Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm?

Abstract

<jats:p>✓ The authors tested the null hypothesis that published literature with a high level of evidence does not support the assertion that subarachnoid hemorrhage (SAH) causes cerebral vasospasm, which in turn causes cerebral infarction and poor outcome after aneurysmal SAH. The medical literature on SAH was searched in MEDLINE. The author's personal files of all published literature on SAH were reviewed. References cited in Cochrane reviews as well as the published papers that were reviewed were also retrieved.</jats:p> <jats:p>There is no question that SAH causes what the authors have chosen to call “angiographic vasospasm.” However, the incidence and severity of vasospasm in recent series of patients is not well defined. There is reasonable evidence that vasospasm causes infarction, but again, accurate data on how severe and how diffuse vasospasm has to be to cause infarction and how often vasospasm is the primary cause of infarction are not available. There are good data on the incidence of cerebral infarction after SAH, and these data indicate that it is highly associated with poor outcome. The link between angiographic vasospasm and poor outcome is particularly poorly described in terms of what would be considered data of a high level of evidence.</jats:p> <jats:p>The question as to whether there is a clear pathway from SAH to vasospasm to cerebral infarction to poor outcome seems so obvious to neurosurgeons as to make it one not worth asking. Nevertheless, the obvious is not always true or accurate, so it is important to note that published literature only weakly supports the causative association of vasospasm with infarction and poor outcome after SAH. It behooves neurosurgeons to document this seemingly straightforward pathway with high-quality evidence acceptable to the proponents of evidence-based medicine.</jats:p>

Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1)

“…In support of the central review opinion, the incidence of new infarcts related to vasospasm in the placebo group was similar to that reported in the literature. 25 These findings support the notion that decreasing vasospasm will improve clinical outcome. They emphasize the need to assess the etiology of CT-based hypodensities in a consistent manner to avoid confounders unrelated to vasospasm and is in agreement with the assessments made in some but not all previous SAH trials.…”

Molsidomine for the prevention of vasospasm-related delayed ischemic neurological deficits and delayed brain infarction and the improvement of clinical outcome after subarachnoid hemorrhage: a single-center clinical observational study

“…2,9,16 Despite nimodipine treatment, vasospasm-associated infarcts occur in 20%-50% of patients with SAH, DINDs in 27%-37% of patients, and severe morbidity in 30%-40% of patients. 9,13,17 A favorable outcome has been reported in less than 10% of patients with DIND, and the majority of those patients (62%) have a poor outcome (severe disability, coma, death).…”

Defining Vasospasm After Subarachnoid Hemorrhage

“…Angiographic vasospasm occurs in up to 70% of patients, 3,4,7 but the relationship between angiographic spasm and clinical symptoms can be inconsistent, and just how extensive or severe angiographic spasm must be to become clinically relevant remains unclear. 8 Transcranial Doppler ultrasound (TCD) is commonly used to diagnose vasospasm, although its positive and negative predictive values for angiographic spasm of the middle cerebral artery is adequate, its sensitivity for detecting angiographic vasospasm of the anterior cerebral artery and distal cerebral vasculature is poor, and the relationship between TCD abnormalities and clinical worsening is unreliable. 9,10 In this study, we aimed to determine the clinical relevance of each definition of vasospasm.…”