Arterial pulsation—dependent perivascular cerebrospinal fluid flow into the central canal in the sheep spinal cord

1997 ◽  
Vol 86 (4) ◽  
pp. 686-693 ◽  
Author(s):  
Marcus A. Stoodley ◽  
Sally A. Brown ◽  
Christopher J. Brown ◽  
Nigel R. Jones

✓ The impetus for the enlargement of syringes is unknown. The authors hypothesize that there is a flow of cerebrospinal fluid (CSF) from perivascular spaces into the central canal and that the flow is driven by arterial pulsations. Using horse-radish peroxidase as a tracer, the CSF flow was studied in normal sheep, in sheep with damped arterial pulsations, and in sheep with lowered spinal subarachnoid pressure. The CSF flow from perivascular spaces into the central canal was demonstrated in the normal sheep, and two patterns of flow were identified: 1) from perivascular spaces in the central gray matter; and 2) from perivascular spaces in the ventral white commissure. Flow into the central canal was also observed in the sheep with lowered spinal subarachnoid pressure, but not in those with reduced arterial pulse pressure. This study provides evidence that CSF flow from perivascular spaces into the central canal is dependent on arterial pulsations. Arterial pulsation—driven CSF flow may be the impetus for the expansion of syringes.

2000 ◽  
Vol 8 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Marcus A. Stoodley ◽  
Nigel R. Jones ◽  
Liqun Yang ◽  
Christopher J. Brown

The pathogenesis of noncommunicating syringomyelia is unknown, and none of the existing theories adequately explains the production of cysts that occur in association with conditions other than Chiari malformation. The authors' hypothesis is that an arterial pulsation–driven perivascular flow of cerebrospinal fluid (CSF) is responsible for syrinx formation and enlargement. They investigated normal CSF flow patterns in 20 rats and five sheep by using the tracer horseradish peroxidase; the effect of reducing arterial pulse pressure was examined in four sheep by partially ligating the brachiocephalic trunk; CSF flow was examined in 78 rats with the intraparenchymal kaolin model of noncommunicating syringomyelia; and extracanalicular cysts were examined using the excitotoxic model in 38 rats. In the normal animals there was a rapid flow of CSF from the spinal subarachnoid space into the spinal cord perivascular spaces and then into the central canal. This flow ceased when arterial pulsations were diminished. In animals with noncommunicating syringomyelia, there was rapid CSF flow into isolated and enlarged segments of central canal, even when these cysts were causing pressure damage to the surrounding spinal cord. Exitotoxic injury of the spinal cord caused the formation of extracanalicular cysts, and larger cysts were produced when this injury was combined with arachnoiditis, which impaired subarachnoid CSF flow. The results of these experiments support the hypothesis that arterial pulsation–driven perivascular fluid flow is responsible for syrinx formation and enlargement.


1978 ◽  
Vol 48 (6) ◽  
pp. 970-974 ◽  
Author(s):  
A. Everette James ◽  
William J. Flor ◽  
Gary R. Novak ◽  
Ernst-Peter Strecker ◽  
Barry Burns

✓ The central canal of the spinal cord has been proposed as a significant compensatory alternative pathway of cerebrospinal fluid (CSF) flow in hydrocephalus. Ten dogs were made hydrocephalic by a relatively atraumatic experimental model that simulates the human circumstance of chronic communicating hydrocephalus. The central canal was studied by histopathology and compared with 10 normal control dogs. In both groups the central canal of the spinal cord was normal in size, configuration, and histological appearance. In this experimental model dilatation of the canal and increased movement of CSF does not appear to be a compensatory alternative pathway.


1983 ◽  
Vol 58 (4) ◽  
pp. 557-561 ◽  
Author(s):  
Mitsuhiro Hara ◽  
Chikafusa Kadowaki ◽  
Yoshifumi Konishi ◽  
Motohide Ogashiwa ◽  
Mitsuo Numoto ◽  
...  

✓ An implantable device for measurement of cerebrospinal fluid (CSF) flow in a ventriculoperitoneal shunt tube has been developed. The unit is energized by an extracorporeal high-frequency generator (200 KHz), and electrolysis creates bubbles in the shunt tube. Velocity of bubble flow is detected by a pair of ultrasonic Doppler probes placed a certain distance apart on the skin surface and in parallel with the implanted tube. The CSF flow rate is calculated taking into account velocity and tube diameter, and is expressed in ml/min. The unit consists of a coil with a capacitor, a silicon diode to rectify the high frequency, and a Zener diode to regulate maximum output voltage of 20 V. The output is fed to a pair of platinum electrodes placed inside the unit's tunnel through which the CSF flows. These components are molded in epoxy resin and coated with medical-grade silicone rubber. In animal experiments, CSF flow rates ranging from 0.033 to 1.0 ml/min could be measured by this flowmeter. Clinically, CSF flow has been measured to date in several cases. In two cases of communicating hydrocephalus occurring after the onset of cerebrovascular disease, and in which the CSF flow was continuously monitored for 24 hours, the flow rate ranged between 0.05 and 0.78 ml/min. The CSF flow rate fluctuates in a 24-hour period, increasing in the morning, especially between 12 midnight and 6 a.m., which suggests a circadian rhythm.


1971 ◽  
Vol 35 (3) ◽  
pp. 263-271 ◽  
Author(s):  
George J. Dohrmann ◽  
Franklin C. Wagner ◽  
Paul C. Bucy

✓ Fine structural alterations in the microvasculature, primarily of the gray matter, occur as one aspect of experimental spinal cord contusion. A force of 300 gm-cm, shown by the authors to produce a transitory paraplegia, was applied to the T-10 level of exposed primate spinal cord. At 5 min post-contusion, the muscular venules of the central gray matter were distended with erythrocytes. Erythrocytes were seen within the perivascular spaces of the post-capillary venules and muscular venules at 15 and 30 min post-contusion, and there was hemorrhage into the gray matter at 1 hour post-contusion. The appearance of erythrocytes within the perivenular spaces was apparently due to small ruptures in the walls of the muscular venules, which were first demonstrated by electron microscopy 15 min after contusion. Alterations in capillary and post-capillary venule endothelium of both gray and white matter were present at 4 hours post-contusion and consisted of vacuolation and endothelial swelling. In conclusion, following experimental contusion of the spinal cord sufficient to cause a transitory paraplegia, the principal changes were early perivascular and parenchymal hemorrhages followed by later evidence of ischemic endothelial injury in the microvasculature.


1993 ◽  
Vol 78 (2) ◽  
pp. 274-279 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Fariborz Nobandegani ◽  
John I. Miller ◽  
Chandrakant Rao

✓ This report describes a new and reliable technique for producing experimental noncommunicating syringomyelia. In 30 rats, 1.2 to 1.6 µl of kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at C-6. The inoculations caused transient neurological deficits in four animals and no deficits in 26 animals. Within 24 hours, kaolin and polymorphonuclear leukocytes entered the central canal and drained rostrally. The clearance of inflammatory products induced a proliferation of ependymal cells and periependymal fibrous astrocytes, which formed synechiae and obstructed the canal at the level of injection and at one or more levels up to C-1. In 22 animals followed for 48 hours or longer, the upper end of the central canal became acutely dilated and formed an ependyma-lined syrinx that enlarged to massive dimensions within 6 weeks. The rostral syrinxes did not communicate with the fourth ventricle and were not associated with hydrocephalus. The histological findings in acute noncommunicating syringomyelia were characterized by progressive stretching and thinning of the ependyma, elongation of intracanalicular septae, and the formation of periependymal edema. After 3 weeks, there was progressive compression of the periependymal tissues associated with stretching of axons, fragmentation of myelin sheaths, and the formation of myelin droplets. These findings and the sequence in which they evolved were identical in most respects to those occurring in acute and subacute noncommunicating hydrocephalus.


2011 ◽  
Vol 31 (3) ◽  
pp. E5 ◽  
Author(s):  
Uwe Max Mauer ◽  
Andreas Gottschalk ◽  
Carolin Mueller ◽  
Linda Weselek ◽  
Ulrich Kunz ◽  
...  

Object The causal treatment of Chiari malformation Type I (CM-I) consists of removing the obstruction of CSF flow at the level of the foramen magnum. Cerebrospinal fluid flow can be visualized using dynamic phase-contrast MR imaging. Because there is only a paucity of studies evaluating CSF dynamics in the region of the spinal canal on the basis of preoperative and postoperative measurements, the authors investigated the clinical usefulness of cardiacgated phase-contrast MR imaging in patients with CM-I. Methods Ninety patients with CM-I underwent preoperative MR imaging of CSF pulsation. Syringomyelia was present in 59 patients and absent in 31 patients. Phase-contrast MR imaging of the entire CNS was used to investigate 22 patients with CM-I before surgery and after a mean postoperative period of 12 months (median 12 months, range 3–33 months). In addition to the dynamic studies, absolute flow velocities, the extension of the syrinx, and tonsillar descent were also measured. Results The changes in pulsation were highly significant in the region of the (enlarged) cistern (p = 0.0005). Maximum and minimum velocities (the pulsation amplitude) increased considerably in the region where the syrinx was largest in diameter. The changes of pulsation in these patients were significant in the subarachnoid space in all spinal segments but not in the syrinx itself and in the central canal. Conclusions The demonstration of CSF flow pulsation can contribute to assessments of surgical outcomes. The results presented here, however, raise doubts about current theories on the pathogenesis of syringomyelia.


2000 ◽  
Vol 93 (2) ◽  
pp. 237-244 ◽  
Author(s):  
Henry W. S. Schroeder ◽  
Christiane Schweim ◽  
Klaus H. Schweim ◽  
Michael R. Gaab

Object. The purpose of this prospective study was to evaluate aqueductal cerebrospinal fluid (CSF) flow after endoscopic aqueductoplasty. In all patients, preoperative magnetic resonance (MR) imaging revealed hydrocephalus caused by aqueductal stenosis and lack of aqueductal CSF flow.Methods. In 14 healthy volunteers and in eight patients with aqueductal stenosis who had undergone endoscopic aqueductoplasty, aqueductal CSF flow was investigated using cine cardiac-gated phase-contrast MR imaging. For qualitative evaluation of CSF flow, the authors used an in-plane phase-contrast sequence in the midsagittal plane. The MR images were displayed in a closed-loop cine format. Quantitative through-plane measurements were performed in the axial plane perpendicular to the aqueduct. Evaluation revealed no significant difference in aqueductal CSF flow between healthy volunteers and patients with regard to temporal parameters, CSF peak and mean velocities, mean flow, and stroke volume. All restored aqueducts have remained patent 7 to 31 months after surgery.Conclusions. Aqueductal CSF flow after endoscopic aqueductoplasty is similar to aqueductal CSF flow in healthy volunteers. The data indicate that endoscopic aqueductoplasty seems to restore physiological aqueductal CSF flow.


1981 ◽  
Vol 54 (6) ◽  
pp. 833-835 ◽  
Author(s):  
Russell L. Blaylock

✓ The case of a 73-year-old woman found to have hydrosyringomyelia associated with a lower thoracic meningioma is reported. Possible mechanisms for the formation of the hydrosyrinx are discussed, with particular attention being paid to the possibility of transmural passage of cerebrospinal fluid into the central canal.


1988 ◽  
Vol 68 (5) ◽  
pp. 817-819 ◽  
Author(s):  
Charles C. Duncan

✓ Proximal shunt obstruction or obstruction of the ventricular catheter may present with signs and symptoms of shunt failure with either no cerebrospinal fluid flow or a falsely low intracranial pressure (ICP) upon shunt tap. The author reports a technique for lowering the ICP and for measuring the pressure in patients with such obstruction by cannulation of the reservoir and ventricular catheter to penetrate into the ventricle with a 3½-in. No. 22 spinal needle. The findings in 20 cases in which this approach was utilized are summarized.


2005 ◽  
Vol 127 (7) ◽  
pp. 1099-1109 ◽  
Author(s):  
C. D. Bertram ◽  
A. R. Brodbelt ◽  
M. A. Stoodley

A two-dimensional axi-symmetric numerical model is constructed of the spinal cord, consisting of elastic cord tissue surrounded by aqueous cerebrospinal fluid, in turn surrounded by elastic dura. The geometric and elastic parameters are simplified but of realistic order, compared with existing measurements. A distal reflecting site models scar tissue formed by earlier trauma to the cord, which is commonly associated with syrinx formation. Transients equivalent to both arterial pulsation and percussive coughing are used to excite wave propagation. Propagation is investigated in this model and one with a central canal down the middle of the cord tissue, and in further idealized versions of it, including a model with no cord, one with a rigid cord, one with a rigid dura, and a double-length untapered variant of the rigid-dura model. Analytical predictions for axial and radial wave-speeds in these different situations are compared with, and used to explain, the numerical outcomes. We find that the anatomic circumstances of the spinal cerebrospinal fluid cavity probably do not allow for significant wave steepening phenomena. The results indicate that wave propagation in the real cord is set by the elastic properties of both the cord tissue and the confining dura mater, fat, and bone. The central canal does not influence the wave propagation significantly.


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