The Medical Management of Cerebral Edema: Past, Present, and Future Therapies

Abstract

Cerebral edema is commonly associated with cerebral pathology, and the clinical manifestation is largely related to the underlying lesioned tissue. Brain edema usually amplifies the dysfunction of the lesioned tissue and the burden of cerebral edema correlates with increased morbidity and mortality across diseases. Our modern-day approach to the medical management of cerebral edema has largely revolved around, an increasingly artificial distinction between cytotoxic and vasogenic cerebral edema. These nontargeted interventions such as hyperosmolar agents and sedation have been the mainstay in clinical practice and offer noneloquent solutions to a dire problem. Our current understanding of the underlying molecular mechanisms driving cerebral edema is becoming much more advanced, with differences being identified across diseases and populations. As our understanding of the underlying molecular mechanisms in neuronal injury continues to expand, so too is the list of targeted therapies in the pipeline. Here we present a brief review of the molecular mechanisms driving cerebral edema and a current overview of our understanding of the molecular targets being investigated.

An amplitude-based characteristic parameter extraction algorithm for cerebral edema detection based on electromagnetic induction

“…Aiming at the distinction between the acute and chronic phases of cerebral edema, this study also evaluated those characteristic parameters data within 0–6 h and 6–24 h. We assumed that it is possible to distinguish between the acute and chronic phases of cerebral edema. Figure 6 plots the characteristic parameter of rabbits in the experimental group within 0–6 h and within 6–24 h, during which cytotoxicity and vasogenic cerebral edema, respectively, dominate the process in this cerebral edema model [ 2 , 56 ]. The contrast between the acute phase and the chronic phase of rabbits is not as clear as that between experimental group and control group.…”

The meningeal lymphatic vessels and the glymphatic system: Potential therapeutic targets in neurological disorders

“…147,148 Traditionally, brain edema is divided into two phases: an early cytotoxic phase and a later vasogenic phase. 149 The cytotoxic phase is predominant in the early stages of acute ischemic stroke and traumatic brain injury, and it is related to cellular energy depletion, failure of membrane integrity, and cellular swelling. Glymphatic inflow of CSF appears to be the primary event in the early phase of acute ischemic stroke: in one study, CSF flow into the brain along the PVS doubled within a few minutes after middle cerebral artery occlusion, driving acute brain swelling.…”

A Diagnostic Dilemma of White Matter Lesions and Cerebral Oedema without Identifiable Cause—A Neurological Conundrum

“…Cerebral oedema is often associated with trauma, intracranial space occupying lesions, vascular ischemia, or obstructive hydrocephalus [ 1 , 2 , 3 ]. Vasogenic oedema, resulting from breakdown of the blood–brain barrier, is often seen in malignant processes [ 1 ].…”

“…Cerebral oedema is often associated with trauma, intracranial space occupying lesions, vascular ischemia, or obstructive hydrocephalus [ 1 , 2 , 3 ]. Vasogenic oedema, resulting from breakdown of the blood–brain barrier, is often seen in malignant processes [ 1 ]. Several auto-immune and para-neoplastic phenomena also present with cerebral oedema and often warrant an expansive evaluation [ 4 ].…”