Sagittal Sinus Pressure Research Articles

A Starling resistor regulates cerebral venous outflow in dogs.

This investigation was undertaken to determine whether a Starling resistor or venous waterfall effect exists between the sagittal sinus and the cerebral veins such that increases in sagittal sinus pressure (Pss) do not abolish cerebral venous outflow and to examine two possible contributions of extracranial venous valves in regulating outflow. Anesthetized dogs were subjected to positive end-expiratory pressure (PEEP) before and after intracranial pressure (Pic) was elevated by inflation of an epidural balloon. PEEP raised Pss equally in all animals, but Pic and cerebral venous pressure (Pcv) increased less in the presence of intracranial hypertension. When Pss was low, passage of a catheter in the cerebral vein in and out of the sagittal sinus demonstrated an abrupt drop in pressure as the sinus was entered. When Pss was raised and lowered independently of superior vena caval pressure (Psvc) the changes in Pic and Pcv were less when Pss was decreased than when it was increased. Sustained increases and decreases in Psvc caused increases and decreases in Pcv, Pic, Pss, and external jugular venous pressure (Pejv) regardless of whether external jugular venous valves were present or absent. We conclude that a Starling resistor between the sagittal sinus and the cerebral veins regulates cerebral venous outflow when Pss is increased by PEEP and other maneuvers that raise Psvc. The waterfall maintains Pcv and Pic at normal levels when Psvc and Pss are reduced. Extracranial venous valves are not essential to this mechanism.

Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation.

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.

Benign intracranial hypertension and disorders of CSF absorption

Sixteen patients suffering from benign intracranial hypertension were studied by a continuous measurement of intraventricular pressure, a simultaneous recording of intraventricular and sagittal sinus pressures, and a measurement of the cerebrospinal fluid (CSF) resistance to drainage. Isotope cisternography was performed and the patency of the dural sinuses verified by direct sinography or phlebography or both. The same procedure was used to study 6 other patients suffering from disorders leading to the same type of intracranial hypertension. In 16, our results confirm a defect in CSF absorption mechanisms linked to an abolition of the pressure gradient between CSF and sagittal sinus in 6 patients, as well as an important increase in CSF resistance to drainage in 10 others. Despite this defect, the CSF circulation was normal in most patients (10 of 12) as demonstrated by isotope cisternography.

Cerebral venous pressure during actively induced hypertension and hypercapnia in cats.

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.

CSF formation and absorption estimates by constant flow infusion method.

The constant-flow infusion method has been used to calculate conductance and the rate of CSF formation in 54 patients with varied but stable clinical pictures, normal CSF pressures, and dilated ventricles. Values for conductance varied from 0.00203 to 0.0263 mL/min/mm H2O, with a peak between 0.005 and 0.010, mL/min/mm H2O. Values for CSF formation uncorrected for a small, negative linear term containing the sagittal sinus pressure varied from 0.114 to 3.0 mL/min, with a peak between 0.5 and 1.0 mL/min, a range considerably larger than that given by earlier studies. Results indicate that CSF formation is reduced in the presence of low conductance. There is a possibility that the syndrome of normal pressure hydrocephalus results from underformation with ventricular stagnation. Low conductance values may identify shunt-responsive syndromes.

Megalencephaly in infants and children. The possible role of increased dural sinus pressure.

Seven children studied because of clinical macrocephaly and suspected hydrocephalus ultimately proved to have megalencephaly apparently due to an increase in sagittal sinus venous pressure as established from infusion studies. Unexplainably, these patients were all males. All were seen initially between 2 and 8 months of age. Head enlargement exceeded two standard deviations in all seven. Pneumoencephalography, ventriculography, or computerized tomography demonstrated normal or minimally enlarged ventricles that did not progress in size. Isotope cisternography was abnormal. Studies of CSF formation and absorption demonstrated normal absorption rates but high calculated sagittal sinus pressures. Though therapy was usually not required, in one unusual infant, severe progressive macrocephaly with minimal hydrocephalus required a shunt. Another had a transient episode of acute hydrocephalus associated with a low CSF absorption rate and ventricular enlargement. In this report, we review the intracranial hydrodynamics of benign intracranial hypertension (BIH), communicating hydrocephalus, and the pathogenesis of megalencephaly. Benign intracranial hypertension and the type of megalencephaly demonstrated by our patients appear to develop similarly except that the presence of open cranial sutures may allow a transient nonhydrostatic loading of brain parenchyma in infants, resulting in mild, nonprogressive macrocephaly.

Pre- and postoperative cerebrospinal fluid absorption studies in patients with myelomeningocele shunted for hydrocephalus.

Nine infants with myelomeningocele and hydrocephalus had cerebrospinal fluid formation and absorption studies before insertion of a ventriculoperitoneal shunt. Six were also tested postoperatively. The preshunt formation rate varied from 0.21-0.42 ml.min-1 and the cerebrospinal fluid absorption rate or CSF conductance (Ccsf) varied from 0.008 to 0.031 ml.min-1.mm Hg-1. The postoperative formation rate varied from 0.21 to 0.39 ml.min-1. The postoperative CSF conductance (Ct) was calculated as the sum of Ccsf and the shunt conductance (Cs). The relationship between the Ccsf and Cs curves was determined by matching the sum of these curves to the postoperative data points using the method of least-squares. The data suggests that the shunt may work directly or indirectly to establish a new resting pressure; the latter by stabilizing the sagittal sinus pressure which preoperatively increased concomitantly with the CSF pressure and thus enhanced an already-existing absorption deficit.

Dural posterior fossa AVM producing raised sagittal simus pressure. Case report.

A patient with raised intracranial pressure secondary to a dural arteriovenous malformation (AVM) of the posterior fossa is presented. Direct shunting of arterial blood into the transverse sigmoid sinus caused a considerable increase of the sagittal sinus pressure (SSP) and elevation of intracranial pressure (ICP). Both ICP and SSP returned to normal values following obliteration of the dural AVM by selective embolization.

The effect of increased intracranial pressure on pressure in the superior sagittal sinus.

It is difficult to explain why rises in ICP provoke different types of response in superior sagittal sinus pressure. In most of our experimental animals there was close correlation between rises in ICP and SSSP. In the remainder, SSSP showed little increase when ICP rose. The animals with marked increase in SSSP showed a greater capacity for compensation for increased amounts of intracranial fluid.

Effects of arterial hypoxaemia, hypercapnia, and changes in cerebral perfusion pressure on mean cerebrospinal fluid and sagittal sinus pressure.

In 20 anaesthetised, artificially ventilated dogs the influence of arterial hypoxaemia, hypercapnia, and decreased systemic arterial blood pressure on mean cerebrospinal fluid pressure and on the pressure in the superior sagittal sinus was studied. Below a PaO2 of 40 Torr and above a PaCO2 of 70 Torr, CSFP was significantly increased. The pressure rise in the torcular, however, was only moderate. Simultaneous CBF measurements showed marked cerebral hyperaemia to be the essential cause of the increase in CSFP. In deep normovolaemic arterial hypotension (MABP below 50 mm Hg), CSFP and SSP were significantly decreased. CBF fell sharply by about 50% compared to the resting values. In arterial normotension and under normocapnic-normoxic conditions, a pressure difference of about 3 mm Hg existed between CSFP and SSP. This pressure difference increased in hypoxia and hypercapnia and fell in arterial hypotension below the “opening-pressure” of the arachnoid villi. An artificially induced rise of CSFP in another 5 experimental animals was reflected to a minor degree in the torcular pressure. However, during rapid reduction of raised intracranial pressure, a transient, but marked pressure rise occurred in the torcular, persisting as long as systemic arterial blood pressure was increased (Cushing response). This is explained by post-compression cerebral hyperaemia and by the undamped transmission of the hypertensive arterial pressure to the dilated cerebral vessels. The origin of the rapid CSF pulse waves was studied in simultaneous recordings of intracranial CSF, cerebral venous, systemic arterial and central venous pressure, and it was shown that the height of CSFP is dependent on MABP, whereas the contour of the CSF pulse waves is shaped by rapid changes of cerebral blood volume in the post-capillary cerebral vascular bed.

Pressure in the sagittal sinus during intracranial hypertension in man.

✓ Intracranial pressure (ICP) and sagittal sinus pressure (SSP) were measured simultaneously in 12 patients with brain tumors and secondary intracranial hypertension (ICH). In nine, the mean SSP was largely unaffected by changes in ICP. In three, SSP changed with the ICP. In all but one patient, the ICP remained higher than SSP and, as the ICP increased, the difference between the two also increased. Sinograms performed during ICH demonstrated partial collapse of the sinuses in some patients and not in others. The mean SSP in adults with brain tumors appears to respond unpredictably to changes in ICP. Since the rate of cerebrospinal fluid drainage depends upon the gradient between ICP and SSP, intracranial spatial compensation is probably influenced by the response of SSP to ICP. Individuals with gradients that rapidly increase because their sinuses do not collapse probably compensate more rapidly than those whose sinuses do collapse. This assumed difference in the rate of spatial compensation may account for some of the variability of the ICP response to an enlarging intracranial mass or a change in cerebral blood volume.

Raised intracranial pressure and cerebral blood flow. 3. Venous outflow tract pressures and vascular resistances in experimental intracranial hypertension.

Pressure changes within the venous outflow tract from the brain were studied in anaesthetized baboons. Segmental vascular resistance changes were also calculated and the results correlated with the changes in cerebral blood flow, measured by the (133)Xenon clearance method. Three different methods were used to raise intracranial pressure: cisterna magna infusion, a supratentorial subdural balloon, and an infratentorial subdural balloon. A close correlation was found between the cortical vein pressure and intracranial pressure with all methods of raising intracranial pressure: the overall correlation coefficient was 0·98. In the majority of animals sagittal sinus pressure showed little change through a wide range of intracranial pressure. In three of the six animals in the cisterna magna infusion group, however, sagittal sinus pressure increased to levels approaching the intracranial pressure during the later stages of intracranial hypertension. Jugular venous pressure showed little change with increasing intracranial pressure. The relationship between cerebral prefusion pressure and cerebral blood flow differed according to the method of increasing intracranial pressure. This was due to differing patterns of change in prevenous vascular resistance as venous resistance increased progressively with increasing pressure in all three groups. The present results confirm, therefore, the validity of the current definition of cerebral perfusion pressure-that is, cerebral perfusion pressure is equal to mean arterial pressure minus mean intracranial pressure-by demonstrating that intracranial pressure does represent the effective cerebral venous outflow pressure.

Arachnoid granulations of the sheep. Structural and ultrastructural changes with varying pressure differences.

Sheep arachnoid granulations were examined to determine the morphologic changes induced by varying pressure differences between the subarachnoid space and the superior sagittal sinus. With the superior sagittal sinus pressure maintained at zero, increasing subarachnoid space pressures caused increasing distention of the arachnoid granulations. Granulations fixed in the distended state by combined subarachnoid and arterial perfusion of aldehydes remained distended even when the gradient was reduced to zero. Electron microscopic studies showed that as the pressure difference was increased (1) neighboring endothelial cell overlappings were shorter and the intercellular spaces were irregularly widened, (2) the endothelial-lined tubules became distended, (3) the endothelial cells showed increased pinocytotic activity, and (4) the stromal cellular and extracellular components were more separated.

Circulatory disturbance of the venous system during experimental intracranial hypertension.

✓ The venous drainage system during increased intracranial pressure (ICP) was studied in dogs. The ICP was gradually increased to the level of the systemic blood pressure while related arterial and venous pressures were monitored. The blood flow through the parasagittal intradural venous channels (lateral lacuna) was also measured to test the collapsibility of these vessels. The cortical venous pressure was constantly 50 to 200 mm H2O higher than the ICP regardless of the degree of elevation, while the sagittal sinus pressure remained at 50 to 75 mm H2O unless the central venous pressure was elevated by respiratory disturbance. Flow through the lateral lacuna decreased as the ICP was increased. The authors conclude that the low pressure in the sinus and the consistency of the walls of the lateral lacuna allow gradual stenosis of the lacuna during increased ICP.

Vascular responses to acute intracranial hypertension.

In 27 rhesus monkeys the cerebrospinal fluid pressure (CSFP) was raised by injections into the cisterna magna to about 40 to 50 mm Hg in steps of 5 mm Hg every five minutes. During the initial phase of the rise of the CSFP to about 15 mm Hg normal animals showed a significant fall in the systolic arterial blood pressure. With a further elevation of the CSFP the BP rose till the CSFP reached 30 to 40 mm Hg. If the CSFP were raised higher than that, a large number of the animals showed a significant fall in the BP. In animals which were shocked before the CSFP was raised there was no drop in the systolic BP during the initial phase. This study indicates that vascular decompensation occurs in the majority of animals when the CSFP goes higher than 30 to 40 mm Hg; there is a significant rise in the pulse rate, superior sagittal sinus pressure (SSP), and internal jugular vein pressure (JVP). The JVP was related to the SSP, indicating that the JVP most probably reflected the pressure changes in the intracranial venous sinuses. Four animals suddenly collapsed at the highest CSFP. In the remaining 23 animals, on a sudden lowering of the CSFP to zero from the highest level, 13 monkeys died in less than half an hour and four in about an hour, while six animals stood this elevation of the CSFP well, with a good recovery. This indicates that, once the vascular decompensation has set in, the prognosis is generally poor even after lowering the CSFP to normal. The drop of the CSFP to zero produced no significant change in the pulse rate but a significant fall in the BP. The SSP rose when its pre-lowering level was less than 7·5 mm Hg and fell when the level was at or above 7·5 mm Hg level. The JVP showed a significant correlation with the variations in the SSP. The fundus examination at the end of the experiment revealed no abnormality.

Response of cereborspinal fluid pressure to hyperbaric oxygenation.

The response of cerebrospinal fluid pressure (CSFP) to hyperbaric oxygenation (OHP) was investigated in 13 patients with acute cerebral damage and in dogs with or without experimentally produced cerebral damage. To elucidate the mechanism of the CSFP response, continuous measurements of carotid blood flow, arterial blood pressure, central venous pressure, and superior sagittal sinus pressure and CSFP were made before, during and after OHP. There was considerable variation in the response of CSFP to OHP in the patients, but three main patterns emerged; type I (nine cases), CSFP decreased at the beginning and rose again at the end of OHP, type II (two cases), CSFP fell with OHP and remained significantly lower than pretreatment level after it, and type III (two cases), CSFP showed little change with OHP. An animal without cerebral damage commonly showed a type I response of CSFP to OHP; the changes of CSFP at the beginning and end of OHP are mainly due to the changes of the cerebral blood flow. There may be two different actions of OHP on cerebral oedema, one decreasing cerebral oedema and another (mainly affecting the normal brain) producing cerebral oedema. Information obtained from the response of CSFP to OHP may be useful in judging the severity and pathophysiological state of cerebral damage.

Ventricular size and chronic increased intracranial venous pressure in the dog.

✓ Intracranial venous pressure was increased by blocking the torcular Herophili in 10 dogs. At intervals of 1 to 29 weeks, pressure in the superior sagittal sinus and cerebrospinal fluid (CSF) were recorded and the size of the ventricles determined at autopsy. Changes in venous pathways were documented by sinograms. Significant increase in both sagittal sinus and CSF pressures occurred after torcular block. CSF pressures remained elevated for as long as 29 weeks at an average of 100 mm above preblock levels. Neurological deficits after torcular block were minimal. Autopsies showed normal-sized ventricles without any stigmata of hydrocephalus.

Compression of cerebral vessels by intracranial hypertension. I. Dural sinus pressures.

In the monkey, sagittal sinus pressure is a complex function of cerebral blood flow and intracranial pressure; jugular vein pressure is a qualitative measure of cerebral blood flow. In the presence of intracranial hypertension, the response of anterior sagittal sinus pressure to blood flow changes is greatly exaggerated, but there is minimal communication of these large fluctuations in pressure to the transverse sinus and jugular vein. On the basis of these observations, we postulated compression of the sagittal sinus in response to increased intracranial pressure, and evidence is presented to localize maximum compression to the region of the interaural line. Reduction in diameter of cerebral vessels proximal to the sinus also appears to occur with intracranial hypertension, and ultimately, the dynamic interaction of these two factors is responsible for sagittal sinus pressure. In the end stage of cerebral decompensation, when intracranial and arterial tensions are equal, anterior sagittal sinus pressure also approaches the diastolic pressure, indicating nearly total collapse of the sinus.