As a rule, patients with normal blood pressure retain mental alertness when ICP rises to 25 to 40 mm Hg unless there is concurrent shift of brain tissue that compresses the brainstem. Stated another way, coma generally cannot be attributed to elevated ICP alone. Only when ICP exceeds 40 to 50 mm Hg does cerebral blood flow diminish to a degree that results in loss of consciousness. Further elevations are followed imminently by global ischemia and brain death. From our own observations, the brain shift and herniation that causes the pupil to dilate on the side of a mass lesion generally occurs at an ICP of 28 to 34 mm Hg. (Again, this is not a direct effect of the elevated ICP.) There are instances in which the dissociation between ICP and clinical signs is striking, for example, a mass in the medial temporal lobe that is contiguous to the third nerve will compress the nerve at a time when ICP is little raised, and slowly growing lesions, which raise ICP slowly and allow for compensation cause few clinical signs. Likewise, unilateral or bilateral abducens palsies do not have a consistent relationship to the degree of elevation of ICP. Rather, abducens palsies are found when raised ICP is a result of diffusely distributed brain swelling, hydrocephalus, meningitic processes, or pseudotumor cerebri.
The consequences of increased ICP take on special features in infants and small children, whose cranial sutures have not closed. The head enlarges and the eyes may bulge. Then the clinical problem involves differentiation from other types of enlargement of the head with or without hydrocephalus, such as constitutional macrocrania or an enlarged brain (megalencephaly; or hereditary metabolic diseases such as Krabbe disease, Alexander disease, Tay-Sachs disease, Canavan spongy degeneration of the brain), and from subdural hematoma or hygroma, neonatal ventricular hemorrhage, and various cysts and tumors.
There had been evidence, mainly from retrospective cohorts of patients with traumatic brain injury, that the outcome in patients with intracranial mass lesions was better if the ICP was maintained at levels well below those that compromise cerebral perfusion. An ICP below 15 or 20 mm Hg is often given as a therapeutic target, as the elastance curve becomes steep beyond this level and small increments in cerebral volume may cause large elevations in pressure. However, guiding treatment by the direct measurement of ICP has not yielded beneficial results, as typified by the BEST-TRIP trial (Chesnut et al) and—after several decades of popularity—the advantage of such devices over clinical and imaging signs of increasing mass effect is less certain. It does appear that lowering ICP and decompressing the brain by craniectomy after traumatic injury (see the DECRA trial, Cooper et al; and RESCUE-ICP, Hutchinson et al) or with cerebral swelling from stroke, greatly reduces mortality and it has been presumed that this is the result of a reduction of ICP. It is difficult, however, to separate this effect of decompression from the parallel amelioration of intracranial tissue shifts. (It should be noted that the reduction in mortality is usually at the expense of increased numbers of survivors in a vegetative or disabled state). Nevertheless, in a patient who cannot be examined because of induced paralysis or sedation, or who will be subjected to a procedure that risks further elevating ICP, monitoring seems sensible.