Raised intracranial pressure (ICP) is a common problem in neurosurgical and neurological practice. It can arise as a consequence of intracranial mass lesions, disorders of cerebrospinal fluid (CSF) circulation, and more diffuse intracranial pathological processes. Its development may be acute or chronic. There are well established methods for the measurement, continuous monitoring, and treatment of raised ICP. Evidence from prospective randomised controlled clinical trials that monitoring and treatment of raised ICP per se improves outcome is currently lacking for many conditions.
The normal range of ICP varies with age (table 1) though values in the paediatric population are not well established. Thresholds for initiating treatment for intracranial hypertension vary according to aetiology and within single conditions there is debate about the appropriate upper limit of normal. For example, various authors have suggested thresholds of 15, 20, and 25 mm Hg for the initiation of treatment for raised ICP in patients with head injury.
Table 2 lists some common causes of raised ICP.
The relation between volume and pressure within the cranium is non-linear (fig 1). The Monro-Kellie hypothesis states that the sum of the intracranial volumes of blood, brain, CSF, and other components (for example, tumour, haematoma) is constant. The skull is considered as an enclosed and inelastic container. An increase in the volume of any one of the intracranial contents must be offset by a decrease in one or more of the others or be associated with a rise in ICP. Intracranial blood (especially in the venous compartment) and CSF are the two components whose volume can adapt most easily to accommodate an increase in the volume of intracranial contents. Once these compensatory mechanisms are exhausted, further increases in volume result in large rises in ICP. Compliance (the change in volume for a given change in pressure) provides an index of compensatory reserve, with low values suggesting a diminished reserve.
Although continuous ventricular pressure monitoring in humans had been reported earlier, Lundberg first classified ventricular pressure fluctuations in humans in 1960 (fig 2).
* A waves or plateau waves--These comprise a steep rise in ICP from near normal values to 50 mm Hg or more, persisting for 5-20 minutes and then falling sharply. These waves are always pathological and indicate greatly reduced compliance. They are frequently accompanied by neurological deterioration.
* B waves--These rhythmic oscillations occur every 1-2 minutes. ICP rises in a crescendo manner to levels 20-30 mm Hg higher than baseline and then falls abruptly. These waves were originally always associated with Cheyne-Stokes respiration. However, they also occur in ventilated patients and are probably related to changes in cerebrovascular tone and cerebral blood volume. B waves are also indicative of failing intracranial compensation.
* C waves--These oscillations occur with a frequency of 4--8 per minute and are of smaller amplitude than B waves. They are synchronous with spontaneous Traub-Hering-Meyer type variations in blood pressure and are probably of limited pathological significance.
ICP pulse amplitude increased linearly with ICP. On occasion the pulse pressure may rise before a rise in mean ICP, indicating impaired compliance and giving advance warning of a rise in baseline ICP.
ICP and brain shifts
The cranial vault is divided into compartments by the dural reflections of the falx cerebri and tentorium cerebelli. Raised ICP frequently results in pressure …