Abstract
Vasospasm is a secondary complication of subarachnoid hemorrhage (SAH), occurring 4–14 days after the bleeding [18,42]. Angiographic investigations have revealed the incidence of “angiographic vasospasm” to be 30%–70% [3,14,17,25,35, 36,42]. This correlates well with the blood flow velocity changes in the basal arteries detected by transcranial Doppler sonography (TCD). A velocity increase of more than twice the baseline value as a sign of a marked vessel diameter reduction is found in TCD in about 70% of patients [1,18–20,37]. Angiographic vasospasm and “Doppler sonographic vasospasm” do not correlate with the clinical symptoms. Only 15%–30% [11,12,21,22] of patients with vasospasm after aneurysmal SAH develop a “clinical or symptomatic vasospasm” with transient or permanent delayed ischemic deficits (DIDs).
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Gilsbach, J., Härders, A. (1990). Prevention of Vasospasm with Nimodipine. In: Bushe, KA., Brock, M., Klinger, M. (eds) Stabilizing Craniocervical Operations Calcium Antagonists in SAH Current Legal Issues. Advances in Neurosurgery, vol 18. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75283-4_43
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DOI: https://doi.org/10.1007/978-3-642-75283-4_43
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