Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought

A good explanation of what follows after a hemorrhage.  I'm sure your doctor explained all this since this is only 3.5 years old.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706525/

INTRODUCTION

When persons in good health are suddenly seized with pains in the head, and straightway are laid down speechless, and breathe with stertor, they die in seven days.

Hippocrates 460–370 BC, Aphorisms on Apoplexy¹

Hippocrates’ 2400-year-old description of delayed death probably caused by a ruptured intracranial aneurysm with subsequent vasospasm is still valid today. Aneurysmal subarachnoid hemorrhage (SAH) affects about 10 out of 100,000 adults annually, and up to half of those affected die soon after²; most of the rest are successfully treated surgically and/or endovascularly. Despite obliterating the offending aneurysm and removing the risk of rebleeding, up to half of the treated patients develop a syndrome of focal and/or cognitive deficits due to cerebral vasospasm (delayed ischemic neurological deficit, symptomatic vasospasm) between the fourth and ninth day after the SAH³. As a result, many die or suffer permanent morbidity², and it has been described as the single most important cause of morbidity and mortality in patients whose ruptured aneurysm is successfully treated⁴.

Patients require vigilant monitoring and treatment for up to 2 weeks, including invasive monitoring of blood pressure, cerebral blood flow and metabolism and often complex treatment with calcium antagonists, hypertensive drugs, hemodilution and hypervolemia (triple H therapy), plus risky and often only temporarily effective intra-arterial administration of vasodilator drugs or balloon angioplasty⁵. These treatments have been documented in nine international conferences on cerebral vasospasm (Table 1).

Table 1

Summary of international conferences on cerebral vasospasm, 1972–2006

Since the demonstration of arterial narrowing in the syndrome of cerebral vasospasm in 1951⁶ and the further emphasis in 1978 by Weir et al.³, it has been proven that SAH gives rise to arterial narrowing and in turn ischemia, causing infarction and poor outcome. Most research into delayed deterioration after SAH has been conducted in concordance with this axiom, with the goal of interrupting this perceived chain of events. There have been many clinical trials, but until the arrival of clazosentan, a selective endothelin 1A receptor antagonist, it has not been possible to reproducibly break this chain. Clazosentan did, however, effectively prevent and reverse arterial narrowing in one work⁷, providing what was thought may at last be an effective treatment. However, the subsequent multi-center CONSCIOUS trial, despite significant reductions in angiographic vasospasm, failed to show any effect on long-term outcome.

The axiom has thus been challenged in such a fashion that it amounts to a paradigm shift.

Accumulated evidence suggests that (1) arterial narrowing is not the only cause of delayed clinical deterioration, (2) arterial narrowing is not necessarily multifactorial but (3) may actually be an effect of a single factor and finally (4) the entire picture of delayed clinical deterioration may be multifactorial. These facts should lead to a search for a more comprehensive and adequate theory that not only can explain observed discrepancies but also will lead to development of a specific and effective treatment strategy.

In recent years, two major concepts in pre-vasospasm research have developed: early brain injury and cortical spreading depression. Basic animal works and some clinical observations have long pointed to the importance of the pre-vasospasm period, with recognition of the importance of transitory ischemia at the onset of SAH ⁸, the opening of the blood–brain barrier^9,10, the existence of early arterial narrowing in clinical settings¹¹ and the detection of cortical spreading ischemia after SAH¹². One or more of these events may replace arterial narrowing as important causes of poor outcomes after SAH¹³.

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PATHOPHYSIOLOGY OF ARTERIAL NARROWING: NEW DEVELOPMENTS

The idea of arterial narrowing has previously been central to understanding the syndrome of cerebral vasospasm, but as outlined above, a paradigm shift is underway. Even so, the association of arterial narrowing with delayed ischemic deficits and the fact that reversal of narrowing by angioplasty can reverse deficits make consideration of pathophysiological events in cerebral arteries still very relevant, as shown in several reviews. Highlights of recent developments are presented below.