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Little is known about intracranial venous pressure in hydrocephalus. Recently, we reported that naturally occurring hydrocephalus in Beagle dogs was associated with an elevation in cortical venous pressure. We proposed that the normal pathway for cerebrospinal fluid (CSF) absorption includes transcapillary or transvenular absorption of CSF from the interstitial space and that the increase in cortical venous pressure is an initial event resulting in decreased absorption and subsequent hydrocephalus. Further analysis, however, suggests that increased cortical venous pressure reflects the effect of the failure of transvillus absorption with increase in CSF pressure on the venous pressure gradient between ventricle and cortex. Normally, the cortical venous pressure is maintained above CSF pressure by the Starling resistor effect of the lateral lacunae. A similar mechanism is absent in the deep venous system, and thus the pressure in the deep veins is similar to that in the dural sinuses. Decreased CSF absorption causes an increase in CSF pressure followed by an increase in cortical venous pressure without a similar increase in periventricular venous pressure. The periventricular CSF to venous (transparenchymal) pressure (TPP) gradient increases. In contrast, cortical vein pressure remains greater than CSF pressure (negative TPP). The elevated periventricular TPP gradient causes ventricular dilatation and decreased periventricular cerebral blood flow (CBF), a condition that persists even if the CSF pressure returns to normal, particularly if tissue elastance is lessened by tissue damage. If deep CBF is to be maintained, periventricular venous pressure must increase. Since the veins are in a continuum, cortical venous pressure will further increase above the CSF pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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To gain a better understanding of cerebrospinal fluid (CSF) hydrodynamics and their relationship to the cerebrovascular system, normal and naturally hydrocephalic dogs were studied to determine transmantle [lateral ventricle (LV) to subarachnoid space] and transparenchymal [LV to cortical vein (CV)] pressures. Pressure was also measured in the sagittal sinus, cisterna magna, and femoral artery. CV pressure has not previously been measured in hydrocephalus. Ventricular volume was determined by computed tomography. Four groups of animals were studied. In Group 1 (n = 5) transmantle pressure was measured; in Group 2 (n = 5), transparenchymal pressure in normal animals was measured. In Group 3 (n = 5) was measured all the pressures in spontaneously normal animals, and in Group 4 (n = 6) was measured the pressures in hydrocephalic animals. The pressure-volume index and CSF outflow resistance were also measured. LV volume in the normal dogs was 1.3 +/- 0.7 ml and in the hydrocephalic dogs was 5.1 +/- 2.7 ml (P less than 0.005). Although LV, subarachnoid space, and sagittal sinus pressures were elevated in the hydrocephalic dogs (15.1 versus 10.2, 16.4 versus 10.5, and 8.4 versus 5.2 mm Hg, respectively), the transmantle pressure and subarachnoid space to sagittal sinus gradients were not significantly altered. CV pressure was markedly elevated in the hydrocephalic animals (21.5 versus 11.7 mm Hg, P less than 0.005). The pressure-volume index and outflow resistance were not significantly different. These results suggest that an elevated CV pressure plays a role in the development and/or maintenance of hydrocephalus, and that the pathway for CSF absorption includes transcapillary or transvenular absorption of CSF from the interstitial space.(ABSTRACT TRUNCATED AT 250 WORDS)

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Compliance is considered a fundamental characteristic of the intracranial system, is measured by the volume pressure test (VPT), and is considered to be related to the cerebrospinal fluid (CSF) pulse pressure (delta Pcsf). This study was carried out to determine the time-dependent relationship of intracranial compliance and the relationship between intracranial pulse pressure and compliance. In nine dogs divided into two groups, the rate of injection of a test volume and the physical compliance of the intracranial system was altered by opening or closing the skull without altering the base line intracranial pressure. The VPT was carried out by three methods: slow infusion--infusion of 0.3 ml at 1.5 to 0.2 ml/second, fast infusion--infusion of 0.2 ml in 0.5 second, and bolus injection--injection of 0.05 ml as rapidly as possible. With the skull closed, there were linear relationships between diastolic CSF pressure (Pcsf-d) and delta Pcsf; Pcsf-d and slow infusion, fast infusion, or bolus injection; and Pcsf-d and CSF respiratory wave amplitude. With the skull open, the linear relationship was retained only for Pcsf-d vs. delta Pcsf and Pcsf-d vs. bolus injection. Furthermore, delta Pcsf amplitude at any level of Pcsf-d was the same whether the skull was open or closed. It is concluded that intracranial compliance can be divided into two components based on the time constant of the injected volume: physical compliance, which has a short time constant and is related to delta Pcsf, and physiological compliance, which has a longer time constant and is related to the VPT.

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Twenty-one dogs were rendered hydrocephalic by the intracisternal injection of kaolin. After various intervals between 1 and 44 days the animals were anesthetized for the measurement of arterial (lingual), ventricular, and sagittal sinus pressures. Following the recordings the animals were sacrificed by formalin infusion, the brains sectioned serially, and ventricular size measured. In general, the longer the period of incubation the larger the ventricles. There was no correlation between the degree of hydrocephalus and mean or pulsatile ventricular pressure. All animals with a pressure of less than 9 torr demonstrated non-linear transmission of the arterial wave into the CSF (which is the same as the pulse in the venous bed). All animals with a pressure greater than 12 torr had linear transmission of the wave. These findings in the hydrocephalic animals are the same as those found in nonhydrocephalic animals with similar pressures. It is concluded that the CSF pulse wave seen in hydrocephalic dogs is a result of how the cerebrovascular bed processes the cardiac pulse wave and is independent of the hydrocephalic process. There is no evidence that the pulse wave produces hydrocephalus.

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Systemic arterial (Ps), cerebrospinal fluid (Pcsf), and sagittal sinus (Pss) pressures were measured in 39 dogs divided into eight groups in which Ps was altered pharmacologically or by bleeding. The pharmaceuticals used were norepinephrine (N-EP), dopamine (DOP), sodium nitroprusside (SNP), and nitroglycerin (NTG). SNP and NTG were examined with and without methohexital (MHX) anesthesia and during chronic infusion and bolus injection. The various pressures were subjected to systems analysis in accordance with a previously published model of myogenic autoregulation. Myogenic autoregulation seemed to be impaired only during infusions of N-EP, DOP, and SNP without MHX and during hypovolemic hypotension. The various observed changes in Pcsf are explained by using a hydraulic model of the cerebrovascular bed in which Pcsf represents the pressure drop across the outflow resistance of the bridging veins and lateral lacunae and myogenic autoregulation at the arteries and arterioles represents the major inflow resistance. Impaired myogenic autoregulation is associated with a rise in Pcsf. In addition, variation in pulse pressure is demonstrated to be related to the arterial pulse pressure and the degree of arterial and arteriolar vasodilation.

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A hydraulic model of the cerebrovascular bed is presented. The model consists of a Starling resistor in series with an upstream resistance. Volume-pressure tests were performed on the model by injecting fluid into the rigid shell of the Starling resistor. An exponential pressure response to the increase in fluid volume was observed, which supports the hypothesis that the origin of the in vivo exponential pressure response to a transient increase in cerebrospinal fluid (CSF) volume can be attributed to compression of the cerebral vessels, most probably the veins. Mathematical expressions for the dependence of pressure on volume change were derived from the model and applied to in vivo volume-pressure data. The correlation between the model and in vivo experiments suggests that the CSF pressure is coupled to cerebral venous pressure and that the volume-pressure test is an indirect measure of the cerebral venous volume and is not a measure of intracranial elastance. The physical basis for the volume-pressure test is clarified, and expressions are derived to improve the utility of the test.

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Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.

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Systems analysis of cerebrospinal fluid pulse wave forms (CSFPWs) was carried out in 19 cats during the inhalation of 5% CO2 + 95% O2. 10% CO2 + 90% O2 and 10% O2 + 90% N2. The results were compared to CSFPWs obtained during the inhalation of 100% O2 and during an intraventricular infusion to the same level of cerebrospinal fluid (CSF) pressure (CSFP) as produced by the test gas. The systemic arterial pressure pulse was utilized as the system input, and the CSFP pulse was used as the output. The harmonic amplitudes of the two pulses and the amplitude transfer function (XFRa) between the pulses were calculated. Hypercapnia and and hypoxia produced an increase in CSF pulse pressure (delta Pcsf), an increase in primarily the XFRa of the fundamental frequency, and as a result, an increase in amplitude of the fundamental frequency of the CSFPW with rounding of the pulse wave. The changes are greater than those noted during an intraventricular infusion (IVI) to the same level of CSFP. In addition, the volume-pressure test was performed on the hypercapnic animals. The volume-pressure response was less during hypercapnia than during the IVI at the same mean level of CSFP. The result suggest that the increase in deltaP csf is related to cerebral arteriolar vasodilation and not to a steepening of the volume-pressure curve and that rounding of the CSFPW is related to a decrease in cerebrovascular tone.

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Systems analysis is explored as a method of evaluating intracranial pressure (ICP). The intracranial cavity is characterized by a transfer function that is evaluated by the blood pressure pulse acting as the system input and the ICP pulse acting as the output. A comparison is made of the ability of systems analysis, volume-pressure test (VPT), and cerebrospinal fluid-pulse amplitude analysis (CSFPAA) to distinguish between an epidural balloon inflation (EBI) and an intraventricular infusion (IVI) at various steady state levels of ICP. The VPT could not distinguish between EBI and IVI at any level of ICP, and above 30 mm Hg the volume-pressure response decreased. Spectral analysis was able to distinguish EBI from IVI above 30 mm Hg, and CSFPAA was demonstrated to be a simplified spectral analysis. Changes in ICP waveform generated during each cardiac cycle appear to be related to changes in vasomotor reactivity and may have value in the clinical monitoring of ICP.

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