Accumulation of extracellular fluid increases brain volume and then intracranial pressure causing the symptoms of cerebral edema.There are several clinical conditions in which vasogenic edema is present:

CNS tumors, like glioblastoma and meningioma
Infections like meningitis, abscess, and encephalitis
Inflammatory central nervous system disease such as multiple sclerosis
Brain hemorrhage
Traumatic brain injuries can lead to increased intracranial pressure, local damage, reduced cerebral blood flow, and focal ischemia secondary to vasogenic edema. Late stage of ischemic stroke after rapid recovery from cytotoxic edema
Hypertensive encephalopathy
Radiation injury

Ionic (Osmotic)
In ionic edema, the solute concentration (osmolality) of the brain exceeds that of the plasma and the abnormal pressure gradient leads to accumulation of water intake into the brain parenchyma through the process of osmosis. The blood-brain barrier is intact and maintains the osmotic gradient.The solute concentration of the blood plasma can be diluted by several mechanisms:

Improper administration of intravenous fluids, isotonic or hypotonic. Excessive water intake, syndrome of inappropriate antidiuretic hormone (SIADH). Rapid reduction of blood glucose in diabetic ketoacidosis or hyperosmolar hyperglycemic state. Hemodialysis has been associated with ionic edema and cellular swelling. Cerebral edema is a potentially life threatening complication of severely decreased sodium ion concentration in the blood (hyponatremia).Ionic brain edema can also occur around the sites of brain hemorrhages, infarcts, or contusions due to a local plasma osmolality pressure gradient when compared to the high osmolality in the affected tissue. Interstitial (hydrocephalic)
Interstitial edema can be best characterized by in noncomunnicating hydrocephalus where there is an obstruction to the outflow of cerebrospinal fluid within the ventricular system.
Hypertonic saline and mannitol are the main osmotic agents in use, while loop diuretics can aid in the removal of the excess fluid pulled out of the brain. Hypertonic saline is a highly concentrated solution of sodium chloride in water and is administered intravenously. It has a rapid-onset, with reduction of pressures within 5 minutes of infusion, lasting up to 12 hours in some cases, and with negligible rebound pressure. The exact volume and concentration of the hypertonic saline varies between clinical studies. Bolus doses, particularly at higher concentrations, for example 23.4%, are effective at reducing ICP and improving cerebral perfusion pressure. In traumatic brain injuries, a responsiveness to hypertonic saline lasting greater than 2 hours was associated with decreased chance of death and improved neurologic outcomes. The effects of hypertonic saline can be prolonged with combination to agents such as dextran or hydroxyethyl starch, although their use is currently controversial. When compared to mannitol, hypertonic saline has been shown to be as effective as mannitol in decreased ICP in neurocritical care and is more effective in many cases. Hypertonic saline may be preferable to mannitol in persons with hypovolemia or hyponatremia. Mannitol is an alcohol derivative of simple sugar mannose, and is historically the most commonly used osmotic diuretic. Mannitol acts as an inert solute in the blood, decreasing ICP through osmosis as discussed above. Additionally, mannitol decreases ICP and increased cerebral perfusion pressure by increasing reabsorption of cerebrospinal fluid, dilutes and decreased the viscosity of the blood, and can cause cerebral vasoconstriction.