Due to increased survival rates among soldiers exposed to explosive blasts, blast-induced traumatic brain injury (bTBI) has become much more prevalent in recent years. Cerebral vasospasm (CVS) is a common manifestation of brain injury whose incidence is significantly increased in bTBI. CVS is characterized by initial vascular smooth muscle cell (VSMC) hypercontractility, followed by prolonged vessel remodeling and lumen occlusion, and is traditionally associated with subarachnoid hemorrhage (SAH), but recent results suggest that mechanical injury during bTBI can cause mechanotransduced VSMC hypercontractility and phenotype switching necessary for CVS development, even in the absence of SAH. Here, we review the mechanisms by which mechanical stimulation and SAH can synergistically drive CVS progression, complicating treatment options in bTBI patients.
Department of Biomedical Engineering, University of Minnesota, Twin Cities, 312 Church St. SE, 7-105 Hasselmo Hall, Minneapolis, MN, 55455, USA.
Transl Stroke Res. 2014 Jun 1; 5 (3): 385-93.
AbstractDue to increased survival rates among soldiers exposed to explosive blasts, blast-induced traumatic brain injury (bTBI) has become much more prevalent in recent years. Cerebral vasospasm (CVS) is a common manifestation of brain injury whose incidence is significantly increased in bTBI. CVS is characterized by initial vascular smooth muscle cell (VSMC) hypercontractility, followed by prolonged vessel remodeling and lumen occlusion, and is traditionally associated with subarachnoid hemorrhage (SAH), but recent results suggest that mechanical injury during bTBI can cause mechanotransduced VSMC hypercontractility and phenotype switching necessary for CVS development, even in the absence of SAH. Here, we review the mechanisms by which mechanical stimulation and SAH can synergistically drive CVS progression, complicating treatment options in bTBI patients.