Carotid near-occlusion pathophysiology: A narrative review and expanded cerebrovascular theory

The purposes of this review are to summarize the pathophysiology of carotid near-occlusion (CNO) and formulate how known hemodynamic theory can be expanded to specifically address CNO. A systematic search revealed 51 articles addressing CNO pathophysiology. ICA flow reduction and collateral pathway activation are hallmarks of CNO. While CNO is associated with a high prevalence of reduced cerebrovascular reserve (CVR), severely impaired CVR was uncommon. Hence, hypoperfusion stroke mechanism is uncommon. Embolic mechanism studies are few and with mixed results. In hemodynamic theory variant, we propose that good collateral capacity results in CNO early during stenosis severity progression and no hemodynamic stroke/TIA. Conversely, we propose that poor collateral capacity results in more severe stenosis for CNO to develop and hemodynamic stroke/TIA will occur when the stenosis is sufficiently severe. This suggested theory predicts that a mismatch between too little distal collapse given a certain stenosis severity might indicate hypoperfusion. In conclusion, CNOs are flow-reducing stenoses associated with collateral use and unclear stroke mechanism. We propose an expansion of known hemodynamic theory to specifically address CNO where collateral capacity is the key factor that determines what stenosis severity is required for CNO to form and for hypoperfusion occur (if it occurs at all).