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In the recumbent position, ICP and consequently CSF pressure measured by lumbar puncture is normally about 8 mmHg or 110 mmH2O (1 mmHg equals 137 mmH2O) As the head and trunk are progressively elevated, the weight of the column of CSF is added incrementally to the pressure in the lumbar subarachnoid space, and the ICP drops correspondingly, so that it is close to zero in the standing position As described above, the CSF pressure is in equilibrium with the capillary or prevenous vascular pressure, which is in uenced mainly by circulatory changes that alter arteriolar tone Rises in systemic arterial pressure cause little or no increase of pressure at the capillary level (because of autoregulation) and hence little increase in CSF pressure The inhalation or retention of CO2 raises the blood PCO2 and correspondingly decreases the pH of the CSF By a mechanism that is not fully understood, this acidi cation of the CSF acts as a potent cerebral vasodilator, causing an increase in cerebral blood ow and leading to intracranial hypertension Hyperventilation, which reduces PCO2, has the opposite effect ie, it increases the pH and the cerebral vascular resistance and thereby decreases CSF pressure; this maneuver of lowering the arterial CO2 content by hyperventilation is utilized in the treatment of acutely raised ICP In contrast to the limited effect caused by changes in arterial blood pressure, increased venous pressure exerts an almost immediate effect on CSF pressure by increasing the volume of blood in the cerebral veins, venules, and dural sinuses If jugular veins are compressed, there is a rise of intracranial pressure that is transmitted to the lumbar subarachnoid space (unless there is a spinal subarachnoid block) This is the basis of the Queckenstedt test, mentioned in Chap 2 In the case of a spinal block, pressure on the abdominal wall, which affects the spinal veins below the point of subarachnoid block, will still increase the lumbar CSF pressure The Valsalva maneuver as well as coughing, sneezing, and straining also causes an increased intrathoracic pressure, which is transmitted to the jugular and then to the cerebral and spinal veins The ICP rises in heart failure, when central and jugular venous pressures become elevated Mediastinal tumors, by obstructing the superior vena cava, have the same effect These increases are manifest despite the presence of valves in the jugular veins When the heart stops, the CSF pressure falls to zero.

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potension induces cerebral vasodilation in order to maintain normal blood ow Upon recovery of the blood pressure, the response in cerebrovascular tone is delayed, thereby allowing intracranial blood volume to accumulate in the dilated vascular bed and raising ICP In support of this explanation is the observation that a brief period of induced elevation of blood pressure paradoxically restores the normal cerebrovascular tone and leads to an abrupt cessation of a plateau wave It has been demonstrated that the high mortality and morbidity of acute cerebral mass lesions is in large part related to uncontrolled elevation in ICP In a normal adult reclining with the head and trunk elevated to 45 degrees, the ICP is in the range of 2 to 5 mmHg Levels up to 15 mmHg are not in themselves hazardous; in fact, adequate cerebral perfusion can be maintained at an ICP of 40 mmHg provided blood pressure (BP) remains normal A higher ICP or a lower BP may combine to reduce cerebral perfusion pressure and cause diffuse ischemic damage, as discussed further on Causes of Raised ICP In clinical practice, one of several general mechanisms causing elevated ICP can be identi ed: 1 A cerebral or extracerebral mass such as brain tumor; massive infarction with edema; extensive traumatic contusion; parenchymal, subdural, or extradural hematoma; or abscess, all of which tend to be localized and deform the adjacent brain The brain deformation is greatest locally, being compartmentalized to a varying degree by dural partitions as already noted Generalized brain swelling, as occurs in ischemic-anoxic states, acute hepatic failure, hypertensive encephalopathy, hypercarbia, and the Reye hepatocerebral syndrome Here the increase in pressure reduces the cerebral perfusion pressure, but tissue shifts are minimal because the mass effect is widely distributed throughout the cranial contents An increase in venous pressure due to cerebral venous sinus thrombosis, heart failure, or obstruction of the superior mediastinal or jugular veins Obstruction to the ow 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 any number of causes (infectious, carcinomatous, granulomatous, hemorrhagic) is another mechanism If the block is con ned 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) Any process that expands the volume of CSF (meningitis, subarachnoid hemorrhage) or, less commonly, increases CSF production (choroid plexus tumor).

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