PubMed · 14490079
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B RAMAMURTHI. 1961. Spinal arachnoiditis.. https://pubmed.ncbi.nlm.nih.gov/14490079/
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AIMS: The dural and arachnoid hole caused by lumbar puncture needles is a determining factor in triggering headaches. The aim of this study is to assess the dimensions and morphological features of the dura mater and arachnoids when they are punctured by a 22 gauge Quincke needle having its bevel either in the parallel or in the transverse position. METHODS: Fifty punctures were made with 22 gauge Quincke needles in the dural sac of four fresh cadavers using an "in vitro" model especially designed for this purpose. The punctures were performed by needles with bevels parallel or perpendicular to the spinal axis and studied under scanning electron microscopy. RESULTS: Thirty five of the 50 punctures done by Quincke needles (19 in the external surface and 16 in the internal) were used for evaluation. When the needle was inserted with its bevel parallel to the axis of the dural sac (17 of 35), the size of the dura-arachnoid lesion was 0.032 mm(2) in the epidural surface and 0.037 mm(2) in the subarachnoid surface of the dural sac. When the needle's bevel was perpendicular to the axis (18 of 35) the measurement of the lesion size was 0.042 mm(2) for the external surface and 0.033 mm(2) for the internal. There were no statistical significant differences between these results. CONCLUSIONS: It is believed that the reported lower frequency of postdural puncture headache when the needle is inserted parallel to the cord axis should be explained by some other factors besides the size of the dura-arachnoid injury.
OBJECTIVE: To apply a theoretical model to analyse the derangement of cerebrospinal fluid (CSF) dynamics in syringomyelia associated with adhesive arachnoiditis. METHODS: An electrical circuit model of CSF dynamics in the spine was used. With this model, the derangement of CSF dynamics in adhesive arachnoiditis was simulated. The effects of various surgical procedures were then analysed, such as syringo-subarachnoid shunting, subarachnoid bypass, and foramen magnum decompression. RESULTS: When CSF flow in the subarachnoid space was obstructed at a certain point, the pressure inside the spinal cord increased in the segment immediately distal to the blockage. This location of increased pressure corresponded to the preferred site of syrinx formation in adhesive arachnoiditis. Syringo-subarachnoid shunting, subarachnoid bypass, and foramen magnum decompression were all effective at reducing this pressure gradient. CONCLUSIONS: Blockage of the spinal subarachnoid CSF pathway produces a relative increase in the pressure inside the spinal cord distal to the blockage point. Repetitive formation of this pressure gradient then induces CSF leakage into the spinal parenchyma, leading to the formation of syringomyelia. Using this model, alternative surgical procedures could be suggested that might be effective in treating this disease.
BACKGROUND AND PURPOSE: Peak CSF velocities detected in individual voxels in the subarachnoid space in patients with Chiari I malformations exceed those in similar locations in the subarachnoid space in healthy subjects. The purpose of this study was to test the hypothesis that the peak voxel velocities are decreased by craniocervical decompression. METHODS: A consecutive series of patients with symptomatic Chiari I malformations was studied before and after craniocervical decompression with cardiac-gated, phase contrast MR imaging. Velocities were calculated for each voxel within the foramen magnum at 14 time points throughout the cardiac cycle. The greatest velocities measured in a voxel during the cephalad and caudad phases of CSF flow through the foramen magnum were tabulated for each patient before and after surgery. The differences in these velocities between the preoperative and postoperative studies were tested for statistical significance by using a single-tailed Student's t test of paired samples. RESULTS: Eight patients with a Chiari I malformation, including four with a syrinx, were studied. Peak caudad velocity diminished after craniocervical decompression in six of the eight patients, and the average diminished significantly from 3.4 cm/s preoperatively to 2.4 cm/s postoperatively (P =.01). Peak cephalad velocity diminished in six of the eight cases. The average diminished from 6.9 cm/s preoperatively to 3.9 cm/s postoperatively, a change that nearly reached the significance level of.05 (P =.055). CONCLUSION: Craniocervical decompression in patients with Chiari I malformations decreases peak CSF velocities in the foramen magnum. The study supports the hypothesis that successful treatment of the Chiari I malformation is associated with improvement in CSF flow patterns.