Cerebrospinal Fluid Outflow Resistance Research Articles

Frontal Brain and Leptomeningeal Biopsy Specimens Correlated with Cerebrospinal Fluid Outflow Resistance and B-wave Activity in Patients Suspected of Normal-pressure Hydrocephalus

Frontal Brain and Leptomeningeal Biopsy Specimens Correlated with Cerebrospinal Fluid Outflow Resistance and B-wave Activity in Patients Suspected of Normal-pressure Hydrocephalus

Frontal brain and leptomeningeal biopsy specimens correlated with cerebrospinal fluid outflow resistance and B-wave activity in patients suspected of normal-pressure hydrocephalus.

Normal-pressure hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space has been suggested as the pathoanatomic basis. The purpose of the present study was to investigate whether meningeal fibrosis causes increased resistance to cerebrospinal fluid outflow (R(out)) and/or increased B-wave activity and whether pathological changes in the brain parenchyma after brain compliance, causing increased B-wave activity. The study involved a group of 38 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 29 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed. Meningeal fibrosis was found in 12 of 25 biopsies containing arachnoid tissue, but no correlation with R(out) or B-waves was found. Pathological parenchymal changes, most often Alzheimer's disease (10 cases) or vascular changes (10 cases), were found in 21 biopsies, but no correlation with B-waves or R(out) was found. The results suggest that leptomeningeal fibrosis is not the only pathoanatomic basis of increased R(out) and/or B-wave activity in patients with NPH and that various degenerative changes in the parenchyma may be responsible for the altered cerebrospinal fluid dynamics characteristic of NPH.

Elevated Cortical Venous Pressure in Hydrocephalus

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)

Subacute hydrocephalus after experimental subarachnoid hemorrhage: its prevention by intrathecal fibrinolysis with recombinant tissue plasminogen activator.

It is investigated whether intrathecal fibrinolysis may prevent subacute hydrocephalus after subarachnoid hemorrhage (SAH). In 19 cats, SAH was induced by the intracisternal infusion of 1 ml/kg body weight of fresh autologous blood at a rate of 0.6 ml/min. Eleven of those animals were treated by intrathecal fibrinolysis performed 24 hours after experimental SAH by intracisternal infusion of 3 mg of recombinant tissue plasminogen activator. Included were eight animals suffering from experimental SAH and four healthy animals retained for control. A computed tomographic scan performed 24 hours after the SAH displayed an acute hydrocephalus from the experimental procedure. Cerebrospinal fluid outflow resistance was 71 +/- 5.0 mm Hg/ml/min in the healthy animals, 265 +/- 19.8 mm Hg/ml/min in the nontreated animals 7 days after SAH, and 151 +/- 6.4 mm Hg/ml/min in the recombinant tissue plasminogen activator-treated animals 7 days after SAH (mean +/- standard deviation; changes significant with P less than 0.01). Postmortem planimetry of both lateral ventricles gives a mean of 3.7 +/- 2.7 mm2 in the healthy animals, 11.1 +/- 3.9 mm2 in the nontreated group after SAH (P less than 0.01), and 3.5 +/- 1.1 mm2 in the animals treated with recombinant tissue plasminogen activator. Intracranial pressure monitoring demonstrated marked intracranial pressure waves only in the nontreated animals after SAH. It is concluded that intrathecal fibrinolysis may prevent subacute hydrocephalus after experimental SAH.

Effects of bilateral jugular vein ligation on intracranial pressure and cerebrospinal fluid outflow resistance in cats

In order to study the effect of jugular venous outflow obstruction on intracranial pressure and cerebrospinal fluid (CSF) reabsorption capability, changes in epidural pressure (EDP) and CSF outflow resistance (Ro) were examined following bilateral jugular vein ligation in cats. EDP increased significantly (P<0.01) immediately after ligation from the control value of 4.9±0.5 mmHg (mean±SEM) to 15.9±0.9 mmHg. Thereafter, EDP gradually decreased back toward the control value. The pressure level had decreased to 6.7±0.5 mmHg by 20 minutes after ligation. The mean Ro was significantly (P<0.01) higher in the ligation group (200.4±9.7 mmHg/ml/min) that in the non-ligation group (120.0±9.9 mmHg/ml/min). These results suggest that bilateral jugular vein ligation impairs CSF reabsorption.

Elevated cortical venous pressure in hydrocephalus

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)

Effect of intrathecal fibrinolysis on cerebrospinal fluid absorption after experimental subarachnoid hemorrhage

The effect of intrathecal fibrinolysis on cerebrospinal fluid (CSF) absorption was investigated after experimental subarachnoid hemorrhage (SAH). In 11 cats, SAH was induced by intracisternal application of 1 to 4 ml of fresh autologous blood. Thirty minutes after the experimental SAH, the CSF outflow resistance was found to be elevated from a median of 77 mm Hg/ml/min (range 41.3 to 109 mm Hg/ml/min) to a median of 580 mm Hg/ml/min (range 104 to 7000 mm Hg/ml/min). A logarithmic relationship could be demonstrated between the volume of subarachnoid blood and the elevation of the CSF outflow resistance. The intrathecal application of 2 mg of recombinant tissue plasminogen activator (rt-PA), which is a fibrinolytic substance suitable for lysis of subarachnoid blood clots in man, resulted in an almost total restoration of CSF absorption after experimental SAH. The CSF outflow resistance after SAH was lowered by application of rt-PA from a median of 1028.05 mm Hg/ml/min (range 394 to 7000 mm Hg/ml/min) to 79 mm Hg/ml/min (range 56.7 to 223 mm Hg/ml/min). It is concluded that the impairment of CSF absorption after SAH may play an important role in the pathogenesis of post-hemorrhagic vasospasm.

Steady-state lumbar infusion tests in the management of children with craniosynostosis

Sixty lumbar steady-state infusion tests were used as a guideline in the management of 30 children with craniosynostosis during a 3-year period. The primary decompressive procedure was performed during the same anesthetic period and was made more extensive in cases with pathological outflow resistance (Ro) values. In 11 children with scaphocephaly the test revealed normal to moderately increased cerebrospinal fluid (CSF) Ro. In 6 children with oxycephaly, 4 with trigonocephaly or combined forms, especially in 7 children with syndromic forms, the need for decompressive surgery was usually more obvious. Also, many of these demonstrated severely increased CSF outflow resistance (above 12 mmHg/ml per min). Spinal infusion tests were particularly helpful in the management of severe syndromic or familial cases where the indication for repeat or further extensive decompression was sometimes difficult to assess on clinical and radiological grounds.

Acute changes in the dynamics of the cerebrospinal fluid system during experimental subarachnoid hemorrhage

Early changes in intracranial pressure (ICP), ICP volume index, and resistance to absorption of cerebrospinal fluid induced by experimental subarachnoid hemorrhage were studied in cats. After SAH, the ICP was slightly elevated, and there was a decrease in the buffering capacity of the intracranial space and a sharp rise in outflow resistance. During infusion of blood into the cisterna magna with a constant infusion rate, an extensive increase in ICP could be demonstrated in contrast to the infusion of saline, which caused only slight elevation of ICP. Furthermore, during blood infusion, the ICP level did not reach a plateau phase of pressure, as was demonstrated during infusion of saline. It is suggested that the marked increase in ICP during blood infusion into the subarachnoid space is caused by intracranial volume loading and the simultaneous increase in cerebrospinal fluid outflow resistance. It is concluded that the reported relationship between increased cerebrospinal fluid outflow resistance and increased ICP supports the hypothesis of a strong increase in ICP during subarachnoid hemorrhage in human subjects.

Hydrocephalus in an achondroplastic child treated by venous decompression at the jugular foramen

A 10-month-old child with achondroplasia with progressive head enlargement, ventriculomegaly, and wide subarachnoid spaces over the hemispheres was referred for evaluation. A steady-state lumbar infusion test revealed increased cerebrospinal fluid (CSF) outflow resistance (14 mm Hg/ml/min), and intra-arterial digital subtraction angiography (DSA) demonstrated bilateral venous outflow obstruction due to stenosis of the jugular foramen. Surgical decompression by opening the right jugular foramen relieved the clinical signs of intracranial hypertension. During the following year, the patient's head enlargement was moderate with relative normalization of size. Repeat DSA demonstrated improved venous runoff on the right side, and a steady-state lumbar infusion test demonstrated reduced CSF outflow resistance (10 mm Hg/ml/min). Venous decompression is causal therapy and may prove to be preferable to shunting in children with hydrocephalus and bilateral stenosis of the jugular foramen.

Cerebrospinal fluid outflow resistance measurements in the selection of patients for shunt surgery in the normal pressure hydrocephalus syndrome. A controlled trial

In an attempt to determine to what extent the measurement of cerebrospinal fluid (CSF) outflow resistance (R(out)) can distinguish patients with normal-pressure hydrocephalus (NPH) who respond to shunt surgery from patients who fail to do so, the authors undertook a controlled trial. Eighteen patients with the diagnosis of NPH entered the study. In connection with the shunt operation all patients who entered the study underwent R(out) measurement by means of the pressure-volume index (PVI) method of bolus manipulation (Marmarou et al.). As a safety measure patients above 70 of age and patients with dementia as the only clinical symptom underwent continuous intraventricular pressure measurement before they entered the final study. As a result a total of fourteen patients underwent PVI test and shunt surgery during the same procedure. Patients with normal R(out) thus served as controls, since all patients underwent shunt surgery irrespective of the result of the R(out) measurement. Eight patients improved following surgery and the outcome did not correlate with result of PVI nor R(out) determinations.

Relationships between intracranial pressure, ventricular size, and resistance to CSF outflow.

In 230 patients with normal-pressure hydrocephalus, high-pressure hydrocephalus, or benign intracranial hypertension, measurements of the intracranial pressure (ICP), ventricular size, and cerebrospinal fluid (CSF) outflow resistance (Ro) have revealed a linear relationship between ICP and Ro. It is shown that on average the CSF formation rate tends to decrease with increasing ICP. It is also shown that the size of the ventricles increases as the ICP levels off toward normal values. The clinical implication of this is that a small or normal ventricular size in acute or subacute phases does not preclude defective CSF resorption.

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients.

The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.

Variations in pressure-volume index and CSF outflow resistance at different locations in the feline craniospinal axis

Pressure volume index (PVI) and cerebrospinal fluid (CSF) outflow resistance (Ro) were estimated in spontaneously breathing anestheized cats by the bolus injection test under normal conditions and also under abnormal conditions produced by slow infusion of saline into the CSF space. Bolus injections were made separately into the lumbar subarachnoid space, cisterna magna, and lateral ventricle. The mean PVI values in the lumbar sac, cisterna magna, and lateral ventricle under normal conditions were 0.70, 0.71, and 0.64 ml, respectively; not significantly different from each other. Saline infusion lowered PVI significantly at every site; PVI values in the lumbar sac, cisterna magna, and lateral ventricle were 0.54, 0.52, and 0.53 ml, respectively; not significantly different from each other. Indirect values of PVI were calculated from the pressure responses observed at sites other than where the bolus had been injected. These indirect PVI values were always greater than PVI at the injection site under normal conditions, but differences between direct and indirect PVI values were abolished during saline loading of the CSF space. The Ro was estimated under normal conditions in the lumbar sac, cisterna magna, and lateral ventricle to be 81.6, 85.6, and 110.3 mm Hg/ml/min, respectively. The lateral ventricle Ro was significantly higher than at other places. These findings suggest that, when there is no blockage in the craniospinal axis, the pressure response to a bolus change in CSF volume is freely transmitted, direct measurements of PVI are independent of location, and indirect measurements are larger because of "buffering" in the CSF space. When PVI is lowered and buffering capacity is exhausted, these differences between direct and indirect PVI values disappear.

Quantification of the Disturbed Cerebrospinal Fluid Circulation and the Elasticity after Subarachnoid Hemorrhage, using Infusion Studies

It is important for adequate treatment after subarachnoid hemorrhage (SAH) to estimate objectively the disturbed cerebrospinal fluid (CSF) circulation and the intracranial spatial compensatory capacity. This paper reports the results of a preliminary trial to apply infusion studies as a method of quantifying the amount of CSF circulatory disturbance and the elasticity of the brain. The infusion studies (bolus injection, bolus withdrawal and steady-state infusion) were performed in 14 adult SAH patients for a total of 19 times. In 12 patients, studies were carried out under two spinal taps (one for CSF manipulation and the other for a pressure transducer). Two other patients received the tests through ventricular drainage. Pressure changes were recorded by a polygraph and a data recorder, and were later analysed by the methods of Marmarou, et al. and Katzman, et al. to calculate three parameters, namely, pressure-volume index (PVI), CSF outflow resistance (Ro) and CSF formation rate. These parameters were compared with computed tomography (CT) findings, radioisotope cisternographic findings (6 cases) and the effectiveness of therapeutic procedures (external decompression in 4 cases and CSF shunt in 9 cases). PVI values showed statistically significant differences between the decompressed group (44.62±30.33 ml) and nondecompressed group (22.23±9.02 ml) (p<0.001, F test). Ro values recorded their peak from 10 to 20 days after SAH, and tended to be higher among the patients who showed a reflux-stasis pattern in cisternography and in whom the shunt procedure was effective. Patients who developed periventricular lucency in the CT scan tended to show higher Ro values. However, there was one case which did not develop hydrocephalic symptoms despite a high Ro value. In some cases Ro remained low despite the fact that other examinations suggested advanced disturbance of CSF absorption. These discrepancies were thought mainly to have occurred because Marmarou's theory did not consider interactions between another two intracranial components (the vascular bed and the brain parenchyme) on volume loading or withdrawal into CSF space. If this problem were solved, the bolus infusion test could be a much more useful and practical method than steady-state infusion.

Validity of measurements of cerebrospinal fluid outflow resistance estimated by the bolus injection method

Estimation of cerebrospinal fluid (CSF) outflow resistance (Ro) using a bolus injection method was carried out under normal conditions and in a state of artificially increased elastance produced by saline loading into the CSF space. These values of Ro were compared with Ro estimated by the steady state infusion method. Saline loading into the subarachnoid space decreased the buffering capacity significantly, as represented by the pressure-volume index (PVI), which was lowered from 0.72 ml under normal conditions of 0.56 ml during saline loading. The estimated values of Ro under normal conditions and during saline loading were 90.6 and 133.6 mm Hg/ml/minute, respectively. The steady state infusion method yielded an Ro value of 166.3 mm Hg/ml/minute. Ro was therefore considerably underestimated by the bolus method when used under normal conditions of resting intracranial pressure. Moreover, its error was bigger when Ro was higher. On the other hand, during the course of saline loading, the estimated value of Ro using the bolus method was not significantly different from that estimated by the steady state infusion method, even in the higher range of Ro. Estimation of Ro by the bolus injection method was more reliable when the buffering capacity of the craniospinal space was reduced. (Neurosurgery 17:63-66, 1985)

Validity of Measurements of Cerebrospinal Fluid Outflow Resistance Estimated by the Bolus Injection Method

Estimation of cerebrospinal fluid (CSF) outflow resistance (Ro) using a bolus injection method was carried out under normal conditions and in a state of artificially increased elastance produced by saline loading into the CSF space. These values of Ro were compared with Ro estimated by the steady state infusion method. Saline loading into the subarachnoid space decreased the buffering capacity significantly, as represented by the pressure-volume index (PVI), which was lowered from 0.72 ml under normal conditions of 0.56 ml during saline loading. The estimated values of Ro under normal conditions and during saline loading were 90.6 and 133.6 mm Hg/ml/minute, respectively. The steady state infusion method yielded an Ro value of 166.3 mm Hg/ml/minute. Ro was therefore considerably underestimated by the bolus method when used under normal conditions of resting intracranial pressure. Moreover, its error was bigger when Ro was higher. On the other hand, during the course of saline loading, the estimated value of Ro using the bolus method was not significantly different from that estimated by the steady state infusion method, even in the higher range of Ro. Estimation of Ro by the bolus injection method was more reliable when the buffering capacity of the craniospinal space was reduced.

Normal pressure hydrocephalus: correlation between CT and measurements of cerebrospinal fluid dynamics.

Twenty-nine patients consecutively admitted for consideration of CSF diversion surgery for suspected communicating ("normal pressure") hydrocephalus underwent cranial computerized tomography (CT) and study of cerebrospinal fluid (CSF) absorption, the latter determined as resistance to outflow of CSF (Ro). From the CT the size of the ventricular system was determined by various linear measurements and ratios and the presence of periventricular lucencies (PVL) and the size of cortical sulci was noted. Except for absence of cortical sulci greater than 3 mm no CT feature was suggestive of compromised CSF absorption. On the other hand, cortical atrophy did not rule out increased resistance to CSF-outflow. Features thought of as characteristic for normal pressure hydrocephalus on CT: large ventricles as compared with the amount of cortical atrophy and presence of PVL, correlated poorly with measured high resistance values. There was no correlation between the size of the ventricular system and resistance to CSF outflow. In the diagnostic distinction between communicating ("normal pressure") hydrocephalus and cerebral atrophy (hydrocephalus ex vacuo) static CT cannot replace an actual determination of CSF outflow resistance.

Cerebrospinal fluid outflow resistance in the developing rat.

Cerebrospinal fluid outflow resistance in the developing rat.

Cerebrospinal fluid outflow resistance in rabbits with experimental meningitis. Alterations with penicillin and methylprednisolone.

Acute bacterial meningitis may be associated with increased intracranial pressure, neurological sequelae such as communicating hydrocephalus, and a slow response to antibiotic therapy. Alterations in cerebrospinal hydrodynamics are at least partially responsible for these complications. Constant, low-flow short-duration manometric infusion studies through a hollow-bore pressure monitoring device in direct continuity with the supracortical subarachnoid space were performed in rabbits with experimental meningitis. Maximal resistance to cerebrospinal fluid (CSF) outflow from the subarachnoid to vascular space was markedly increaed in acute pneumococcal meningitis when compared to control, uninfected animals (6.77 +/- 3.52 vs. 0.26 +/- 0.04 mm Hg/microliter per min, P less than 0.001). Similar elevations (8.93 +/- 4.15 mm Hg/microliter per min were found in experimental Escherichia coli meningitis. Despite eradication of viable bacteria from the CSF by penicillin therapy during the acute stage of pneumococcal meningitis, resistance remained elevated (6.07 +/- 4.68 mm Hg/microliter per min) and had not returned to normal up to 15 d later. Administration of methylprednisolone during the early stages of acute pneumococcal meningitis reduced mean peak outflow resistance towards control values (0.59 mm Hg/microliter per min) and no "rebound" effect was apparent 24 h later. These hydrodynamic alterations in experimental meningitis prevent normal CSF absorption and decrease the ability of the bran to compensate for changes in intracranial volume and pressure.