Marcus A. Stoodley

Post-traumatic syringomyelia: a review

More than a quarter of spinal cord injured patients develop syringes and many of these patients suffer progressive neurological deficits as a result of cyst enlargement. The mechanism of initial cyst formation and progressive enlargement are unknown, although arachnoiditis and persisting cord compression with disturbance of cerebrospinal fluid flow appear to be important aetiological factors. Current treatment options include correction of bony deformity, decompression of the spinal cord, division of adhesions, and shunting. Long-term improvement occurs in fewer than half of patients treated. Imaging evidence of a reduction in syrinx size following treatment does not guarantee symptomatic resolution or even prevention of further neurological loss. A better understanding of the causal mechanisms of syringomyelia is required to develop more effective therapy.

Effect of cervical hard collar on intracranial pressure after head injury

Background:  Patients suffering head trauma are at high risk of having a concomitant cervical spine injury. A rigid cervical collar is usually applied to each patient until spinal stability is confirmed. Hard collars potentially cause venous outflow obstruction and are a nociceptive stimulus, which might elevate intracranial pressure (ICP). This study tested the hypothesis that application of a hard collar is associated with an increase in ICP.

CSF pathways: a review

The treatment of patients with cerebrospinal fluid (CSF) pathway disorders (including hydrocephalus, syringomyelia, and arachnoid cysts), requires an understanding of CSF pathways and the cerebral water system. Although outcome with these disorders has improved, only limited treatment options remain available. Ongoing research has continued to improve our understanding of the cerebral water circulation and is starting to provide insight into the pathogenesis and potential treatment options of this common group of disorders. This article reviews current concepts of CSF function and pathways, following the journey of CSF from conception to absorption.

The influence of the relative timing of arterial and subarachnoid space pulse waves on spinal perivascular cerebrospinal fluid flow as a possible factor in syrinx development

OBJECT The mechanisms of syringomyelia have long puzzled neurosurgeons and researchers alike due to difficulties in identifying the driving forces behind fluid flow into a syrinx, apparently against a pressure gradient between the spinal cord and the subarachnoid space (SAS). Recently, the synchronization between CSF flow and the cardiac cycle has been postulated to affect fluid flow in the spinal cord. This study aims to determine the effect of changes in the timing of SAS pressure on perivascular flow into the spinal cord. METHODS This study uses a computational fluid dynamics model to investigate whether the relative timing of a spinal artery cardiovascular pulse wave and fluid pressure in the spinal SAS can influence CSF flow in the perivascular spaces. RESULTS The results show that the mass flow rate of CSF through a model periarterial space is strongly influenced by the relative timing of the arterial pulse wave and the SAS pressure. CONCLUSIONS These findings suggest that factors that might alter the timing of the pulse wave or the fluid flow in the SAS could potentially affect fluid flow into a syrinx.

Cervical and thoracic juxtafacet cysts causing neurologic deficits.

Study Design. Case reports and review of the literature. Objectives. To review the clinical features, treatment, and outcome of juxtafacet cysts. Summary of Background Data. There have previously been 4 reported cases of thoracic juxtafacet cysts and 19 cases of cervical juxtafacet cysts. Cervical cysts have usually originated from the cruciate ligament and caused myelopathy. Thoracic cysts are usually signaled by myelopathy. Methods. The records of the Neurosurgery Department of Royal Adelaide Hospital from 1980 through 1995 were reviewed for cases of intraspinal juxtafacet cysts. Results. Eight cases of intraspinal juxtafacet cysts were identified; six were in the lumbar spine. One patient had a cervical cyst related to a facet joint and had unilateral radiculopathy. A second patient with a thoracic cyst had the gradual onset of myelopathy. Both patients had surgical excision of the cyst without resection of the adherent dura. The symptoms and neurologic signs improved in each case. Conclusions. Cervical and thoracic juxtafacet cysts are rare lesions that are usually signaled by myelopathy. Results of surgery are excellent in most cases, even if the cyst is not completely excised.

The Origins of Syringomyelia: Numerical Models of Fluid/Structure Interactions in the Spinal Cord

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.

Excitotoxic model of post-traumatic syringomyelia in the rat.

Study Design. A rat model was developed to elucidate the role of excitatory amino acids and spinal subarachnoid block in the genesis of post-traumatic syringomyelia. This excitotoxic model produces intramedullary cavities rather than the dilation of the central canal (canalicular syringomyelia) created by previous animal models. Objectives. To produce extracanalicular cysts in the rat spinal cord with quisqualic acid, a potent agonist of multiple excitatory amino acid receptors, and to compare the effects of excitotoxic injury only with that of excitotoxic injury and subarachnoid block with kaolin. Summary of Background Data. In post-traumatic syringomyelia, primary injury and excitotoxic cell death secondary to elevated levels of excitatory amino acids may initiate a pathologic process leading to the formation of spinal cavities. Subarachnoid block by arachnoiditis may promote enlargement of the cavities. Methods. Three control rats received a unilateral injection of normal saline into the spinal cord, and another five rats received an injection of kaolin into the spinal subarachnoid space. Quisqualic acid was injected unilaterally into the spinal cord of 20 rats, and 13 additional rats received a unilateral injection of quisqualic acid into the spinal cord after injection of kaolin into the subarachnoid space. Histologic and immunocytochemical assessments were undertaken. Results. In the control groups, no parenchymal cyst developed in any of the animals. Spinal cord cyst formation was observed in 16 of 19 animals in the quisqualic acid groups, but no cysts exceeding two segments in the length of the spinal cord developed in any of the rats. Much larger cavities were seen in 9 of 11 animals in the group with quisqualic acid and kaolin, and cysts exceeding two segments developed in all 9 of these (9/11; 82%). Conclusions. In post-traumatic syringomyelia, excitotoxic cell death occurring secondarily to elevated levels of excitatory amino acids may contribute to the pathologic process leading to the formation of spinal cord cysts. Subarachnoid block by arachnoiditis is likely to cause enlargement of the cavity.

Altered subarachnoid space compliance and fluid flow in an animal model of posttraumatic syringomyelia.

Study Design. A histologic study of cerebrospinal fluid tracers in Sprague-Dawley rats undergoing lumboperitoneal shunt insertion in the excitotoxic animal model of posttraumatic syringomyelia (PTS). Objectives. To determine the effects of cerebrospinal fluid (CSF) diversion from the subarachnoid space on perivascular flow (PVS) and syrinx formation in posttraumatic syringomyelia. Summary of Background Data. In an animal model of PTS, fluid enters syringes from the subarachnoid space via perivascular spaces. Preferential PVS flow occurs at the level of the syrinx. It has been suggested that arachnoiditis predisposes to posttraumatic syringomyelia formation by obstructing subarachnoid cerebrospinal fluid flow and enhancing perivascular flow. Materials and Methods. Thirty-two male Sprague-Dawley rats were investigated using the CSF tracer horseradish peroxidase (HRP), the excitotoxic model of PTS, and lumboperitoneal shunt insertion. Five experimental groups consisted of normal controls, syrinx only and shunt only controls, and shunt insertion before or after syrinx formation. In all groups except normal controls, CSF flow studies were performed 6 weeks after the final intervention. Grading scales were used to quantify HRP staining. Results. All excitotoxic model animals formed syringes. Perivascular flow was greatest at the level of the syrinx. Cerebral cortex perivascular flow was significantly reduced after shunt insertion in animals with a syrinx (P < 0.05). Shunt insertion did not alter syrinx length or size. There were no significant differences between shunt and syrinx first groups. Conclusions. Increasing caudal subarachnoid space compliance with a shunt does not affect local CSF flow into the spinal cord and syrinx. These results suggest that localized alterations in compliance, as opposed to obstruction from traumatic arachnoiditis, may act as an important factor in syrinx pathogenesis.

Sutureless nerve repair with laser-activated chitosan adhesive : a pilot in vivo study

OBJECTIVE The anastomosis of peripheral nerves is a demanding procedure that has potential complications due to foreign body reactions elicited by sutures. In this study, the sutureless in vivo anastomosis of rat tibial nerves was successfully performed, using for the first time a chitosan-based laser-activated adhesive. The nerve thermal damage caused by the laser irradiation was quantitatively assessed. MATERIALS AND METHODS A novel adhesive composed of chitosan, indocyanine green, acetic acid, and water, was fabricated in thin sheets. Its adhesive strength was tested in vitro by bonding strips (surface area approximately 20 mm2, thickness approximately 20 microm) onto rat sciatic nerves and sheep intestine by laser activation with low fluence ( approximately 50 J/cm2), using a fiber-coupled diode laser (n = 13). The tensile strength of the adhesive/tissue bonds was measured after tissue repair. The chitosan adhesive was then used to perform sutureless anastomosis of tibial nerves in vivo (n = 6). Adhesive strips were also bonded in vivo onto intact rat sciatic nerves (n = 6) in order to quantitatively assess, by counting myelinated axons, the thermal damage induced by the laser. RESULTS The adhesive bonded well to tissue with a tensile strength of 12.5 +/- 2.6 KPa (mean +/- SD; n = 13). The in vivo anastomosed nerves were in continuity 3 d after surgery. Axon counting showed the number and morphology of myelinated axons were normal proximally ( approximately 96%) compared with intact nerves (100%). Axon demyelination was observed at the operation site ( approximately 49%) and distally ( approximately 27%), and was attributed to laser-induced thermal damage. CONCLUSIONS Nerve anastomosis, performed by the laser-adhesive procedure, was successful 3 d postoperatively. Proximal myelinated axons were not significantly damaged by the low laser fluence.

Ultrastructure of perinidal capillaries in cerebral arteriovenous malformations.

OBJECTIVE:The ultrastructure of perinidal capillaries in cerebral arteriovenous malformations (AVMs) was examined to clarify their pathomorphological features. METHODS:Fifteen AVM specimens were dissected and divided into perinidal and intranidal groups and processed for ultrastructural study immediately after surgical removal. Eleven of the patients had presented with hemorrhage. Tissue from four normal controls was also studied. Electron microscopy was used to compare features of the blood-brain barrier and endothelial cells (ECs) of capillaries in perinidal, intranidal, and controls. RESULTS:Perinidal capillaries demonstrated abnormal ultrastructure of the blood-brain barrier with no basement membranes and astrocytic foot processes. ECs had fenestrated luminal surfaces. Large gaps were observed at endothelial intercellular junctions. ECs contained numerous filopodia, large numbers of cytoplasmic processes, numerous micropinocytotic vesicles, and the cytoplasm contained more filaments than those observed in controls. Pericytes were rich in pinocytotic vesicles, vacuoles, and filaments. Their processes were in close contact with ECs. Weibel-Palade bodies were present in perinidal ECs. CONCLUSION:The absence of blood-brain barrier components in perinidal capillaries may contribute to extravasation of red blood cells into the surrounding brain in the absence of major hemorrhage and explain the gliosis and hemosiderin occasionally seen around AVMs. Cellular differentiation and proliferation in perinidal capillaries should be included in a systematic study aimed at a better understanding of the mechanisms underlying the recurrence of surgically removed AVMs.