Glial cell response after aneurysmal subarachnoid hemorrhage — Functional consequences and clinical implications

• Aneurysmal subarachnoid hemorrhage (SAH) is a severe type of stroke.
• SAH can cause early brain damage, delayed cerebral ischemia and cognitive impairment.
• Glial response after SAH is both beneficial and detrimental for brain functioning.
• Sustained glial response may contribute to cognitive impairment after SAH.

Glial cells, both astrocytes and microglia, respond to neurodegenerative processes and to brain damage by a process called reactive gliosis. This response is highly context dependent, varies from mild to severe, and can be protective or detrimental for neural functioning. In patients with a subarachnoid hemorrhage from a ruptured aneurysm, the acute glial response is important to restrict the initial damage. Patients who survive the hemorrhage and early brain injury, often suffer from delayed cerebral ischemia or persisting cognitive impairment. Glia emerge as versatile cells that can modulate synapses and can control the microcirculatory blood flow in the brain. Therefore, a sustained activation of glial cells can affect normal brain functioning. Here we review the current literature on the glial response induced by aneurysmal subarachnoid hemorrhage in humans and in animal models. We discuss how reactive gliosis can affect brain functioning and how it may contribute to early brain injury, delayed cerebral ischemia and cognitive impairment after aneurysmal subarachnoid hemorrhage. This article is part of a Special Issue entitled: Neuro Inflammation edited by Helga E. de Vries and Markus Schwaninger.