Pathophysiology of Intracranial Hypertension

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The Monro-Kellie doctrine, which dates back over two centuries, defined the cranial vault as a fixed compartment made up of three components: blood, cerebrospinal fluid (CSF), and brain tissue. It established that the sum of the volumes of the brain, CSF, and intracranial blood is constant and that an increase in one compartment causes a compensating decrease in another. Due to compensating mechanisms such as spinal dislocation of CSF or extracranial dislocation of cerebral venous blood, such volume increases initially result in just a tiny or unnoticeable increase in ICP. However, if a crucial threshold of increased volume in any cerebral compartment has been reached, even tiny volume increases can cause an exponential increase in ICP, as seen by the steeper part of the pressure-volume curve (SDC 2: Intracranial compliance curve). It's worth noting that elastance is the proper physiologic term for describing a change in pressure for a given change in volume, whereas compliance is the most commonly used term to describe intracranial dynamics, with poor compliance indicating an increased change in pressure for a given change in volume. Changes in the intracranial pressure waveform are another sign of poor compliance (SDC 3: ICP waveform changes with decrements in compliance).

Idiopathic Intracranial Hypertension

The pressure gradient across the cerebrovascular bed that drives cerebral blood flow is known as cerebral perfusion pressure (CPP). It is typically calculated as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP) (or distal venous pressure if greater). Increases in ICP can lower CPP and, as a result, CBF. When ICP reaches critical closing pressure3, CBF, which is normally continuous throughout the cardiac cycle, becomes discontinuous, and there is no flow during diastole. If the intracranial pressure (ICP) exceeds the systolic blood pressure, and intracranial circulatory arrest may occur4 (SDC 4: Cerebral oligemia with decreased CPP). Furthermore, ICP gradients can cause brain tissue shift or herniation, as well as arterial occlusion.

Taxonomy of Intracranial Hypertension

Increased Blood Volume

  • Cerebral Arterial Hypervolemia  ⇾ Autoregulated Active Vasodilation Dysregulated Passive Vasodilation
  • Cerebral Venous Hypervolemia  ⇾ Starling resistor outflow obstruction, Venous sinus obstruction, Very high extracranial venous pressure

Masses and Edema

  • Brain tissue edema - oligemia ⇾ Vasogenic edema, Cytotoxic edema
  • Masses - oligemia ⇾ Intracranial Neoplasia Hematoma

Increased CSF Volume

  • Hydrocephalus ⇾ Communicating, Non-communicating
While these pathophysiologic subsets provide a conceptual framework for approaching intracranial hypertension, it is important to remember that the processes they describe rarely occur in isolation, but rather frequently in combination. A hyperemic process, for example, may increase ICP initially but then contribute to subsequent edema or hemorrhage with further increases in ICP, but now with oligemia. Following is a detailed description of these ICP subsets.



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