Subdural effusion protects the aging brain from harmful ventriculomegaly.

The human brain loses its volume and its function during aging. The solid part of the brain within the intracranial space, the brain parenchyma, decreases in volume with age; while the cerebrospinal fluid (CSF) volume increases. With progressive loss of brain parenchymal volume (BPV), CSF may shift from cerebral ventricles to the subdural space, forming subdural effusion (SDE), whose role in the brain aging process remains unclear. We hypothesize that damages associated with ventriculomegaly can be lessened after formation of SDE. As the BPV decreases, the enlarged ventricular surface area causes dysfunction of its lining ependymal cells, followed by damages to the periventricular tissue. The periventricular nerve fibers are stretched by the enlarged ventricles. We hypothesize that after the formation of SDE, ventriculomegaly can be stopped or even reversed. By allowing the atrophic brain to reside in a smaller fraction of the intracranial volume, damages associated with ventriculomegaly can be alleviated. If our hypothesis is correct, physicians should continue to maintain a conservative approach for uncomplicated SDE. For focal or global brain parenchymal loss caused by various pathologies, intracranial spacers can be employed to simulate the effect of SDE to protect the brain. For treatment of idiopathic normal pressure hydrocephalus, aggressive ventricular size reduction should be pursued. Finally, the protective effects of SDE have its limits. Extremely enlarged subdural volume can cause acute or chronic subdural hematoma, further damaging the brain.