Adding to the Combat Sports Law blog’s archived combat sports safety studies, a recent article was published in International Journal of Neuroscience discussing the exact physiology at play when a person becomes unconscious from a vascular neck restraint (think rear naked choke). In the study, titled There is more to the mechanism of unconsciousness from vascular neck restraint than simply carotid compression, the authors perform an extensive literature review to explain what is scientifically understood about the technique.
The general understanding is that the technique leads to unconsciousness due to restriction of carotid blood flow. As the authors point out there is a lot more at play that simply this. The authors note, after extensive literature review, that carotid compression, jugular compression, and carotid barosensor stimulation are all at play.
The full abstract reads as follows:
Vascular neck restraint (VNR), an effective technique practiced within police and military combatives and in mixed martial arts and grappling sports, is of both interest and controversy. In any context the goal of VNR (referred to as a choke within combat sports) is to restrict brain blood flow enough to threaten or result in unconsciousness. The physiologic basis for the resultant unconsciousness has been depicted as being solely because of restriction of carotid blood flow due to direct external compression. This view is likely simpler than what is actually going on, but it’s an area not well explored in the medical literature. Brain blood flow is maintained through mechanisms that allow for a relatively wide acceptable cerebral perfusion pressure (CPP). If CPP drops below the threshold of this auto-regulation, blood flow and brain oxygen delivery begin to decline. CPP is the difference of the mean arterial pressure (MAP) coming into the brain and the intracranial pressure (ICP). Lowering the MAP and/or raising the ICP reduce the CPP. The best literature-established physiologic component of VNR is carotid compression and resultant reduction in functional carotid MAP, thus lowering the CPP. Most studies have looked at this essentially to the exclusion of two other contributing entities: jugular compression resulting in increased ICP from reduction of outflow, and reduction of actual whole body MAP due to reduced cardiac output from vagal stimulation coming from a pressure affected carotid body. This article fleshes out some of these physiologic variables and discusses the related available literature.