A cerebral or extracerebral mass such as brain tumor; cerebral infarction with edema; traumatic contusion; parenchymal, subdural, or extradural hematoma; or abscess, all of which are localized but deform the adjacent brain. The brain deformation is compartmentalized, or constrained by the rigid dural partitions surrounding the compartment containing the mass.
2.
Generalized brain swelling, as occurs in ischemic–anoxic states, acute hepatic failure, hypertensive encephalopathy, hypercarbia, and Reye hepatocerebral syndrome. In these disorders, the increase in pressure can reduce cerebral perfusion, but tissue shifts are minimal because the effect of the addition of mass to the brain is uniformly distributed throughout the cranial contents.
3.
An increase in venous pressure because of cerebral venous sinus thrombosis, heart failure, or obstruction of the superior mediastinal or jugular veins.
4.
Obstruction to the flow and absorption of CSF. If the obstruction is within the ventricles or in the subarachnoid space at the base of the brain, hydrocephalus results. Extensive meningeal disease from several potential causes (infectious, carcinomatous, granulomatous, hemorrhagic) is another mechanism of blockage to CSF flow. If the block is confined to the absorptive sites adjacent to the cerebral convexities and superior sagittal sinus, the ventricles remain normal in size or enlarge only slightly, because the pressure over the convexities approximates the pressure within the lateral ventricles (see further on).
5.
Any process that expands the volume of CSF (meningitis, subarachnoid hemorrhage) or hat increases CSF production (choroid plexus tumor). In this situation, there may be a pressure gradient between the cerebral and spinal compartments, resulting in hydrocephalus.
Clinical Features of Raised ICP (See Also Chap. 16)
The typical clinical manifestations of increased ICP in children and adults are headache, nausea and vomiting, drowsiness, ocular palsies, and papilledema. Papilledema may result in periodic visual obscurations and if it protracted, optic atrophy and blindness may follow (see
Chap. 12 for further discussion of papilledema and optic nerve atrophy). The practice of monitoring ICP with a pressure device inserted into the cranial cavity has permitted approximate correlations to be made between clinical signs and the levels of ICP. However, the neurologic signs of a large intracranial mass, namely pupillary dilatation, abducens palsies, drowsiness, and the Cushing response, as discussed below and in Chaps. 16 and 34, are caused, not by raised pressure, but by displacement of brain tissue, and therefore they do not bear a strict relationship to ICP.