Lecture 5 - Cerebral edema

Lecture 5 - Cerebral edema

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain. It is characterized by certain changes in morphology with the brain becoming soft and smooth and oedema fluid overfills the cranial vault. Gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Physiologically it may be characterized by nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.

Causes – Cerebral edema can result from brain trauma or from non-traumatic causes such as ischemic stroke, cancer, or brain inflammation due to meningitis or encephalitis.

Vasogenic edema caused by amyloid-modifying treatments, such as monoclonal antibodies, is known as ARIA-E (amyloid-related imaging abnormalities edema).

The blood–brain barrier (BBB) or the blood–cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain's extracellular space.

Altered metabolism may cause brain cells to retain water, and dilution of the blood plasma may cause excess water to move into brain cells.

Fast travel to high altitude without proper acclimatization can cause high-altitude cerebral edema (HACE).

The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed.

In ayurvedic context cerebral oedema the more likely failure of agni in terms, that it is depleted or variance in parthiv combinations causes changes in osmotic and hydrostatic gradients and these minor shifts on the scale are likely to influence retention of fluid or decreased drainage or even decomposing (conversion of tissue due to decomposition towards jal); any of these can cause grave changes which may become the cause for cerebral oedema.