I believe stroke and cardiovascular researchers may be better able to create models of MS using perfusion--or blood flow. Stroke specialists, like Dr. Peter Stys, have been questioning the autoimmune theory of MS, and suggesting that the immune reaction may be secondary. link
The relatively new concept of neurovascular unit (NVU) helps to clarify the hemodynamic changes due to the intricate interplay between cerebral blood flow (CBF) and vasoactive factors. Several studies have demonstrated the importance of endothelial factors, their neurovascular interaction, and that vascular changes are also highly conducive to neurodegenerative changes and clinical impairment.10–13 Cerebral hypoperfusion and vascular factors are strictly involved in neurovascular dysfunction, vascular oxidative stress, and relative tissue hypoxia, well in advance of any demyelinating lesions. Changes in capillary resistance and neurovascular function may, in fact, represent important common denominators for conditions that increase the risk of developing both demyelinating lesions and progressive MS forms. https://journals.sagepub.com/doi/full/10.1177/1177271918774800
After ischmic events, the brain is reperfused. Reperfusion simply means to redeliver blood. Reperfusion is a good thing and a bad thing. Reperfusion can be a natural occurrence; it returns blood to tissue after there is an event which slows blood flow, like a stroke or ischemia. Reperfusion brings essential O2 and glucose to cells after such an event, but it also brings inflammation and the immune system with it. Blood returns to the area of tissue where it had been absent, at a cost.
6. NEW RESEARCH 2019 which considers newly discovered CNS lymphatic vessels. Impaired cerebrospinal fluid (CSF) drainage in the central nervous system, due to malfunction of neurovascular unit (NVU) after ischemia, may lead to neuronal cell death and reperfusion injury.
In the adverse event of ischemia, pericytes around capillaries constrict, eventually leading to pericyte death in rigor and could cause neutrophil trapping in the arterioles. These findings suggest reconsideration of neutrophil involvement in ischemia and reperfusion. Rather than acting neurotoxic, neutrophil accumulation in arterioles may have an impact on the vascular function including CSF drainage recently shown to occur along these pathways.15,116 In fact, cerebral ischemia results in impaired fluid clearance along the perivascular spaces in the affected cortex117 underscoring a neutrophil-induced malfunction of the NVU in I/R.
Functional impairment of lymphatic drainage from the CNS after ischemic stroke may lead to rapid neuronal cell death due to the accumulation of toxic metabolites in the brain parenchyma.
I did find one animal study which looked at venous hypertension as a complicating factor in reperfusion injury