MRI-based investigation on outflow segment of cerebral venous system under increased ICP condition.

OBJECTIVE

Increased intracranial pressure (ICP) is responsible for causing most nervous system diseases to progress seriously, till death. Recently, volume-targeted therapeutic strategy against increased ICP, which works by releasing excessive intracranial liquid especially from the venous compartment, attracted a great deal of attention. Previous research by us found a structurally special "outflow segment cuff" that is located at the juncture of superior sagittal sinus (SSS) and the brain-bridging veins in porcine model. Sequential observation demonstrated that this special structure appeared to have functional abnormalities. Based on these findings, it was proposed to try and prove a further hypothesis that there exists a similar structure in human beings that might be of importance for cerebral venous system to intervene in volume-initiated ICP regulation. Meanwhile, the diameters of bridging veins under either increased or normal ICP are compared by means of magnetic resonance imaging (MRI).

METHOD

Forty patients who presented with increased ICP were selected to undergo 2D time of flight (TOF) venography and ten normal volunteers were taken as the control group. Increased intracranial pressure status was evaluated by using flash visual evoked potential (fVEP) technique. All the patients and volunteers underwent 2D-TOF MRI imaging for the following parameters: repetition time/echo time, 50/4.9 milliseconds; flip angle, 45 degrees ; field of view, 250x250 mm; matrix, 256x256 pixels; section thickness, 1.5 mm. Syngo fastview imaging system was used to process and analyze the targeted brain-bridging venous section.

RESULTS

By using 2D-TOF method in vivo, most bridging venous profiles as well as SSS and vicinal cortical veins could be clearly visualized. A short and narrow section, as previously described, obviously emerged because of MRI signal weakness even disappearing at the juncture of SSS and bridging veins in increased ICP patients. In combination with previous animal morphological findings we believe that this section with abnormal MRI signal could stand for the human counterpart of "outflow segment cuff" in porcine. Such a special structure could be observed within a majority of increased ICP patients (32/40 cases), whereas only one case presented the existence of similar imaging signal weakness. Furthermore, the diameters of the bridging veins in increased ICP group are statistically larger than the control group.

CONCLUSION

Intracranial venous compartment occupies about 70 to 80% blood volume inside the inflexible cranial cavity. Following volume-targeted rationale, ICP can be regulated effectively by the fluctuation of venous blood volume based on different aspects of morphology, biomechanics, and hemodynamics. In the present study, the coincidence of animal model and human venography in vivo offers strong evidences to support the hypothesis that venous hemodynamics, although passively, influences intracranial pressure environment through a possible key regulator - outflow segment narrow structure. The fact that this narrow formation and proximal vascular dilation appears more in patients under high ICP condition rather than in patients with normal pressure. Both narrow formation and proximal vascular dilation indicate its significant contribution to intracranial venous congestion, resulting from difficult drainage and the close relationship between intracranial venous volume and ICP.