A case of hypertensive intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion]

We report a case of intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion. The patient was a 54-year-old man, who developed a small cerebral hemorrhage in the left internal capsule. He was admitted with mild right hemiparesis to out hospital. Left carotid angiography showed an occlusion at the origin of the internal carotid artery. Right cerebral angiography revealed the slow filling of cerebral arteries of left hemisphere by the cross flow. He was treated conservatively. Two days after admission, the neurological examination revealed no notable abnormalities. The etiology of hemorrhage of this case is presumed as the arterial necrosis due to hypertension. There has been no report on the intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion. Our case suggests that the volume and enlargement of cerebral hemorrhage may be influenced by cerebral perfusion pressure.     

Massive cerebral air embolism after cardiopulmonary resuscitation.

We report a case of massive intracerebral air embolism after cardiopulmonary resuscitation in a patient with a fatal head injury. There was no pneumothorax or extravascular pneumocephalus, however, air was found in the internal carotid artery. Massive cerebral air embolism may occur after entrance of air into the circulatory system via ruptured pulmonary vessels during cardiopulmonary resuscitation.     

Acute Spontaneous Subdural Hematoma due to Rupture of a Tiny Cortical Arteriovenous Malformation

Acute subdural hematoma (SDH) of arterial origin is rare, especially SDH associated with an arteriovenous malformation (AVM) is extremely rare. The authors report a case of acute spontaneous SDH due to rupture of a tiny cortical AVM. A 51-year-old male presented with sudden onset headache and mentality deterioration without a history of trauma. Brain CT revealed a large volume acute SDH compressing the right cerebral hemisphere with subfalcine and tentorial herniation. Emergency decompressive craniectomy was performed to remove the hematoma and during surgery a small (5 mm sized) conglomerated aciniform mass with two surrounding enlarged vessels was identified on the parietal cortex. After warm saline irrigation of the mass, active bleeding developed from a one of the vessel. The bleeding was stopped by coagulation and the vessels were removed. Histopathological examination confirmed the lesion as an AVM. We concluded that a small cortical AVM existed at this area, and that the cortical AVM had caused the acute SDH. Follow up conventional angiography confirmed the absence of remnant AVM or any other vascular abnormality. This report demonstrates rupture of a cortical AVM is worth considering when a patient presents with non-traumatic SDH without intracerebral hemorrhage or subarachnoid hemorrhage.     

Primary intracerebral hemorrhage and heart weight: a clinicopathologic case-control review of 218 patients

The mean heart weight as a measure of arterial hypertension of patients who died from spontaneous intracerebral hemorrhage (primary intracerebral hemorrhage or PIH) was compared with that of controls from the same autopsy population. All patients with valvular or congenital heart disease or disease processes associated with myocardial infiltration were excluded. In 206 cases of PIH, hypertension was diagnosed if heart weight greater than or equal to the mean heart weight of autopsy controls for either sex, plus 1.5 SD. Only 94 (46%) of all cases of PIH were hypertensive by this criterion. However, hypertension was five times more frequent in the cases than in the controls. The site of hemorrhage was clearly defined in 183 cases (88.8%) only. Of these, 80 (43.7%) had lobar hemorrhage and 69 (37.7%) bled in the basal ganglia. Only 26 cases (12.6%) had evidence of previous cerebral or myocardial infarction and there was no instance of previous intracerebral hemorrhage. These data show that arterial hypertension was present in about half the cases of PIH and suggest that other as yet unidentified risk factors for PIH may be more common than is realized. Patients who died from PIH had been healthy all their lives with no evidence of cardiovascular or cerebrovascular disease, and the PIH was their first evidence of disease.     

A change in injured corticospinal tract originating from the premotor cortex to the primary motor cortex in a patient with intracerebral hemorrhage

Many studies have attempted to elucidate the motor recovery mechanism of stroke,but the majority of these studies focus on cerebral infarct and relatively little is known about the motor recovery mechanism of intracerebral hemorrhage.In this study,we report on a patient with intracerebral hemorrhage who displayed a change in injured corticospinal tract originating from the premotor cortex to the primary motor cortex on diffusion tensor imaging.An 86-year-old woman presented with complete paralysis of the right extremities following spontaneous intracerebral hemorrhage in the left frontoparietal cortex.The patient showed motor recovery,to the extent of being able to extend affected fingers against gravity and to walk independently on even ground at 5 months after onset.Diffusion tensor imaging showed that the left corticospinal tract originated from the premotor cortex at 1 month after intracerebral hemorrhage and from the left primary motor cortex and premotor cortex at 5 months after intracerebral hemorrhage.The change of injured corticospinal tract originating from the premotor cortex to the primary motor cortex suggests motor recovery of intracerebral hemorrhage.     

Hypertension as a risk factor for spontaneous intracerebral hemorrhage

To better define the etiologic importance of hypertension for spontaneous intracerebral hemorrhage, hospital records were studied for all patients sustaining intracerebral hemorrhage during 1982 in the Cincinnati metropolitan area. Hypertension pre-dating the hemorrhage was present in 45% (69 of 154), as determined by history. A more inclusive definition of hypertension, combining those with a positive history with those found to have left ventricular hypertrophy by electrocardiogram or cardiomegaly by chest radiography, applied in 56% (87 of 154). The cases were compared to controls with and without hypertension derived from the NHANES II study of blood pressure (n = 16,204) to determine relative risk. For the presence of hypertension by history, the relative risk of intracerebral hemorrhage was 3.9 (95% confidence interval, 2.7 to 5.7). For the inclusive definition of hypertension, the relative risk was 5.4 (3.7 to 7.9). Relative risk was also determined for hypertension in blacks (= 4.4), age greater than 70 (= 7), prior cerebral infarction (= 22), and diabetes (= 3). We conclude that the term "hypertensive hemorrhage" should be used very selectively, particularly in whites, and propose that hypertension be viewed as one of several important risk factors for spontaneous intracerebral hemorrhage.     

Pseudoephedrine-induced hemorrhage associated with a cerebral vascular malformation

BACKGROUND: Sympathomimetic-related intracerebral hemorrhage is well-documented. Most cases are associated with phenylpropanolamine use. CASE REPORT: We report a case of intracerebral hemorrhage occurring in a middle-aged man who suffered from chronic sinusitis and had been ingesting pseudoephedrine daily for one year. This patient was previously well with no known cardiovascular risk factors. Clinical examination revealed no evidence of vasculitis nor coagulopathy and initial neuroimaging (i.e., computed tomography, angiography, magnetic resonance imaging) demonstrated no features consistent with aneurysm, arteriovenous malformation (AVM), cavernoma, nor cerebral metastases. A follow-up cerebral angiogram demonstrated a small AVM arising off a branch of the pericallosal artery and a small arteriovenous fistula arising off the costal marginal branch. The AVM was embolized without incident, however, the AVF was not accessible. CONCLUSIONS: Sympathomimetics have long been associated with intracerebral hemorrhage. Since 1979, over 30 published case reports have documented the relationship between phenylpropanolamine and stroke. Only one report links phenylpropanolamine consumption to an intracerebral hemorrhage in a patient with an AVM. There is a paucity of literature etiologically inculpating other ephedra alkaloids in the causation of intracerebral hemorrhage. This is a case of pseudoephedrine-induced intracerebral hemorrhage in a patient with an underlying vascular malformation.     

Anticoagulant-related hemorrhage in acute cerebral embolism

Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.     

Kinetics of Elimination and Acute Consequences of Cerebral Air Embolism

The pathophysiology of arterial air embolism inducing brain injuries remains unclear. Previous experiments demonstrated the usefulness of computed tomography (CT) in the detection of air emboli in canine brain. This canine study investigates CT's ability to detect small air bubbles and to determine the kinetics of air elimination from cerebral arteries and it's relationship with clinical, electroencephalographic (EEG), and histological manifestations. CT detects small air embolism, and intracerebral air volume strongly correlates with injected air dose (r² = 0.86, p = 2 × 10 ³) Air clearance time significantly depends on intracerebral air volume (r² = 0.86, p = 0 04) and on the number of bubbles (r² = 0.71, p = 0 03), whereas half–life of air elimination does not. No relationship was found between injected air dose, air clearance time, intracerebral volume of air, and clinical, EEG, and histological findings. The data indicate that CT accurately detects small air bubbles in the early course of cerebral air embolism, that air elimination from cerebral arteries follows a first–order compartment model, and that early CT findings do not correlate with clinical, EEG, and histological manifestations.     

脑出血并脑微出血的临床与影像特征

目的 探讨脑出血并脑微出血的临床与影像特点.方法 分析16例自发性脑出血并脑微出血患者的临床资料与MRI-SWI影像表现.结果 患者平均年龄67.9岁.14例患者合并高血压病,9例为首次发病的脑出血患者,7例为再发脑出血患者.再发脑出血患者SWI检查全部发现脑微出血,其中6例(85.7％)微出血同时累及双侧半球多个脑叶及深部脑组织.首发脑出血组合再发脑出血组患者脑微出血的病灶数量均数分别为5.22±2.82和9.71±3.50,2组间微出血病灶数量存在统计学差异(P=0.013).结论 脑微出血与自发性脑出血关系密切,较多的脑微出血病灶可能预示着再发脑出血的风险增高.     

Intracerebral hemorrhage in two patients with Down’s syndrome and cerebral amyloid angiopathy

Cerebral amyloid angiopathy (CAA) is an important cause of spontaneous intracerebral hemorrhages in the elderly and is often seen in the brains of patients with Alzheimer’s disease, Down’s syndrome (DS), and hereditary cerebral hemorrhage with amyloidosis of the Dutch type. We report two patients with DS and extensive CAA who died of intracerebral hemorrhage; only two other such case reports exist in the literature. We believe the incidence of such cases is higher than is reported and that the likelihood of hemorrhage in the setting of CAA is independent of the patient’s underlying disease. Received: 27 March 1997 / Revised, accepted: 8 August 1997     

非高血压性自发性颅内出血病因及治疗研究

目的 分析非高血压性自发性颅内出血的病因,并对其治疗进行探讨.方法 对60例非高血压性自发性蛛网膜下腔出血(SAH)和42例脑实质内出血患者进行分析,均行DSA检查并采取相应治疗措施.结果 60例SAH的患者中,动脉瘤52例(86.67%),脑动静脉畸形(CAVM)1例(1.67%),动脉瘤合并CAVM 1例(1.67%),血液病1例(1.67%),造影阴性5例(83.33%);在42例脑实质出血(包括脑室出血)的患者中,动脉瘤15例(35.71%),CAVM 9例(21.43%),moyamoya病3例(7.14%),右侧椎动脉变细1例,海绵窦血栓性静脉炎1例,13例(30.95%)造影未发现异常.结论非高血压性SAH的主要原因为动脉瘤破裂,自发性脑实质出血的主要原因为动脉瘤和脑动静脉畸形破裂,临床DSA检查是确诊其病因的重要手段之一,自发性颅内出血病因的早期诊断和对因治疗具有重要临床意义.     

Early seizures following intracerebral hemorrhage: implications for therapy

Seizures occurred in 19 of 112 patients (17%) with nontraumatic, supratentorial intracerebral hemorrhage (ICH). All seizures occurred at ICH onset; patients without seizures at hemorrhage onset remained seizure-free until the last recorded follow-up. Seizures were significantly associated with extension of blood into the cerebral cortex. We found no association between seizures and hemorrhage size or the presence of subarachnoid or intraventricular blood. These data suggest that (1) seizures, in ICH, occur at hemorrhage onset, (2) patients without seizures at hemorrhage onset are at very low risk for subsequent seizures during their hospitalization, (3) hemorrhage involving the cerebral cortex, regardless of site of origin, predisposes to seizures, and (4) the prophylactic use of anticonvulsants in the acute management of these patients appears unwarranted, especially in patients without cortical extension.     

植入异物法构建自发性脑出血实验动物模型

目前对于自发性脑出血的病理生理机制及治疗方法的研究大多基于动物试验。国内外不同实验室已经针对多种动物制作了实验性脑出血模型。根据其脑内移植的组织不同，分为缺血诱发脑出血、外伤导致脑出血、自发性脑出血和颅内植入异物导致脑出血4类。颅内植入异物导致脑出血根据植入异物的不同，又分为植入惰性物质导致的脑出血、植入生物制剂诱导脑出血、植入自体动脉血模拟脑出血3种。文章归纳总结实验性脑出血动物模型总类、制作方法和特点。     

Intracerebral hemorrhage due to cerebral amyloid angiopathy after head injury: Report of a case and review of the literature

Cerebral amyloid angiopathy (CAA) is an important cause of spontaneous intracerebral hemorrhage in the elderly. A few case reports of CAA‐related intracerebral hemorrhage after head injury, usually following a fall, have been published. More rarely, it may occur in the setting of a traffic accident, with only four cases having been reported. We describe a case of CAA‐related intracerebral hemorrhage in an 88‐year‐old man injured in a road traffic accident. The patient died 14 h after the accident. Autopsy examination revealed a left frontoparietal hematoma and CAA of most of the small leptomeningeal and cortical arteries, as well as several capillaries, predominantly in the parietal and occipital lobes. Except for bruises in the frontal and zygomatic regions, elbow and forearm, to the left, there were no skull fractures or traumatic lesions in other parts of the body. We review the literature on CAA‐related intracerebral hemorrhage associated with head injury. CAA‐related intracerebral hemorrhage after head injury may occur due to a minor trauma, minor and severe falls, or in the setting of a traffic accident. However, even in this last condition, it seems to happen mostly in patients who had a mild to moderate head injury. These facts show that replacement of the contractile components of the arterial tunica media by amyloid renders the affected cerebral blood vessels more vulnerable to head injury associated with acceleration and deceleration, independently of the severity of the dynamic loading acting on the head.     

Unexpected air embolism during an aneurysmal operation in supine position--a case report and a speculation about its pathogenesis]

The occurrence of air embolism in supine position operation is extremely rare. We reported a case of air embolism during the operation of a ruptured middle cerebral artery aneurysm in supine position. A 58-year-old woman was admitted to our hospital in semicomatous state. A CT scan revealed diffuse subarachnoid hemorrhage. Cerebral angiogram showed a middle cerebral artery aneurysm. Massive pinkish foamy sputum and butterfly shadow on chest x-ray strongly suggested an association of neurogenic pulmonary edema (NPE). Barbiturate therapy and controlled ventilation with positive end-expiratory pressure (5cmH2O) were started. Her airway pressure was about 35cmH2O. Decrease of pinkish foamy sputum and an improvement of chest x-ray findings on the next day encouraged us to perform a clipping operation. Just before a clip application, air bubbles were observed to pass through the middle cerebral artery under the microscope. Subsequently cardiac standstill was brought out. Fortunately, she was resuscitated, and a clip application was finished. A postoperative CT scan revealed an infarction in the middle cerebral artery area. A postoperative cerebral angiogram showed occlusion of a temporal branch of the right middle cerebral artery, P1 portion of the left posterior cerebral artery, and the right superior cerebellar artery. We speculated that high endotracheal pressure brought out pulmonary alveolar rupture, and in spite of supine position operation massive air, which flowed into systemic circulation from ruptured alveoli, caused cerebral infarction and cardiac arrest. We consider that unrecognized air embolism might be the one of the factors influencing the prognosis of severe subarachnoid hemorrhage, especially in the cases associated with neurogenic pulmonary edema.     

Prognostic parameters in spontaneous intracerebral hematomas with special reference to anticoagulant treatment

We examined a series of 200 consecutive patients with spontaneous intracerebral hematoma clinically and by computed tomography, excluding patients with trauma, aneurysm, or tumor. Hematoma volume varied from 1 to 230 (average 35) ml, and overall mortality was 30% (60 patients). Of the 200 patients, 14% (28) were receiving anticoagulants; among these 28 patients hematoma volume averaged 72 ml and mortality 57% (16 patients). The 140 survivors were followed for 2-24 months. Our findings indicate that anticoagulation therapy after previous cerebral infarction or embolism of cardiogenic origin did not predispose to intracerebral hemorrhage. Prognosis was poor when the initial level of consciousness was low and the hematoma volume exceeded 50 ml in combination with dilatation of the contralateral ventricle. An intracerebral hematoma of greater than 80 ml volume was always fatal, regardless of therapy. With volumes of 40-80 ml, early surgical evacuation of the lobar hematoma may improve outcome.     

Massive pontine hemorrhagic transformation associated with an anticoagulant for basilar artery occlusion

Symptomatic hemorrhagic transformation is common in supratentorial and cerebellar infarction, but is rare in brainstem infarction. It is seldom reported in basilar artery occlusion. Although early arterial recanalization by thrombolytic agent has became the new trend of treatment, for some neurologists anticoagulant is still a conventional alternative treatment of basilar artery occlusion, especially in longer-existing ischemic deficits. We report a case of massive pontine hemorrhage associated with enoxaparin (low-molecular-weight heparin) treatment for basilar artery occlusion. On the basis of the clinical information and neuroimaging, an embolism was the most likely cause of stroke. The case presented herein adds massive pontine hemorrhagic transformation to the list of possible complications of anticoagulants for basilar artery occlusion. Apart from no evidence-based benefit in treatment of basilar artery occlusion, anticoagulant may contribute to devastating hemorrhagic transformation.     

Small vessel pathology and cerebral hemorrhage

Spontaneous intracerebral hemorrhage may be due to two main arteriolopathies: HTA and age-related small vessel disease and cerebral amyloid angiopathy. Historical study of the CHARCOT-BOUCHARD microaneurysm controversy leads to conclude that altered arterioles may be ruptured with or, probably more often, without microaneurysms. Recent neuroradiological studies with gradient-echo T2*W MR imaging have confirmed a classical neuropathological fact: there is a strong correlation between subcortical ischemic lesions (lacune, leukoaraiosis) and subcortical hemorrhage (hematomas, microbleeds). Sporadic Cerebral Amyloid Angiopathy is the first cause of spontaneous intracerebral hemorrhage after 70 years. Hemorrhages are lobar, typically recurrent and/or associated with cortical microbleeds at T2*W imaging.     

An autopsy case of subarachnoid and intracerebral hemorrhage and necrotizing angitis associated with methamphetamine abuse

We report an autopsy case of methamphetamine-related intracranial hemorrhage and vasculitis. The possible relationship between drug usage and the occurrence of intracranial bleeding and cerebral vasculitis in such patients is discussed. A 22-year-old woman died after an intravenous injection of unknown dose of methamphetamine. A computed tomography head scan demonstrated massive subarachnoid hemorrhage and hematoma in corpus callosum. Cerebral angiography revealed nonfilling of bilateral intracranial carotid arteries and extravasation of contrast medium from right pericallosal artery which was visualized retrogradely via vertebral artery. Postmortem studies showed cerebral edema, subarachnoid and intracerebral hemorrhage, and intracranial vasculitis in the absence of aneurysm, arteriovenous malformation or chronic hypertension. Histological findings of necrosis of blood vessel walls with destruction of the elastica and smooth muscle layer, and without leukocytotic infiltration of the blood vessel walls were observed in order of anterior cerebral, middle cerebral, vertebral, posterior cerebral and basilar arteries. These angiographic and histological evidence suggests that such hemorrhage results from the development of fibrinonecrosis in the large intracerebral vessels, in addition to a sudden rise in blood pressure.