ICP and Cerebral Blood Flow

The skull is a rigid structure with a fixed volume. Intracranial pressure is determined by the volume of the three contents of the skull:

Brian CSF Blood

A compensatory mechanism exists to ensure this ration remains constant, but when this changes and fails, ICP changes.

Cerebral blood flow depends on vascular resistance and blood pressure. ICP must be considered due to the fixed volume of the skull. There are two types of regulatory mechanism that serve to maintain cerebral blood flow at an appropriate level:

1. Chemoregulation2. Autoregulation (change in vessel calibre)

Autoregulation means that cerebral perfusion pressure can fluctuate within limits without casuing a significant change to cerebral blood flow.

Autoregulation is impaired in the damaged brain. Consequently, a decrease in cerebral perfusion pressure is more likely to result in reduced cerebral blood flow and secondary ischaemia. Equally, high cerebral perfusion may increase cerebral blood flow, damage the blood-brain barrier and cause cerebral oedema.

There are two compensatory mechanism for an expanding intracranial mass lesion:

1. Immediate – CSF outflow to lumbar theca and decreased cerebral blood flow2. Delayed – Decreased ECF

Cerebral Oedema

The skull contains 0.9 – 1.2l of ICF, and 100-150 ml of ECF. An increase in the volume of either of these two components results in cerebral oedema.

The pathogenesis can be devided into:

1. Vasogenic2. Cytotoxic3. Interstitial

These types coexist to variable degrees depending on the primary pathology.

Treatment relies on identifying the underlying cause. Vasogenic is usually responsive to corticosteroids, osmotic diuretics and hyperventilation, whereas cytotoxic is often less responsive.

1. Vasogenic:- Increased permeability of capillary endothelia cells- Caused either by tight junction defects, or increased active transport- Develops around tumours, abscesses, and MS plaques

- Predominantly affects white matter.

2. Cytotoxic:- Intracellular oedema- Damage to ATP dependent Na+ pump- Leads to Na+, Ca2+, H2O accumulation within neurons and glia. - Affects both grey and white matter- Commonly seen early in ischaemic brian damage, and dilutional hyponatraemia

3. Interstitial:- Extracellular, primarily seen in hydrocephalus- Results from extravasation of CSF through ependymal cells into the EC space of the

periventricular white matter.

There are several clinical effects of raised ICP:

Headache – worse in morning, aggravated by stooping/bending Vomiting – occurs with sudden rise in ICP Papilledema – occurs in some patients

Raised ICP does not case neuronal damage until cerebral blood flow is compromised. However, damage does result from brain-shift and subsequent herniation.