Venous system in acute brain injury: Mechanisms of pathophysiological change and function

Abstract

Cerebral vascular injury is a major component of acute brain injury. Currently, neuroprotective strategies primarily focus on the recanalization of cerebral arteries and capillaries, and the protection of insulted neurons. Hitherto, the role of vein drainage in the pathophysiology of acute brain injury has been overlooked, due to an under appreciation of the magnitude of the impact of veins in circulation. In this review, we summarize the changes in the vein morphology and functions that are known, or likely to occur related to acute brain injury, and aim to advance the therapeutic management of acute brain injury by shifting the focus from reperfusion to another term: recirculation. Recent progress in the neurobiological understanding of the vascular neural network has demonstrated that cerebral venous systems are able to respond to acute brain injury by regulating the blood flow disharmony following brain edema, blood brain barrier disruption, ischemia, and hemorrhage. With the evidence presented in this review, future clinical management of acutely brain injured patients will expand to include the recirculation concept, establishing a harmony between arterial and venous systems, in addition to the established recanalization and reperfusion strategies.

Keywords: Acute brain injury; Pathophysiology; Vascular neural network; Vein.

Figure 1

Examination images of the patients. A and B: Computerized tomography scan did not reveal any abnormity in the brain at his first administration. C and D: Computerized tomography scan revealed multiple hematomas with edema in the left cerebral at his second administration. E and F: Computerized tomography angiography did not reveal aneurysms and vascular malformation. G and H: Magnetic resonance venography indicated thrombosis in superior sagittal sinus and right transverse sinus.

Figure 2

Pathogenesis of cerebral venous system abnormality after acute brain injury. Venous drainage abnormalities might be attributed to several interwoven factors after brain injury, including elevated ICP due to brain edema, active constriction caused by pericyte contraction and phenotypic transformation in smooth muscle cells, and leukocyte-platelet aggregate with microthrombsis. ICP: intracranial pressure.

Figure 3

Vein-mediated pathophysiology after acute brain injury. The changes of cerebral venous may lead to venous congestion, BBB disruption, microthrombosis, infarction and hemorrhage, which subsequently cause ICP increase and brain edema. TBI: traumatic brain injury; SAH: subarachnoid hemorrhage; ICH: intracerebral hemorrhage; ICP: intracranial pressure; BBB: Blood Brain Barrier.