ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Within 3 weeks of the event, 505 patients with cerebral infarction, minor or major stroke, were randomly assigned to treatment with acetylsalicylic acid (ASA) 1.5 g/day or placebo in a double—blind clinical trial with a follow—up of 2 years in all patients. Primary events were considered to be recurrent stroke or death; secondary events, myocardial infarction and transient ischemic attack. There was no difference in stroke recurrence rate in the ASA and placebo groups (12 and 13%, respectively), nor was there any significant difference in the rate of recurrent stroke or death, first event counted (23% in the ASA and 22% in the placebo group). The risk of transient ischemic attack and myocardial infarction was not reduced in the ASA group. In the present study there was no prophylactic effect of high—dose ASA after cerebral infarction. A compilation of the major trials of ASA after transient ischemic attack and cerebral infarction is presented. (Stroke1987; 18:325–334)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

A 7‐year prospective study of a cohort of 107 neurologically normal elderly hypertensive volunteers (mean age, 65.8 ± 8.3 years) was undertaken to investigate the predictive validities of additional risk factors for atherothrombotic cerebrovascular disease including stroke, transient ischemic attacks, reversible ischemic neurological deficits, and multi—infarct dementia. This longitudinal study has been in progress now for 7 years with a mean follow—up interval of 50.12 ± 5.76 months. Among 107 formerly symptom—free, normal hypertensive volunteers, 25 (23%) have developed cerebrovascular disease, 7 (6.5%) sustained a stroke, 10 (9.3%) developed multi—infarct dementia, and 18 (16.8%) have transient ischemic attacks. None have suffered intracranial hemorrhage. Mean gray matter cerebral blood flow (CBF) values measured at the initial visit were sensitive predictors of cerebrovascular disease. Eight of 16 hypertensives (50%) with initial CBF values below 60.0 ml/100 g/min now exhibit signs and symptoms of cerebrovascular disease, while 11 of 43 hypertensives (25.6%) with initial CBF values between 60.1 and 69.9 ml/100 g/min and only 6 of 48 (12.5%) with initial CBF levels above 70.0 developed cerebrovascular disease. Incidence of cerebrovascular disease among cigarette smoking hypertensive volunteers (32.5%) was significantly greater than among nonsmokers (17.2%). (Stroke1987;18:335–341)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

True, three—dimensional proton nuclear magnetic resonance imaging at 0.147 tesla was performed postmortem on 2 patients embodying various stroke syndromes, including chronic (4 and 15 years) infarction, subacute (within 1 week) bland infarction, acute (2 days) hemorrhagic Infarction, and hematoma secondary to ruptured aneurysm. A third patient, with subcortical arteriosclerotic encephalopathy, so—called Binswanger's disease, was examined antemortem using a 0.6 tesla scanner. Nuclear magnetic resonance images were reconstructed at levels matching the pathologic specimens. Qualitative and, when available, quantitative comparisons between the results of nuclear magnetic resonance imaging and pathology were carried out. Areas of qualitatively prolonged Tl and T2 relaxation times on nuclear magnetic resonance imaging were more extensive than the corresponding areas of chronic infarction noted pathologically and were determined to be infarcts plus the adjacent areas of Wallerian degeneration. Hemorrhagic infarction, without evidence of blood on computed tomography, was found to have mildly prolonged Tl and T2 relaxation times, between those of normal brain and chronic infarction; a 10‐day—old hematoma had a very short Tl, slightly shorter than that of white matter, and a mildly prolonged T2, with values between those of white and gray matter. Subcortical arteriosclerotic encephalopathy was found to have areas of prolonged Tl and T2 relaxation times involving almost the entire white matter of the corona radiata. (Stroke1987;18:342–351)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The therapeutic efficacy of prostacyclin in nonhemorrhagic cerebral infarction was assessed in a placebo—controlled double—blind trial. A total of 80 patients with stroke onset within 24 hours were randomized into placebo (37 patients) and prostacyclin (43 patients) groups. Demographic data and risk factors were comparable. Patients in the prostacyclin group received a continuous i.v. infusion of prostacyclin at an average rate of 8.5 ng/kg/min for an average of 64 hours. The placebo group received vehicle only in a similar fashion. During treatment hemodynamic changes were more prominent in the patients receiving prostacyclin and included reduction of systolic and diastolic blood pressure and increase in pulse rate. In contrast there was only a slight (but significant) reduction of diastolic blood pressure in the placebo group. Neurologic deficit scores were determined on admission, at Day 3, and at Weeks 1,2, and 4. Mean neurologic deficit scores upon entry were comparable in the placebo and prostacyclin groups, and a significant improvement in the score for neurologic deficit was noted in both. The placebo group tended to fare better throughout the study, with a significant difference in neurologic deficit score favoring the placebo group at Week 2 (p = 0.0048). Two patients in the placebo and one in the prostacyclin group died. The only difference in adverse reactions was flushing (6 patients in prostacyclin vs. 0 in placebo group, p < 0.05). The results of this study suggest a lack of therapeutic efficacy of prostacyclin in a defined population of patients with nonhemorrhagic cerebral infarction.Stroke1987;18:352–358)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To assess the role of acute alcohol ingestion as a risk factor for cerebral infarction, we administered a pretested questionnaire to 205 middle—aged and elderly acute ischemic stroke patients and 410 outpatient controls matched by age, sex, race, and method of hospital payment. Paired Mantel—Haenszel analysis revealed that alcohol ingestion within 24 (p = 0.07) and 72 (p = 0.001) hours of stroke onset and medical histories of smoking (p < 0.0001), hypertension (p < 0.001), and transient ischemic attacks (p = 0.051) were more common among stroke index cases than controls. Matched multiple logistic analysis revealed that both hypertension (p < 0.05) and smoking (p < 0.05) were independently associated with stroke, while alcohol consumption was not. In analyses to assess the possibility of mutual confounding effects of independent variables, the effect of alcohol ingestion was lost when adjusting for smoking. We conclude that acute alcohol ingestion is not an independent risk factor for cerebral infarction in middle—aged and elderly patients. The apparent association between alcohol ingestion and ischemic stroke may be the result of the confounding effects of smoking. (Stroke1987; 18:359–364)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following subarachnoid hemorrhage using a uniform management protocol over a 24‐month period. One hundred eighteen consecutive patients were admitted to the neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not attributed to trauma, tumor, or vascular malformation (113 patients had aneurysms). Early surgery was performed whenever possible, and hypertensive hypervolemk hemodilution therapy was instituted at the first sign of clinical vasospasm. Forty—two patients (35.6%) developed characteristic signs and symptoms of clinical vasospasm with angiographic verification of spasm in 39 cases. All patients with clinical vasospasm received hypervolemic hemodilution therapy aiming for a hematocrit of 33–38%, a central venous pressure of 10–12 mm Hg (or a pulmonary wedge pressure of 15–18 mm Hg), and a systolic arterial pressure of 160–200 mm Hg (120–150 mm Hg for undipped aneurysms) for the duration of clinical vasospasm. Over the course of treatment, 60% of patients with clinical vasospasm had sustained improvement by at least 1 neurologic grade, 24% maintained a stable neurologic status, and 16% continued to worsen. At the end of hyper volemic hemodilution therapy, 47.6% had become neurologically normal, 33.3% had a minor neurologic deficit, and 19% had a major neurologic deficit or were dead. There were 3 Instances of cardiopulmonary deterioration (7%), all of which were in patients without Swan—Ganz catheters, and all resolved with appropriate diuresis. One patient rebled and died while on hypervolemic hemodilution therapy. Death or major neurologic deficit from clinical vasospasm occurred in < 7% of all patients with subarachnoid hemorrhage. This compares favorably with the morbidity and mortality attributed to vasospasm in recent reports. The authors conclude that early surgery and aggressive management of clinical vasospasm with hypervolemic hemodilution therapy can be accomplished with minimal morbidity. This management strategy may lower the incidence of death and disability from vasospasm after subarachnoid hemorrhage. (Stroke1987;18:365–372)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The results of clinical trials investigating various therapies in acute ischemic stroke have been inconsistent. The effect of glycerol therapy and a combination therapy of glycerol and dextran was evaluated in a double—blind, placebo—controlled study. Repeated neurologic examinations (Day 0, Weeks 1, 6, 12, and 24) according to a modified Mathew score were performed on 62 patients. Statistical analysis showed no superiority of either treatment compared with placebo in acute ischemic stroke. A retrospective estimation of the Type II error of the study yielded approximately p = 0.25. A major side effect was hemolysis in 98% of patients treated with glycerol. (Stroke1987; 18:373–379)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The paramedian diencephalic syndrome is characterized by a clinical triad: hypersomnolent apathy, amnesic syndrome, and impaired vertical gaze. We studied 4 cases with computed tomography evidence of bilateral diencephalic infarctions. Each case began abruptly with hypersomnolent apathy followed by fluctuations from appropriate affect, full orientation, and alertness to labile mood, confabulation, and apathy. Speech varied from hypophonia to normal; handwriting varied from legible script to gross scrawl. Psychological testing revealed poor learning and recall, with low performance scores. In 3 patients the predominant abnormality was in downward gaze. (Stroke1987;18:380–385)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Transient arterial hypertension occurs sporadically following cerebral air embolism and may occur during the acute phase of stroke. This study used an animal model of multifocal cerebral ischemia induced by air embolism and reversed by recompression to assess the effect of induced hypertension on the evoked response recovery, local cerebral blood Bow, intracranial pressure, and brain water in 19 anesthetized dogs (Canis familiaris). Six received 0.4 ml of air via the internal carotid artery, 8 received intracarotid air and 10 /μg/kg norepinephrine to produce transient hypertension, and 5 received intracarotid saline and norepinephrine. The average evoked response recovery in the air—only group was 58.3 ± 7.7% (mean ± SEM) of control after 4 hours of recompression; the air plus hypertension group recovery was 15.4 ±2.7% (p < 0.01). The final evoked response in the dogs receiving hypertension alone did not differ from control values. Seven of 8 dogs in the air plus hypertension group had very low blood flows; only 1 of 4 in the air—only group had very low Bows. The amount of brain water and the intracranial pressure were not detectabh/different at the end of treatment among all 3 groups. These results support a role for endothelial damage produced by air and hypertension in potentiating the process of postischemic hypoperfusion. (Stroke1987;18:386–395)

ISSN:0039-2499    

出版商:OVID    

年代:1987

数据来源: OVID