摘要:

Antifibrinolytic drags reduce the risk of rebleeding during the first 2 weeks after aneurysmal subarachnoid hemorrhage. However, they do not lower overall mortality, largely because of an increased incidence of cerebral ischemia. The usefulness of antifibrinolytic drugs might be increased if a method to prevent or control vasospasm in patients were to be developed. We recently completed late Phase I and Phase II studies of the calcium ion blocking drug nicardipine in 67 patients treated within 1 week of subarachnoid hemorrhage. Of these 67 patients, 42 had delayed operations and were treated concomitantly with the antifibrinolytic drug aminocaproic add (1.5 g/hr) for an average of 6 days before surgery. The outcome of these 42 patients is the subject of this report. Fifteen of 42 patients were treated with the lower dosage levels of nicardipine (0.4–4.5 mg/m2/hr), and 27 patients were treated at the highest dosage level (6.0 mg/m2/hr). Using the World Federation of Neurological Surgeons scale for subarachnoid hemorrhage, at admission 18 patients were Grade 1,15 were Grade II, 6 were Grade HI, and 3 were Grade IV. Five patients (12%) developed clinical signs of deterioration suggestive of cerebral ischemia with concomitant evidence of vasospasm on arteriography. These patients were all treated with hypervolemic hypertensive therapy. Only one patient (2%) developed an Infarction from vasospasm. Two patients developed symptomatic hydrocephalus requiring ventriculoperitoneal shunting, and a third patient required a temporary ventriculostomy. The 3‐month postoperative outcomes were excellent. Three patients (7%) rebled. Three patients died, two from rebleeding of the aneurysm and one who never regained consciousness from the initial hemorrhage. Thirty‐two patients (76%) were Grade I at 3 months after the subarachnoid hemorrhage. These data suggest that the incidence of vasospasm and cerebral ischemia among patients with antifibrinolytic drugs can be lowered by the concomitant use of a calcium ion blocker. Further investigation of this combination of drugs in patients with recent subarachnoid hemorrhage is warranted. (Stroke1988;19:63–67)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In an effort to determine which blood elements play a critical role in the development of cerebral vasospasm, adult cats were subjected to prepontine injection of either autogenous whole blood or erythrocyte‐free blood containing latex beads as a substitute morphologic marker. Seven or 10 days later the cats were anesthetized and perfused with fixative, and the basilar arteries were prepared for light and electron microscopy. Successful clot deposition was confirmed by the presence of numerous erythrocytes or latex beads within the adventitia of vessels. In agreement with previous studies, instillation of whole blood produced luminal narrowing associated with profound ultrastructural changes in all layers of the vascular wall. No significant alterations, however, occurred in arteries bathed in erythrocyte‐free blood. These findings suggest first, that erythrocytes are essential for the development of the vasculopathy associated with chronic cerebral vasospasm, and second, that the role, if any, of other blood elements is not autonomous. (Stroke1988;19:68–72)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Diltiazem given 48 hours before experimental subarachnoid hemorrhage protects the cerebral vasculature of monkeys against the widespread cerebrovascniar spasm seen on angiography after 5–6 days and against associated neurologic defects. In vitro examination of the cerebral arteries from treated monkeys shows that compared with untreated animals, the functional changes in the vascular smooth muscle cells, the increase in arterial wall stiffness, and the decrease in contractility, all of which were prominent in untreated monkeys, were relatively small. Other changes such as abnormal spontaneous myogenic tone, decreased responsiveness to constrictor and dilator nerve activation, and other indexes of neuronal function were little influenced by the drug. We suggest that chronic cerebrovasospasm may be initiated by the combined action of exceptionally high concentrations of a number of putative spasmogens causing injury to the larger cerebral arteries. However, the later development of intractable spasm is related to the location of blood clot and to the involvement of the vascular wall in an inflammatory process. The combined insult results in pathologic changes in the artery wall resulting in increased thickness and stiffness. Diltiazem acts on cerebrovascular smooth muscle in lower concentrations than on smooth muscle in other vascular beds, interfering with calcium entry through receptor‐operated and potential‐sensitive channels, and may protect against calcium‐induced cell death through these and additional actions. Protection against early events presumably prevents the genesis of the subsequent chronic state. (Stroke1988;19:73–79)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The nature of α‐adrenergic receptors in human cerebral arteries was characterized, and alteration of these receptors after subarachnoid hemorrhage was examined using a radioligand binding assay. Norepinephrine content of control arteries was also analyzed and compared with that of arteries after subarachnoid hemorrhage. Norepinephrine content in human cerebral arteries in cases of subarachnoid hemorrhage was about 5% of the control group. Specific binding of [3H]yohimbine, a selective α2‐antagonist, to cerebral arteries of the control group indicated two classes of binding sites: high‐affinity sites with KDof 0.5 nM and Bmaxof 18 fmol/mg protein and low‐affinity sites with KDof 29 nM and Bmaxof 248 fmol/mg protein. In cerebral arteries obtained from the subarachnoid hemorrhage group, [3H]yohimbine binding sites were of a single class with KDof 53 nM and Bmax, of 456 fmol/mg protein. These results suggest that sympathetic denervation and subsequent alterations in α2‐adrenergic receptors occurred after subarachnoid hemorrhage in human cerebral arteries. These changes in sympathetic innervation to cerebral arteries were considered to be one of the antecedents of delayed vasospasm after subarachnoid hemorrhage. (Stroke 1988;19:80–83)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

A relation between hypertension, atherosclerosis, and stroke is well documented in humans. We report a similar relation in two hypertensive cynomolgus monkeys with severe cerebral atherosclerosis. In our primate model hypertension is induced by surgical coarctation of the aorta. These monkeys, when fed an atherogenic diet, develop severe cerebrovascular atherosclerosis. In this setting two monkeys developed spontaneous cerebral hemispheric strokes that occurred during treatment of hypertension. Since the strokes were topographically related to severe atherosclerotic narrowing of cerebral arteries and occurred without evidence of either thrombosis or embolization, they are presumed to be related to disturbances of blood flow. In both humans and animals cerebral perfusion is autoregulated to a constant flow over a wide range of mean arterial blood pressures. In hypertension both the upper and lower limits of autoregulation are increased. With treatment of hypertension readaptation to more normal levels is reported to be inconsistent and slow to develop. It is therefore postulated that the strokes in these two monkeys were due to hypoperfusion as a result of the combination of pharmacologic reduction in blood pressure and severe occlusive atherosclerosis. (Stroke1988;19:84–90)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

We studied whether the biomechanical properties of brain play an important role in the development of early ischemic brain edema in cats with middle cerebral artery occlusion. Brain tissue pressure, tissue compliance, and tissue resistance were measured from the gray matter in the core and the periphery of the middle cerebral artery territory for 6 hours after occlusion. Regional cerebral blood flow and water content were also measured from the same areas. Ventricular fluid pressure was recorded. Tissue pressure rose gradually in the core, where flow was 6 ml/100 g/min, over 4 hours and then stabilized. The pressure gradient measured between edematous tissue and ventricular fluid was 5.3 mm Hg. Tissue resistance increased 1 hour after occlusion when water content increased to 10 mg/g. Later, when water content increased by 40 mg/g, tissue resistance decreased and tissue compliance increased significantly. In the periphery, where flow was 17.6 ml/100 g/min, tissue pressure rose slightly while tissue compliance and tissue resistance did not change within 6 hours. Our data indicate that as ischemic injury progresses, edema fluid accumulates in highly compliant brain parenchyma, then migrates through highly conductive tissue into the cerebrospinal fluid spaces, driven by the hydrostatic pressure gradient between the edematous tissue and the cerebrospinal fluid. (Stroke1988;19:91–97)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Acute transient amnesia has not been previously associated with vertebral artery dissection. We describe two men with acute onset of dense anterograde amnesia and partial retrograde amnesia resulting from spontaneous vertebral artery dissection. Both amnesic syndromes completely resolved with conservative management. (Stroke1988;19:98–101)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Carotid body tumors are an unusual cause of transient ischemic attacks. The cases reported in the literature have been limited to the postoperative period. We report a patient with bilateral carotid body tumors and transient ischemic attacks as the presenting syndrome. A low‐perfusion state could explain his symptomatology. (Stroke1988;19:102–103)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Pure motor hemiplegia is the most commonly encountered lacunar syndrome and is classically associated with small infarctions in the contralateral internal capsule or basis pontis. Pure motor hemiplegia has also been observed secondary to a wide variety of other vascular and nonvascular focal central nervous system processes. We describe a patient with pure motor hemiplegia associated with a saccular basilar artery aneurysm causing a lacunar infarction of the cerebral peduncle. (Stroke1988;19:104–107)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Forty‐five patients with symptomatic (20 with transient ischemic attack, 25 with minor stroke)⩾ 75% stenosis of the cervical internal carotid artery had no endarterectomy and received only medical therapy because the surgical risks (severe cardiac disease, chronic obstructive pulmonary disease, hypertension or diabetes with systemic complications, aortic aneurysm) were believed to be unacceptable. During follow‐up (mean 48 months), occlusion of the internal carotid artery developed without symptoms in two patients and with symptoms in three patients. The cumulative stroke and/or death rate was 24% at 2 years and 50% at 6 years. The ipsilateral infarct rate was 10% after the first year, but decreased markedly thereafter (2.4% per year), and one third of these infarcts were probably lacunes due to hypertensive small vessel disease. Overall, stroke related to previously symptomatic internal carotid artery stenosis was not the major problem during follow‐up but was largely overcome by other strokes and cardiac death. (Stroke1988;19:108‐lll)

ISSN:0039-2499    

出版商:OVID    

年代:1988

数据来源: OVID