Morphologic Manifestations of Vascular Injury

Most researchers agree that severe structural damage occurs in the arterial wall following SAH (18-28). Subendothelial edema develops, the endothelial layer and internal lamina are disrupted, and vascular SMCs (VSMCs) infiltrate the endothelium. Endothelial cell vacuolization and desquamation can be observed, followed by progressive intimal fibrosis and proliferation (Fig. 1) (21). The medial layer also exhibits SMC proliferation, vacuolization, and a generalized loss of myofilaments (phenotypic modulation). Cell necrosis and an increase in collagen in the extracellular matrix are well described. These structural changes are progressive, correlate with the development of angiographic vasospasm, and clearly represent a significant injury or vascular response to injury (24,27,29).

The importance of these arterial morphologic changes in the pathogenesis of clinical vasospasm is not clear, however. Some authors argue that structural changes, in particular intimal proliferation, generally tend to follow the angiographic phase of vasospasm (30,31). Nevertheless, although some microscopic manifestations of arterial injury might not be evident during the early phases of vasospasm, precursor events, such as subtle phenotypic modulation of VSMCs, including calcium sensitization and switching of contractile VSMC to a noncontractile state, might occur (32,33 ).

The mechanism of injury is not entirely clear either but is almost certainly multifactorial. The extent of the injury is related to the size of the blood clot, and reducing the clot size by either irrigation or fibrinolytic therapy reduces the severity of vasospasm (34-36). The adventitial layer of the cerebral arteries is thin and lacks an external elastic lamina and vasavasorum. Cerebral arteries probably receive their nourishment from the CSF, which penetrates the adventitia through pores (37), leaving the cerebral arteries extremely vulnerable to the toxic milieu that develops following SAH.

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