Magnetic resonance imaging—based measurements of cerebrospinal fluid and blood flow as indicators of intracranial compliance in patients with Chiari malformation

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Object

The diagnosis of Chiari malformation (CM) is based on the degree of tonsilar herniation, although this finding does not necessarily correlate with the presence or absence of symptoms. Intracranial compliance (ICC) and local craniocervical hydrodynamic parameters derived using magnetic resonance (MR) imaging flow measurements were assessed in symptomatic patients and control volunteers to evaluate the role of these factors in the associated pathophysiology.

Methods

Seventeen healthy volunteers and 34 symptomatic patients with CM were studied using a 1.5-tesla MR imager. Cine phase-contrast images of blood and cerebrospinal fluid (CSF) flow to and from the cranium were used to quantify local hydrodynamic parameters (for example, cord displacement and systolic CSF velocity and flow rates) and ICC. The ICC was derived using a previously described method that measures the small, natural changes in intracranial volume and pressure with each cardiac cycle.

Differences in the average cord displacement and systolic CSF velocity and flow, comparing healthy volunteers and patients with CM were not statistically significant. Note, however, that a statistically significant lower ICC (20%) was observed in patients compared with controls.

Conclusions

Previous investigators have focused on CSF flow velocities and cord displacement to explain the pathogenesis of CM. Analysis of results have indicated that ICC is more sensitive than local hydrodynamic parameters to changes in the craniospinal biomechanical properties in symptomatic patients. The authors concluded that decreased ICC better explains CM pathophysiology than local hydrodynamic parameters such as cervical CSF velocities and cord displacement. Low ICC also better explains the onset of symptoms in adulthood given the decline in ICC with aging.

Abstract

Object

The diagnosis of Chiari malformation (CM) is based on the degree of tonsilar herniation, although this finding does not necessarily correlate with the presence or absence of symptoms. Intracranial compliance (ICC) and local craniocervical hydrodynamic parameters derived using magnetic resonance (MR) imaging flow measurements were assessed in symptomatic patients and control volunteers to evaluate the role of these factors in the associated pathophysiology.

Methods

Seventeen healthy volunteers and 34 symptomatic patients with CM were studied using a 1.5-tesla MR imager. Cine phase-contrast images of blood and cerebrospinal fluid (CSF) flow to and from the cranium were used to quantify local hydrodynamic parameters (for example, cord displacement and systolic CSF velocity and flow rates) and ICC. The ICC was derived using a previously described method that measures the small, natural changes in intracranial volume and pressure with each cardiac cycle.

Differences in the average cord displacement and systolic CSF velocity and flow, comparing healthy volunteers and patients with CM were not statistically significant. Note, however, that a statistically significant lower ICC (20%) was observed in patients compared with controls.

Conclusions

Previous investigators have focused on CSF flow velocities and cord displacement to explain the pathogenesis of CM. Analysis of results have indicated that ICC is more sensitive than local hydrodynamic parameters to changes in the craniospinal biomechanical properties in symptomatic patients. The authors concluded that decreased ICC better explains CM pathophysiology than local hydrodynamic parameters such as cervical CSF velocities and cord displacement. Low ICC also better explains the onset of symptoms in adulthood given the decline in ICC with aging.

Despite the fact that CM was first described more than 110 years ago, its pathophysiology remains unclear. Chiari malformation Type I—the most common of these malformations—is characterized by the displacement of the cerebellar tonsils more than 5 mm caudally through the foramen magnum with preserved fourth ventricle architecture.10 These malformations are sometimes associated with spinal abnormalities, such as syringomyelia and scoliosis, and occasionally with hydrocephalus.9 With the development of MR imaging, sagittal images of the craniospinal junction have been used in the diagnosis of CM. Although its prevalence has not been formally studied, CM has been estimated to occur in between 56010 and 77015 of every 100,000 people and is more common in women.

Typical symptoms associated with CM include severe headache (often brought on by coughing and straining), neck pain, and sensory and motor deficits. Although CM is considered to be a congenital malfomation, the onset of symptoms occurs mainly during adulthood. Also puzzling is the fact that the presence or absence of these symptoms does not correlate with the anatomical severity of herniation. Tonsilar herniation is often found accidentally in asymptomatic persons,15 whereas severe symptoms are often associated with only mild herniation. Hence, the evaluation of the anatomical herniation alone is of limited prognostic value and therefore a better understanding of CM pathophysiology is needed.

Tonsilar herniation is assumed to obstruct partially CSF flow between the cranium and the spinal canal, modifying the local craniocervical hydrodynamics. Several authors have evaluated parameters such as tonsilar motion, cord displacement, and CSF velocities at the craniospinal junction in patients with CM by using phase-contrast MR imaging.5,8,11,17,21 Wolpert, et al.,21 reported greater caudal velocities of tonsils, and Pujol, et al.,17 reported higher tonsilar pulsations in patients harboring CM compared with those in control volunteers. In a similar study, Hofmann, et al.,11 found an increase in maximal systolic and diastolic cord displacement rates in patients with CM. Bhadelia, et al.,8 measured systolic and diastolic CSF flow velocities at four different regions in the craniospinal junction by using MR imaging. They reported statistically significant lower maximal CSF velocities in patients with CM only at the anterior subarachnoid space at the foramen magnum level. On the other hand, Armonda, et al.,5 measured significantly reduced CSF velocities only dorsal to the spinal cord at the level of C-2. This discrepancy in results is not surprising given that CSF velocities have been found to exhibit considerable intersubject variability.3,7,20 Although higher tonsillar velocities and cord displacement rates as well as reduced CSF velocities have been documented in patients with CM, these parameters cannot explain the pathophysiology of the defect including the presence and severity of symptoms.

Despite these remaining questions, posterior fossa decompression surgery has been the treatment of choice in patients with CM. The aim of decompression surgery is the alleviation of hindbrain congestion by removing a portion of bone at the base of the skull. A variety of surgical decompression procedures—with or without opening of the dura mater, opening of the dura with or without closing or patching—have been proposed.13,16 Both successes and failures of decompression have been reported.4,6 The absence of standard guidelines for surgical treatment may be due to the lack of noninvasive means of quantifying the effect of decompression surgery on craniospinal biomechanical properties. Using a recently described MR imaging—based method of measuring intracranial elastance and pressure,2 investigators from our lab reported a significant increase in ICC following decompression surgery in patients whose symptoms improved.19 To establish further the role of ICC in CM, in the present study we quantified ICC in patients with symptomatic CM and in controls. We also compared the sensitivity of ICC with that of local hydrodynamic parameters in detecting abnormal craniospinal biomechanics in patients suffering from CM.

Clinical Material and Methods
Patient Population

Thirty-four patients (nine men and 25 women) with symptomatic CM Type I and a mean age of 42 ± 12 years (range 18–68 years) and 17 healthy control volunteers (16 men and one woman) with no history of neurological problems and a mean age of 27 ± 9 years (range 20–52 years) were studied using a 1.5-tesla MR imager (GE Medical systems, Milwaukee, WI). The study protocol was approved by the respective institutional review boards and signed consent was obtained from each participant. Among the patients with CM, three had hydrocephalus and seven had syringomyelia. Symptoms most commonly present in these patients included severe headache, neck pain, and sensory and motor difficulties such as ataxia, numbness in arms and legs, and dysmetria. The mean tonsilar herniation measured 9.8 ± 4.5 mm.

Magnetic Resonance Imaging Parameters

Standard anatomical sagittal T1-weighted MR images were used to estimate herniation levels in all patients. The ICC and local hydrodynamic parameters were obtained from measurements of CSF and blood flows to and from the cranium by using velocity-encoded cine phase-contrast scans. Blood flow was measured using velocity encoding that ranged from 60 to 90 cm/second; the slower CSF flow was quantified using velocity encoding that ranged from 5 to 9 cm/second. Cerebrospinal fluid flow was measured at a level just below the tonsilar herniation in patients and at the mid—C-2 level in the control group, where the luminal cross-sectional area is relatively constant to minimize the partial volume effect on velocity and VFR measurements. Other imaging parameters included slice thickness 5 to 6 mm, field of view 14 to 16 cm, TR 17 to 22 msec, TE 6.5 to 9 msec, and flip angle 20 and 25° for the CSF and blood flow scans, respectively.

Derivation of Hydrodynamic Parameters

The CSF flow between the cranium and spinal canal was measured using the low velocity encoding images. Cerebrospinal fluid velocities inside the cross-sectional area of the CSF space were averaged to obtain the mean CSF velocity at the different phases of the cardiac cycle. The VFR was obtained by integrating the velocities within cross-sectional area of the CSF space. The cord displacement rate was derived by multiplying the cord velocity by the cord cross-sectional area. Cord displacement was then calculated by integration with respect to time over the cardiac cycle. For increased measurement accuracy and reproducibility, lumen boundaries were delineated using a recently developed automated method for the segmentation of lumens conducting pulsatile flow, that is, the pulsatility-based segmentation technique.1 The following parameters were derived: maximal cord displacement, maximal mean systolic CSF velocity, and maximal systolic CSF VFR. The amount of CSF volume that flows to and from the intracranial vault (that is, oscillatory CSF volume) was obtained by integrating the absolute values of the CSF flow waveform over the cardiac cycle and dividing the sum by two. Intersubject means and standard deviations for patients with CM and control volunteers were then calculated.

Derivation of ICC

Compliance is defined as the ratio of the volume change associated with a small pressure change. The MR imaging—based method measures the small changes in intracranial volume and pressure (CSF pulse pressure) that occur naturally with each cardiac cycle. The derivation of ΔICV during the cardiac cycle is explained using a simplified compartmental model of the craniospinal system (Fig. 1). The ΔICV is derived from the instantaneous difference among volumetric arterial inflow, venous outflow, and oscillating CSF flow between the cranium and spinal canal. During systole the arterial inflow is greater than the venous and the CSF outflows, resulting in a small temporary increase in volume, which in turn causes an increase in pressure. The total arterial inflow to the cranium was calculated by summing the VFR through each of the four vessels carrying blood to the brain (right and left internal carotid arteries and vertebral arteries). Venous outflow was obtained by summation of the flow through the internal jugular veins and epidural, vertebral, and deep cervical veins when present. Unmeasured venous outflow through other secondary channels, such as cavernous-facial outflow, is usually small and is compensated by scaling the measured venous outflow to equate total arterial inflow.

Fig. 1.
Fig. 1.

Illustration depicting a compartmental model of the craniospinal system used in the derivation of the ΔICV and ICC. The model shows arterial inflow, venous outflow, and oscillating CSF flow between the cranium and spinal canal. Given that blood, CSF, and brain tissue are not compressible, the volume change can be derived from the instantaneous difference between volumetric inflow and outflow rates.

Pressure change during the cardiac cycle is derived from the change in the CSF pressure gradient, which is calculated from the velocity-encoded MR images of the CSF flow by using the Navier-Stokes relationship.2 An ICC index is then calculated from the ratio of these ICV and pressure changes.2,18 Method validity and measurements accuracy and reproducibility were evaluated using a nonhuman primate model, flow phantoms, computer simulations of the CSF dynamics,14 and healthy human volunteers. The inherent accuracy of the maximal volume change measurements obtained on phase-contrast MR imaging studies under controlled conditions was well within the 18% measurement reproducibility, estimated by repeated measurements in healthy humans.2 The accuracy and reproducibility of the pressure change measurements in baboons and humans were within 8%.2

Statistical Analysis

The significance of differences in the derived parameters between patients with CMs and control volunteers were tested by applying a single-tailed, unpaired t-test with a probability value less than 0.05 indicating statistical significance. The test was implemented using commercially available software (Microsoft Excel, version 2002; Microsoft Corp., Redmond, WA).

Results

A representative phase-contrast MR image used to quantify blood flow to and from the brain is shown in Fig. 2 (left). A scout MR angiography image is also shown to indicate the location of the imaging plane used for blood flow velocity measurements (Fig. 2 right). In the velocity encoded image, black pixels indicate flow in the cranial-to-caudal direction, that is, arterial inflow, and the white pixels indicate flow in the caudal-to-cranial direction (venous outflow). Graphs of total arterial and venous VFR waveforms in a control volunteer and a patient with CM are featured in Fig. 3. An example of an MR image used for the quantification of CSF flow is represented in Fig. 4 (left). A sagittal T1-weighted MR image with the location of the imaging plane used for the CSF flow measurements is also shown (Fig. 4 right). Graphs of the CSF VFR waveforms in a control volunteer and a patient with CM are shown in Fig. 5. Note that the maximal VFR in the patient with CM is lower than that in the control volunteer.

Fig. 2.
Fig. 2.

Left: A velocity-encoded phase-contrast MR image revealing the blood flow to and from the cranium. Black pixels indicate flow in the caudocranial direction (arterial flow), and white pixels flow in the craniocaudal direction (venous flow). Right: A midsagittal MR image of the blood vessel demonstrating the location of the imaging plane used for the arterial and venous flow measurements.

Fig. 3.
Fig. 3.

Graphs depicting representative MR imaging—derived waveforms of total arterial inflow and total venous outflow in a healthy volunteer (left) and a patient with CM (right). Note that the venous flow is much more pulsatile in the patient compared with that in the healthy volunteer. total_art = total arterial inflow; total_ven = total venous outflow.

Fig. 4.
Fig. 4.

Left: Phase-contrast MR image obtained during the systolic phase, exhibiting the CSF flow velocities through the CSF space in the cervical spine. Right: Anatomical midsagittal T1-weighted MR image demonstrating the location of the imaging plane.

Fig. 5.
Fig. 5.

Graphs depicting the oscillatory CSF VFR waveform in a control volunteer (left) and a patient with CM (right). Positive values indicate flow from the cranium to the spinal canal. In the patient with CM, the maximal VFR is lower than that in the healthy control.

The average intersubject values of the following local hydrodynamic parameters in all study participants are summarized in Table 1: maximal cord displacement, maximal CSF systolic velocity, maximal CSF systolic VFR, CSF oscillatory volume, global biomechanical parameters, ΔICV, and ICC index. Mean values in the patient group for cord displacement was 18% greater; CSF systolic velocity, 17% lower; and maximal CSF VFR, 12% lower. The average oscillatory CSF volume was similar between the two groups. None of the differences in these parameters reached statistical significance. In contrast, the differences in the global intracranial parameters—ΔICV and ICC—reached statistical significance. Compared with those in the controls, the ΔICV was 28% lower in patients harboring CM and ICC was 20% lower. The probability values are listed in Table 1. There was no statistically significant difference in the average ICC, which was measured separately in patients with CM with and without syrinx.

TABLE 1

Summary of MR imaging—derived local hydrodynamic parameters and global biomechanical parameters in patients with CM and control volunteers*

ParameterControlsPatients w/ CMp Value
max cord displacement0.33 ± 0.13 0.39 ± 0.17 0.077
 (mm)  
max mean CSF1.89 ± 0.71 1.56 ± 0.55 0.053
 velocity (cm/sec)  
max CSF VFR215.6 ± 64.7 189.5 ± 57.3 0.084
 (ml/min)  
oscillatory CSF0.57 ± 0.19 0.56 ± 0.21 0.496
 vol (ml)  
ΔICV (ml)0.6 ± 0.18 0.43 ± 0.2 0.002†
ICC index8.3 ± 2.5 6.7 ± 2.9 0.025†

* Values are presented as the means ± standard deviation.

† Statistical significance was set at a probability value less than 0.05.

The lower ICC in a patient with CM compared with that in a control is depicted in the relationship between the CSF and the net transcranial blood flow waveforms shown in Fig. 6. The CSF VFR waveform is shown together with the net transcranial blood flow (arterial inflow − venous outflow) waveform. In the patient harboring a CM the CSF waveform follows the net transcranial blood flow waveform more closely than those in the control.

Fig. 6.
Fig. 6.

Graphs illustrating representative net transcranial blood flow (arterial inflow — venous outflow [A-V]) and the CSF flow waveforms in a healthy volunteer (left) and a patient with CM (right). Note that the CSF waveform follows the A-V waveform more closely in the patient with CM compared with those in the control volunteer, indicating a less compliant intracranial compartment.

Discussion

In this study we expanded on earlier work by others who used dynamic phase-contrast MR imaging measurements of cord displacement and CSF flow velocities at the craniospinal junction to characterize differences in the local hydrodynamics between patients with CM and healthy controls. Data from these earlier studies revealed higher tonsilar pulsations,17 faster rates of cord displacement,11 and lower systolic CSF velocities at different locations of the craniospinal junction5,8 in patients harboring CM compared with those in healthy volunteers. In these studies, global biomechanical properties of the craniospinal system, for example, the compliance state of the intracranial compartment, were also measured as were the local hydrodynamic parameters. A similar trend in the local hydrodynamic parameters was found in the current study as were greater cord displacement and lower CSF velocities and VFRs. Nevertheless, these differences did not reach statistical significance between patients and controls. In contrast, a statistically significant lower ICC and ΔICV were measured in the patients with CM compared with those in healthy volunteers. Therefore, it is apparent from these results that the ICC and the ΔICV are more sensitive than the local hydrodynamic parameters to the abnormal state of the craniospinal system in patients with symptomatic CM.

The ICC state can be visualized from the relationship between transcranial CSF and blood flows. The net transcranial blood flow (arterial inflow — venous outflow) can be regarded as the driving force behind the oscillatory CSF flow between the cranium and the spinal canal. In a less compliant intracranial compartment the CSF waveform follows the net transcranial blood flow more closely, whereas in a more compliant compartment the CSF flow is less pulsatile. As can be seen in the example shown in Fig. 6, the CSF waveform measured in a patient with CM follows its driving force more closely than it does in a control volunteer. Note that the venous outflow itself is affected by the intracranial compliance (Fig. 4). Venous outflow follows systolic arterial inflow more closely. These relationships may explain why parameters such as ICC and ΔICV, which are derived from measurements of both the blood and CSF flows into and out of the cranium, are more sensitive to changes associated with CM than are hydrodynamic parameters derived from the CSF flow measurement alone.

The maximal ΔICV during the cardiac cycle measured in patients with CM is also statistically significantly smaller than that measured in the control group. A lower ΔICV is another manifestation of reduced ICC. Due to the reduced compliance of the intracranial compartment, venous and CSF outflow occur more immediately following the systolic increase in arterial blood inflow, which in turn results in a smaller systolic increase in intracranial volume.

Lower ICC and the Pathophysiology of CM

The lower ICC in patients with CM in this study supports an earlier hypothesis by Hofmann, et al.,11 who associated the increased cord displacement with reduced ICC.10 In fact, a reduced ICC in patients with CM better explains the associated pathophysiology than the changes in local craniocervical hydrodynamics. For example, lower ICC explains a common clinical symptom associated with CM Type I, that is, the cough-strain headaches. Low ICC indicates reduced buffering capability to accommodate the temporary increase in intracranial blood volume caused by coughing. Therefore, in patients with CM coughing will cause a temporary increase in intracranial pressure, which could trigger the headaches. A lower ICC in patients with CM also explains the delayed onset of symptoms, which commonly occurs in adulthood. It has been shown that ICC declines with age.12 Therefore, it is possible that symptoms occur once ICC decreases below a certain threshold.

The fact that decompression surgery often alleviates symptoms associated with CM further supports the importance of ICC to the understanding of the associated pathophysiology of CM. Decompression surgery is currently performed to alleviate the apparent obstruction to CSF flow in the craniocervical junction by removing a portion of the bone to enlarge the foramen magnum. Because a larger opening in the skull increases compliance, the decompression procedure increases ICC and thereby alleviates the associated symptoms. In a recent study, we evaluated the effect of decompression surgery on local hydrodynamic parameters and ICC in 12 patients with CM.19 A significant increase in ICC was measured after decompression surgery, whereas changes in the local hydrodynamic parameters did not reach statistical significance. Note that ICC increased after surgery in 10 of 12 patients, was relatively unchanged in one patient, and decreased in one patient. The increase in ICC was associated with improved clinical outcome, whereas the decrease in ICC in one of the patients was associated with persistent symptoms.

Results from the current study further establish the association between reduced ICC and the presence of symptoms in patients diagnosed with CM Type I. Nevertheless, further studies are warranted to correlate symptom type and severity with the ICC value. Finding of a positive correlation between a certain type and severity of symptoms and reduced ICC would enable tailoring of treatment to address a patient's specific symptoms. Furthermore, because MR imaging is already being used to establish a diagnosis of CM, MR imaging—based ICC measurements are a practical way of augmenting anatomical information with relevant quantitative physiological parameters.

Conclusions

We evaluated for the first time ICC in patients with CM and controls. The statistically significant lower ICC in patients harboring CM explains the pathophysiology of the disorder better than any previously reported changes in local hydrodynamic parameters. This finding potentially establishes the MR imaging—derived ICC index as a more sensitive marker of the biomechanical state of the system than local hydrodynamic parameters such as maximal CSF velocities and flow rates.

Abbreviations used in this paperCM =

Chiari malformation

;
CSF =

cerebrospinal fluid

;
ICC =

intracranial compliance

;
MR =

magnetic resonance

;
VFR =

volumetric flow rate

;
ΔICV =

change in intracranial volume

.

References

  • 1.

    Alperin NLee SH: PUBS: Pulsatility-based segmentation of lumens conducting non-steady flow. Magn Reson Med 49:9349442003Magn Reson Med 49:

  • 2.

    Alperin NLee SHLoth FRaksinPBLichtor T: MR-Intracranial pressure (ICP). a method to measure intracranial elastance and pressure noninvasively by means of MR imaging: baboon and human study. Radiology 217:8778852000Radiology 217:

  • 3.

    Alperin NVikingstad EMGomez-Anson BLevin DN: Hemodynamically independent analysis of cerebrospinal fluid and brain motion observed with dynamic phase contrast MRI. Magn Reson Med 35:7417541996Magn Reson Med 35:

  • 4.

    Alzate JCKothbauer KFJallo GIEpstein FJ: Treatment of Chiari type I malformation in patients with and without syringomyelia: a consecutive series of 66 cases. Neurosurg Focus 11(1):E32001Neurosurg Focus 11(1):

  • 5.

    Armonda RACitrin CMFoley KTEllenbogen RG: Quantitative cine-mode magnetic resonance imaging of Chiari I malformations: an analysis of cerebrospinal fluid dynamics. Neurosurgery 35:2142241994Neurosurgery 35:

  • 6.

    Bejjani GKCockerham KPRothfus WEMaroon JCMaddock M: Treatment of failed Adult Chiari Malformation decompression with CSF drainage: observations in six patients. Acta Neurochir 145:1071162003Acta Neurochir 145:

  • 7.

    Bhadelia RABogdan ARWolpert SM: Analysis of the cerebrospinal fluid flow waveforms using gated phase-contrast MR velocity measurements. AJNR 16:3894001995AJNR 16:

  • 8.

    Bhadelia RABogdan ARWolpert SMLev SAppignani BAHeilman CB: Cerebrospinal fluid flow waveforms: analysis in patients with Chiari I malformation by means of gated phase-contrast MR imaging velocity measurements. Radiology 196:1952021995Radiology 196:

  • 9.

    Caviness VS: The Chiari malformations of the posterior fossa and their relation to hydrocephalus. Dev Med Child Neurol 18:1031161976Caviness VS: The Chiari malformations of the posterior fossa and their relation to hydrocephalus. Dev Med Child Neurol 18:

  • 10.

    Elster ADChen MYM: Chiari I malformations: clinical and radiologic reappraisal. Radiology 183:3473531992Radiology 183:

  • 11.

    Hofmann EWarmuth-Metz MBendszus MSolymosi L: Phase-contrast MR imaging of the cervical CSF and spinal cord: volumetric motion analysis in patients with Chiari I malformation. AJNR 21:1511582000AJNR 21:

  • 12.

    Kiening KLSchoening WNLanksch WRUnterberg AW: Intracranial compliance as a bed-side monitoring technique in severely head-injured patients. Acta Neurochir Suppl 81:1771802002Acta Neurochir Suppl 81:

  • 13.

    Levy WJMason LHahn JF: Chiari malformation presenting in adults: a surgical experience in 127 cases. Neurosurgery 12:3773901983Neurosurgery 12:

  • 14.

    Loth FYardimci MAAlperin N: Hydrodynamic modeling of cerebrospinal fluid motion within the spinal cavity. J Biomech Eng 123:71792001J Biomech Eng 123:

  • 15.

    Meadows JKraut MGuarnieri MHaroun RICarson BS: Asymptomatic Chiari Type I malformations identified on magnetic resonance imaging. J Neurosurg 92:9209262000J Neurosurg 92:

  • 16.

    Park JKGleason PLMadsen JRGoumnerova LCScott RM: Presentation and management of Chiari I malformation in children. Pediatr Neurosurg 26:1901961997Pediatr Neurosurg 26:

  • 17.

    Pujol JRoig CCapdevila APou AMarti-Vilalta JLKulisevsky Jet al: Motion of the cerebellar tonsils in Chiari type I malformation studied by cine phase-contrast MRI. Neurology 45:174617531995Neurology 45:

  • 18.

    Raksin PBAlperin NSivaramakrishnan ASurapaneni SLichtor T: Noninvasive intracranial compliance and pressure based on dynamic MR imaging of blood flow and cerebrospinal fluid flow: review of principles, implementation, and other noninvasive approaches. Neurosurg Focus 14(4):E42003Neurosurg Focus 14(4):

  • 19.

    Sivaramakrishnan AAlperin NSurapaneni SLichtor T: Evaluating the effect of decompression surgery on cerebrospinal fluid flow and intracranial compliance in patients with Chiari malformation using magnetic resonance imaging flow studies. Neurosurgery 55:134413512004Neurosurgery 55:

  • 20.

    Thomsen CStahlberg FStubgaard MNordell B: Fourier analysis of cerebrospinal fluid flow velocities: MR imaging study. The Scandinavian Flow Group. Radiology 177:6596651990Radiology 177:

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    Wolpert SMBhadelia RABogdan ARCohen A: Chiari I malformations: assessment with phase-contrast velocity MR. AJNR 15:129913081994AJNR 15:

This study was supported in part by the Ed and Gayle Labuda Charitable Fund of the Vanguard Charitable Endowment Program.

Article Information

Address reprint requests to: Noam Alperin, Ph.D., Physiological Imaging and Modeling Lab, Department of Radiology (M/C 711), University of Illinois at Chicago, 830 South Wood Street, Chicago, Illinois 60612. email: alperin@uic.edu.

© AANS, except where prohibited by US copyright law.

Headings

Figures

  • View in gallery

    Illustration depicting a compartmental model of the craniospinal system used in the derivation of the ΔICV and ICC. The model shows arterial inflow, venous outflow, and oscillating CSF flow between the cranium and spinal canal. Given that blood, CSF, and brain tissue are not compressible, the volume change can be derived from the instantaneous difference between volumetric inflow and outflow rates.

  • View in gallery

    Left: A velocity-encoded phase-contrast MR image revealing the blood flow to and from the cranium. Black pixels indicate flow in the caudocranial direction (arterial flow), and white pixels flow in the craniocaudal direction (venous flow). Right: A midsagittal MR image of the blood vessel demonstrating the location of the imaging plane used for the arterial and venous flow measurements.

  • View in gallery

    Graphs depicting representative MR imaging—derived waveforms of total arterial inflow and total venous outflow in a healthy volunteer (left) and a patient with CM (right). Note that the venous flow is much more pulsatile in the patient compared with that in the healthy volunteer. total_art = total arterial inflow; total_ven = total venous outflow.

  • View in gallery

    Left: Phase-contrast MR image obtained during the systolic phase, exhibiting the CSF flow velocities through the CSF space in the cervical spine. Right: Anatomical midsagittal T1-weighted MR image demonstrating the location of the imaging plane.

  • View in gallery

    Graphs depicting the oscillatory CSF VFR waveform in a control volunteer (left) and a patient with CM (right). Positive values indicate flow from the cranium to the spinal canal. In the patient with CM, the maximal VFR is lower than that in the healthy control.

  • View in gallery

    Graphs illustrating representative net transcranial blood flow (arterial inflow — venous outflow [A-V]) and the CSF flow waveforms in a healthy volunteer (left) and a patient with CM (right). Note that the CSF waveform follows the A-V waveform more closely in the patient with CM compared with those in the control volunteer, indicating a less compliant intracranial compartment.

References

1.

Alperin NLee SH: PUBS: Pulsatility-based segmentation of lumens conducting non-steady flow. Magn Reson Med 49:9349442003Magn Reson Med 49:

2.

Alperin NLee SHLoth FRaksinPBLichtor T: MR-Intracranial pressure (ICP). a method to measure intracranial elastance and pressure noninvasively by means of MR imaging: baboon and human study. Radiology 217:8778852000Radiology 217:

3.

Alperin NVikingstad EMGomez-Anson BLevin DN: Hemodynamically independent analysis of cerebrospinal fluid and brain motion observed with dynamic phase contrast MRI. Magn Reson Med 35:7417541996Magn Reson Med 35:

4.

Alzate JCKothbauer KFJallo GIEpstein FJ: Treatment of Chiari type I malformation in patients with and without syringomyelia: a consecutive series of 66 cases. Neurosurg Focus 11(1):E32001Neurosurg Focus 11(1):

5.

Armonda RACitrin CMFoley KTEllenbogen RG: Quantitative cine-mode magnetic resonance imaging of Chiari I malformations: an analysis of cerebrospinal fluid dynamics. Neurosurgery 35:2142241994Neurosurgery 35:

6.

Bejjani GKCockerham KPRothfus WEMaroon JCMaddock M: Treatment of failed Adult Chiari Malformation decompression with CSF drainage: observations in six patients. Acta Neurochir 145:1071162003Acta Neurochir 145:

7.

Bhadelia RABogdan ARWolpert SM: Analysis of the cerebrospinal fluid flow waveforms using gated phase-contrast MR velocity measurements. AJNR 16:3894001995AJNR 16:

8.

Bhadelia RABogdan ARWolpert SMLev SAppignani BAHeilman CB: Cerebrospinal fluid flow waveforms: analysis in patients with Chiari I malformation by means of gated phase-contrast MR imaging velocity measurements. Radiology 196:1952021995Radiology 196:

9.

Caviness VS: The Chiari malformations of the posterior fossa and their relation to hydrocephalus. Dev Med Child Neurol 18:1031161976Caviness VS: The Chiari malformations of the posterior fossa and their relation to hydrocephalus. Dev Med Child Neurol 18:

10.

Elster ADChen MYM: Chiari I malformations: clinical and radiologic reappraisal. Radiology 183:3473531992Radiology 183:

11.

Hofmann EWarmuth-Metz MBendszus MSolymosi L: Phase-contrast MR imaging of the cervical CSF and spinal cord: volumetric motion analysis in patients with Chiari I malformation. AJNR 21:1511582000AJNR 21:

12.

Kiening KLSchoening WNLanksch WRUnterberg AW: Intracranial compliance as a bed-side monitoring technique in severely head-injured patients. Acta Neurochir Suppl 81:1771802002Acta Neurochir Suppl 81:

13.

Levy WJMason LHahn JF: Chiari malformation presenting in adults: a surgical experience in 127 cases. Neurosurgery 12:3773901983Neurosurgery 12:

14.

Loth FYardimci MAAlperin N: Hydrodynamic modeling of cerebrospinal fluid motion within the spinal cavity. J Biomech Eng 123:71792001J Biomech Eng 123:

15.

Meadows JKraut MGuarnieri MHaroun RICarson BS: Asymptomatic Chiari Type I malformations identified on magnetic resonance imaging. J Neurosurg 92:9209262000J Neurosurg 92:

16.

Park JKGleason PLMadsen JRGoumnerova LCScott RM: Presentation and management of Chiari I malformation in children. Pediatr Neurosurg 26:1901961997Pediatr Neurosurg 26:

17.

Pujol JRoig CCapdevila APou AMarti-Vilalta JLKulisevsky Jet al: Motion of the cerebellar tonsils in Chiari type I malformation studied by cine phase-contrast MRI. Neurology 45:174617531995Neurology 45:

18.

Raksin PBAlperin NSivaramakrishnan ASurapaneni SLichtor T: Noninvasive intracranial compliance and pressure based on dynamic MR imaging of blood flow and cerebrospinal fluid flow: review of principles, implementation, and other noninvasive approaches. Neurosurg Focus 14(4):E42003Neurosurg Focus 14(4):

19.

Sivaramakrishnan AAlperin NSurapaneni SLichtor T: Evaluating the effect of decompression surgery on cerebrospinal fluid flow and intracranial compliance in patients with Chiari malformation using magnetic resonance imaging flow studies. Neurosurgery 55:134413512004Neurosurgery 55:

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