Hypoplasia or Occlusion of the Ipsilateral Cranial Venous
Drainage Is Associated With Early Fatal Edema of Middle
Cerebral Artery Infarction
Conclusions—In this small case series, we demonstrated that only the patients with hypoplasia or occlusion of the
ipsilateral cranial venous drainage developed early fatal edema after large middle cerebral artery infarction. Our results suggest a role of cranial venous outflow abnormalities in the development of brain edema after arterial ischemic stroke.
The intracranial venous compartment occupies approximately
70% of blood volume inside the inflexible cranial
cavity. Following volume-targeted rationale, ICP can be
regulated effectively by the fluctuation of venous blood
volume. Venous hemodynamics passively influence the ICP
through a possible key regulator, outflow obstruction. This
outflow obstruction contributes to intracranial venous congestion
more in patients with high ICP than in patients with
normal ICP. In case of normal ICP, venous collaterals may be
sufficient to prevent cerebral venous congestion and edema.
However, in the setting of large MCA infarction with widespread
ischemic injury, pre-existing abnormalities of cranial
venous drainage may pose significant resistance to venous
outflow, accelerating the development of cerebral edema
This is very specific to our chances of stroke survival, but pwCCSVI would not do well in the aftermath of a stroke.
The specific patients had hypoplasia of the IJV and hypoplasia or atresia of the transverse sinus, or a ligated jugular vein.