Background:Cerebrospinal fluid (CSF) transport across the central nervous system (CNS) is no longer believed to be on the conventional lines. The Virchow–Robin space (VRS) that facilitates CSF transport from the basal cisterns into the brain interstitial fluid (ISF) has gained interest in a whole new array of studies. Moreover, new line of evidence suggests that VRS may be involved in different pathological mechanisms of brain diseases.Methods:Here, we review emerging studies proving the feasible role of VRS in sleep, Alzheimer's disease, chronic traumatic encephalopathy, and traumatic brain injury (TBI).Results:In this study, we have outlined the possible role of VRS in different pathological conditions.Conclusion:The new insights into the physiology of the CSF circulation may have important clinical relevance for understanding the mechanisms underlying brain pathologies and their cure.

Brain edema after severe traumatic brain injury (TBI) plays an important role in the outcome and survival of injured patients. It is also one of the main targets in the therapeutic approach in the current clinical practice. To date, the pathophysiology of traumatic brain swelling is complex and, being that it is thought to be mainly cytotoxic and vasogenic in origin, not yet entirely understood.However, based on new understandings of the hydrodynamic aspects of cerebrospinal fluid (CSF), an additional mechanism of brain swelling can be considered. An increase in pressure into the subarachnoid space, secondary to traumatic subarachnoid hemorrhage, would result in a rapid shift of CSF from the cisterns, through the paravascular spaces, into the brain, resulting in an increase of brain water content. This mechanism of brain swelling would be termed as "CSF-shift edema."This "CSF-shift," promoted by a pressure gradient, leads to increased pressure inside the paravascular spaces and the interstitium of the brain, disturbing the functions of the paravascular system, with implications of secondary brain injury.Cisternostomy, an emerging surgical treatment, would reverse the direction of the CSF-shift, allowing for a decrease in brain swelling. In addition, this technique would reduce the pressure in the paravascular spaces and interstitium, leading to a recovery of the functionality of the paravas- The principal mechanisms of TBI can be classified as focal brain damage related to a contact injury, resulting in contusion, laceration, and/or intracranial hemorrhage; or diffuse brain damage due to acceleration/deceleration-type injuries, resulting in diffuse axonal injury or brain swelling (Baethmann et al., 1998;Marshall, 2000;McIntosh et al., 1996).It is well known that the outcome from TBI depends on two mechanisms: the primary insult, strictly related to the impact for which the available treatments are symptomatic but not therapeutic.The secondary insult, delayed non-mechanical damage, represents consecutive pathological processes initiated at the moment of injury with a delayed clinical presentation. Brain edema, cerebral ischemia, and intracranial hypertension refer to secondary insults and, in treatment terms, SignificanceThis mini-review provides a succinct synopsis of the main mechanisms underlying brain edema following traumatic brain injury (TBI). We introduce the concept of CSF-shift edema and its role in TBI. We conclude that cisternostomy, an emerging surgical technique, may counteract brain edema following TBI, and holds promise in improving morbidity and mortality following severe TBI.

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