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A method using chronically prepared, anesthetized dogs was devised for studying the effects of treatments of intracranial hypertension induced by applying a reversible extradural mass lesion while simultaneously measuring production of cerebrospinal fluid. This was measured with a ventricular-cisternal perfusion technique in which the rate of cisternal outflow could be controlled by a pump and matched to the inflow, allowing intracranial pressure to fluctuate despite simultaneous measurement of cerebrospinal fluid formation. Elevations of intracranial pressure to the range 20 to 35 Torr were induced and maintained during perfusion, but elevations above 35 Torr would not permit continued perfusion. At normal intracranial pressure, 10 Torr or less, rates of cerebrospinal fluid formation were the same whether the outflow controlling pump or free outflow was used. Formation of cerebrospinal fluid decreased progressively as intracranial pressure increased above 20 Torr. It also decreased with time after the start of perfusion during the course of 5 h, but returned to the initial range during the control phase of subsequent experiments in the same animal. Furosemide, 3 mg kg-1, i.v., had no significant effect on rate of formation but did induce a small decrease in ICP in time-controlled experiments in which i.v. fluid replacement limited net fluid losses to 20 ml kg-1 with no change in mean arterial or central venous pressures.

Intracranial pressure (ICP) is often measured from intraventricular catheters, a technique that allows therapeutic drainage of ventricular cerebrospinal fluid (CSF) as an aid in controlling ICP and circumventing obstruction. Drainage of CSF simultaneously with ongoing ICP measurement has been advocated as safe and efficient, and devices are commercially available to permit this practice; however, this concept has been seriously challenged, based on clinical observations. The inaccuracy induced by simultaneous CSF drainage and ICP monitoring is quantitated in this report in a mechanical brain model using a standard ventricular catheter. The following conclusions have been confirmed: 1) rapid CSF drainage induces a severe artifactual reduction in measured ICP, more extreme at higher pressures; 2) calibrated slower rates of CSF drainage produce a severe, although less immediate, reduction in measured ICP; 3) severe artifact appears even in the presence of continuous CSF outflow, so a system that measures ICP only in the presence of CSF flow does not prevent artifact; 4) with simultaneous CSF drainage, measured ICP is determined more by the outflow pressure setting than by actual brain pressure; 5) Since ICP elevation of 25 to 30 mm Hg blocks CSF production, even slow fluid drainage at high pressures should ultimately lead to ventricular collapse and severe artifact.

The authors have attempted to find a clinically reliable method of measuring intracranial pressure (ICP) compliance or reactivity that does not require volumetric manipulation. An analysis was undertaken of ICP, pulse widths and of the presence or absence of B waves, both experimentally in dogs and clinically in postoperative human patients. In both dogs and humans, ICP pulse width generally increased with increasing ICP and with increasing intracranial mass, and definitely increased with systolic arterial blood pressure. Nonetheless, ICP pulse width commonly failed to increase with increasing cerebral reactivity, and low ICP pulse width measurements were at times recorded in distinctly pathological situations. From the clinical study it was found that B waves were encountered more commonly in patients with increased ICP or increased ICP pulse width. However, the correlation between B waves alone or in combination with increased ICP or ICP pulse width and quantitative measurements of ICP reactivity was not significant. Mean reactivity and the range of reactivity measurements were almost identical in patient groups with and without B waves. For the time being the "ICP reserve test" remains the most accurate, the safest, and the most clinically useful method of quantitating ICP reserve.

Quantitating cerebral "elastance" or "ICP reserve" has added considerably to the value of continuous monitoring of intracranial pressure (ICP). Intracranial pressure reserve is a measure of the capacity of the brain's natural compensatory mechanisms for countering increases in ICP secondary to increases in intracranial volume. Intracranial pressure reserve testing was studied in dogs with known volumes of extracerebral intracranial mass, both in normal and in edematous brains and at various ICPs. Ten thousand measurements were made with five different methods of measuring ICP reserve. Testing when multiple increments of subdural saline infusion were used over a five-minute period to quantitate ICP reactivity to volumetric stress seemed most reliable and most adaptable to clinical application. Methods of measuring cerebral "elastance" using only a single subdural infusion proved to be variable and difficult to read.

Sequential subdural injections of fluid through an intracranial pressure (ICP) monitoring cup catheter have been employed to measure "ICP reserve" in a series of 136 determinations in 30 patients over a total of 155 days of recordings. This dynamic method of quantitating the brain's ability to adapt to increased intracranial volume tests the brain's compensatory mechanisms over a five-minute time span. The test, incorporating several safety features, has been found to be reliable, safe, and well tolerated. A series of observations have been made using this test in patients with subdural drains and in response to fluid, mannitol, and dexamethasone therapy. Deteriorating ICP reserve gave early warning of the need for reoperation for postoperative hematoma, massive brain swelling, or cystic reaccumulation. Intracranial pressure reserve testing also quantitated the evolution of postoperative brain edema. Changes in ICP reserve could be detected as much as 48 hours before changes in baseline ICP and as much as 72 hours before clinical deterioration was evident.

The author describes a simple catheter designed for use in the measurement of intracranial pressure, especially during the initial stage following craniotomy. The device has been studied in experimental animals, and has been used in 40 neurosurgical patients for periods up to 15 days.

The intracranial pressure "reserve" test seems to be the most reliable method of determining when the brain's natural mechanisms for pressure compensation for added intracranial volume have been compromised or exhausted. The test employs a timed sequence of intracranial fluid injections, but as a safety precaution injections are discontinued if intracranial pressure remains elevated more than 10 Torr over baseline. In this case, a linear extrapolation is then calculated to determine the elevation which might have been achieved by a full series of injections. However, this linear extrapolation has been criticised on the expectation that an exponential response should be expected. A series of experimental observations in dogs and baboons and a review of clinical records in humans have been made to determine the observed slope of increase following aliquot injection during performance of the intracranial pressure reserve test. In these species the observed response was actually linear in shape rather than exponential. This held true even for different initial baseline values and with different volumes of "lesion" balloon inflations in experimental animals. A theoretic explanation is proposed.