The Pathophysiology of Delayed Cerebral Ischemia

Area of Science:

• Neurology
• Neurosurgery
• Critical Care Medicine

Background:

• Subarachnoid hemorrhage (SAH) impacts 30,000 individuals annually in the US.
• Delayed cerebral ischemia (DCI) affects one-third of SAH survivors, presenting a treatable cause of morbidity.
• Traditionally attributed to vasospasm, DCI is now understood as a complex post-SAH syndrome.

Purpose of the Study:

• To elucidate the multifaceted pathophysiology of delayed cerebral ischemia following subarachnoid hemorrhage.
• To highlight the evolving nature of DCI and its contributing factors beyond vasospasm.
• To emphasize the need for novel therapeutic strategies targeting multiple pathways.

Main Methods:

• Review of emerging evidence on DCI pathophysiology.
• Analysis of early and late contributors to post-SAH injury.
• Synthesis of current understanding of DCI development.

Main Results:

• DCI involves early arteriolar vasospasm, microthrombosis, perfusion mismatch, neurovascular uncoupling, spreading depolarizations, and inflammation.
• These processes initiate at hemorrhage onset and evolve over time, leading to cortical infarction.
• Large-vessel vasospasm is considered a late contributor to established injury.

Conclusions:

• Delayed cerebral ischemia is a complex syndrome with multifactorial origins.
• Effective DCI treatment necessitates early detection of pathophysiologic changes.
• Therapeutic interventions must target multiple pathways involved in DCI development.