Vasospasm As The Sole Cause of Cerebral Ischemia
Vasospasm As The Sole Cause of Cerebral Ischemia
The authors review literature that challenges the view that vasospasm involving large arteries is the exclusive cause of delayed ischemic neurological deficits (DINDs) following subarachnoid hemorrhage. They discuss alternative mechanisms and review the evidence supporting a potential role for thromboembolism. They conclude that vasospasm and thromboembolism play interrelated and additive roles in the development of DINDs, and that this interaction provides opportunities for novel therapeutic approaches.
Whenever a theory appears to you as the only possible one, take this as a sign that you have neither understood the theory nor the problem which it was intended to solve.Karl Popper
Early observations of the cortical surface revealed that electrical, chemical, and mechanical stimuli often caused arterial constriction. Echlin demonstrated in 1942 that this induced vasospasm could in turn impair CBF. In 1949, Robertson investigated cerebral infarction after SAH, and was the first to speculate on arterial spasm as a possible cause. Soon thereafter, a small study of patients with SAH was published in which vasospasm was demonstrated angiographically, and the connection between vasospasm and ischemia after SAH was established.
In subsequent studies, researchers confirmed that angiographically demonstrated vasospasm is quite common after aneurysm rupture and is frequently associated with clinical evidence of cerebral ischemia. In 1965, Kagstrom, et al., demonstrated that vasospasm is usually "de layed" for at least 3 days after the initial SAH. Other investigators have elaborated on the association and temporal relationship between angiographically demonstrated and "clinical" vasospasm. Considerable effort over the years has gone into clarifying the pathogenesis, clinicopathological associations, and treatment of vasospasm. A recent MEDLINE search revealed that since 1953 more than 38,000 scientific articles that address one or more aspects of cerebral vasospasm have been published. This research has established a strong association between angiographically demonstrated and clinically apparent vasospasm.
The authors review literature that challenges the view that vasospasm involving large arteries is the exclusive cause of delayed ischemic neurological deficits (DINDs) following subarachnoid hemorrhage. They discuss alternative mechanisms and review the evidence supporting a potential role for thromboembolism. They conclude that vasospasm and thromboembolism play interrelated and additive roles in the development of DINDs, and that this interaction provides opportunities for novel therapeutic approaches.
Whenever a theory appears to you as the only possible one, take this as a sign that you have neither understood the theory nor the problem which it was intended to solve.Karl Popper
Early observations of the cortical surface revealed that electrical, chemical, and mechanical stimuli often caused arterial constriction. Echlin demonstrated in 1942 that this induced vasospasm could in turn impair CBF. In 1949, Robertson investigated cerebral infarction after SAH, and was the first to speculate on arterial spasm as a possible cause. Soon thereafter, a small study of patients with SAH was published in which vasospasm was demonstrated angiographically, and the connection between vasospasm and ischemia after SAH was established.
In subsequent studies, researchers confirmed that angiographically demonstrated vasospasm is quite common after aneurysm rupture and is frequently associated with clinical evidence of cerebral ischemia. In 1965, Kagstrom, et al., demonstrated that vasospasm is usually "de layed" for at least 3 days after the initial SAH. Other investigators have elaborated on the association and temporal relationship between angiographically demonstrated and "clinical" vasospasm. Considerable effort over the years has gone into clarifying the pathogenesis, clinicopathological associations, and treatment of vasospasm. A recent MEDLINE search revealed that since 1953 more than 38,000 scientific articles that address one or more aspects of cerebral vasospasm have been published. This research has established a strong association between angiographically demonstrated and clinically apparent vasospasm.
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