Results 241 to 250 of about 760,534 (303)

Treatment of cerebral vasospasm with self-expandable retrievable stents: proof of concept

Journal of NeuroInterventional Surgery, 2016
Objective To report our preliminary experience with the use of stent retrievers to cause vasodilation in patients with delayed cerebral vasospasm secondary to subarachnoid hemorrhage.
P. Bhogal, Y. Loh, P. Brouwer, T. Andersson, M. Söderman   +4 more
semanticscholar   +1 more source

Cerebral vasospasm

Current Opinion in Anaesthesiology, 2016
With recent research trying to explore the pathophysiologic mechanisms behind vasospasm, newer pharmacological and nonpharmacological treatments are being targeted at various pathways involved. This review is aimed at understanding the mechanisms and current and future therapies available to treat vasospasm.Computed tomography perfusion is a useful ...
Radhakrishnan Muthuchellappan, Ganne S. Umamaheswara Rao   +1 more
openaire   +2 more sources

Management of cerebral vasospasm

Neurosurgical Review, 2006
Cerebral vasospasm is delayed narrowing of the large arteries of the circle of Willis occurring 4 to 14 days after aneurysmal subarachnoid hemorrhage (SAH). It is but one cause of delayed deterioration after SAH but, in general, is the most important potentially treatable cause of morbidity and mortality after SAH.
openaire   +3 more sources

Phosphodiesterase Inhibitors and Cerebral Vasospasm

Archives of Neurology, 1975
Experimental cerebral vasospasm was studied in cat and monkey models. In the cat, the basilar artery was exposed by a transclival approach and spasm induced by the application of blood to the vessel. In the monkey, spasm was produced by injecting blood into the subarachnoid space.
Eugene S. Flamm, Joseph P. Lin, Jhino Kim, Joseph Ransohoff   +3 more
openaire   +4 more sources

The History of Cerebral Vasospasm

Neurosurgery Clinics of North America, 1990
In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain,
openaire   +3 more sources

The pathophysiology of cerebral vasospasm

British Journal of Neurosurgery, 1995
The current state of knowledge about the physiology, pathology and treatment of cerebral vasospasm is reviewed.
openaire   +3 more sources

The Pharmacology of Cerebral Vasospasm

Pharmacology, 1984
About 3 days after subarachnoid hemorrhage the cerebral blood vessels often undergo a sustained constriction (cerebral vasospasm) which is associated with increased morbidity and mortality. Examination of the literature suggests that interactions of hemoglobin, various prostaglandins, and perhaps some other agents are responsible for this condition ...
openaire   +3 more sources

Results of a national cerebrovascular neurosurgery survey on the management of cerebral vasospasm/delayed cerebral ischemia

Journal of NeuroInterventional Surgery, 2014
Objective Following aneurysmal subarachnoid hemorrhage, cerebral vasospasm/delayed cerebral ischemia accounts for significant morbidity and mortality. In this paper we provide the first glimpse of actual practice in the management of cerebral vasospasm ...
K. Bulsara, Murat Günel, S. Amin‐Hanjani, Peng Roc Chen, E. S. Connolly, Robert M Friedlander   +5 more
semanticscholar   +1 more source

The Nature of Cerebral Vasospasm

Journal of Vascular Research, 1981
The article comprises mainly the personal views of the author on the following aspects of cerebral vasospasm: the definition of vasospasm; historical physiological concepts of cerebral bloodflow regulation; relation of spasm development in cerebral arteries to their functional behavior during regulation of cerebral blood flow; the essence of vasospasm ...
openaire   +3 more sources

Cerebral infarction caused by vasospasm

Medical Journal of Australia, 1982
Fifteen patients with cerebral infarction, the majority of them being under the age of 40 years, were reviewed. Patients in whom an underlying structural disease, such as atheroma or thromboembolism, was suspected on clinical grounds were excluded. On the basis of either a personal or family history of migraine, or a concomitant vascular headache, or a
Richard Burns, Gregory M. Stone
openaire   +3 more sources