored the frequency of the APOE ϵ2 allele in intracranial haemorrhage due to three different pathophysiological mechanisms to determine the specificity of the association. APOE genotypes in 207 autopsies with intracranial haemorrhage (96 subarachnoid haemorrhage, 71 deep intracerebral haemorrhage, 40 cerebral amyloid angiopathy (CAA)-related haemorrhage patients) were compared with 41 autopsy controls without neuropathological abnormalities and 406 living patients admitted to hospital following head injury. As identified previously the ϵ2 allele frequency was significantly over-represented in CAA-related haemorrhage (frequency 0.24, P<0.01); this association was stronger among patients with multiple CAA-related haematomas (0.31). The ϵ2 frequencies of the deep haemorrhage (0.13) and subarachnoid haemorrhage (0.09) groups were not significantly different from the control autopsies (0.07) or live patients (0.08). The findings indicate that the ϵ2 allele is associated with haemorrhage only in the context of cerebral blood vessels laden with amyloid.

Stereotactically guided thrombolysis of deep cerebral hemorrhage: preliminary results.

The neurologic outcome from conventional medical or surgical therapy of intracerebral hemorrhage (ICH) is poor; however, stereotactically guided instillation of thrombolytic agents to dissolve parenchymal clots due to hypertensive hemorrhage has recently produced results equal to or better than those obtained with conventional therapies. To determine whether stereotactic thrombolysis of deep ICH is safe and effective. We administered urokinase to clots in four patients with hypertensive ICH. After the hemorrhage was localized using angiography and computed tomography-assisted stereotactic technique, a ventricular catheter was used to administer urokinase to the clot. Preliminary results showed dramatic reduction in clot volume within 48 hours of initiating treatment and modest clinical improvement in all four patients. No further hemorrhages were seen after treatment. Three patients ultimately died of non-neurologic causes. With careful patient selection, stereotaxy-assisted thrombolytic therapy may be an advance in the treatment of certain cases of ICH.

Anticardiolipin Antibodies: Clinical Characteristics of Antibody-Positive Patients with Recent Cerebrovascular Events

Using a solid-phase enzyme-immunosorbent assay in sera of 84 patients with recent transient ischemic attack, ischemic stroke, or deep intracerebral hemorrhage, anticardiolipin antibodies (ACLA) were found in 34 cases (40%; 95% confidence interval = 30–51 %). Thirteen patients had class IgM antibodies, 11 had class IgG antibodies, and 10 had antibodies belonging to both classes. Patients with ACLA more frequently had histories of previous cerebrovascular events (CVE) (44 vs. 16%) and clinical features of occlusive peripheral vascular disease (76 vs. 38%) than patients without antibodies. The distribution of other stroke risk factors was similar in both groups. Further clinical observations are needed to establish the significance of ACLA in the pathogenesis of CVE.