Table 2.

Facts that challenged the concept of angiographic vasospasm as the main factor leading to delayed cerebral ischaemia

A. Approximately 70 % of patients with subarachnoid haemorrhage (SAH) will develop some degree of angiographic vasospasm within 2 weeks of haemorrhage [64, 165]; however, only 30 % will develop symptoms (i.e., delayed cerebral ischaemia, or DCI) [88]. B. DCI-associated cerebral infarct is an independent factor for poor outcome after SAH [166]; however, cerebral infarction can happen asymptomatically [88] or in vascular territories not affected by vasospasm [167]. C. Large-vessel angiographic vasospasm detected by modalities such as transcranial Doppler has a poor temporal relationship with the development of DCI [167]. D. There is no evidence that nimodipine decreases the rate of angiographic vasospasm or promotes cerebral vasodilation; however, it remains the sole pharmacological intervention proven to improve outcomes from DCI [108, 111]. E. There is an important dissociation between vasospasm-related morbidity and functional outcome after SAH [168, 169]. F. The prevention and treatment of angiographic vasospasm do not necessarily translate into improved outcome [169].