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Previous studies of samples from cranial meninges have created doubts about the existence of a virtual subdural space. We examined the ultrastructure of spinal meninges from three human cadavers immediately after death to see whether there is a virtual subdural space at this level. The arachnoid mater had two portions: a compact laminar portion covering the dural sac internal surface and a trabecular portion extending like a spider web around the pia mater. There was a cellular interface between the laminar arachnoid and the internal layer of the dura that we called the dura-arachnoid interface. There was no subdural space in those specimens where the dura mater was macroscopically in continuity with the arachnoid trabecules. In the specimens where the dura mater was separated from the arachnoid, we found fissures in between the neurothelial cells that extended throughout the interface. We hypothesize that the subdural space would have its origin within the dura-arachnoid interface when the neurothelial cells break up, creating in this way a real subdural space. IMPLICATIONS: The subdural space was not seen under transmission electron microscopy in samples of human spinal meninges where surgical manipulation was avoided. Scanning electron microscopy in other samples showed the presence of broken neurothelial cells giving up fissures that extended along the dura-arachnoid interface. These findings may explain the origin of a real subdural space.
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A study using scanning electron microscopy showed that although the laminas forming the dura mater are concentric and parallel to the surface of the medulla, the fiber layers' orientations are different in each sub-lamina, dispelling the conventional knowledge that all the fibers of the dura are arranged in a parallel direction. Thus, this study evaluated the dural lesions produced by Whitacre and Quincke spinal needles in the external and internal surface of the dura mater of the lower spine area in an attempt to gain more insight into the pathophysiology of postdural puncture headaches (PDPH).
The T11-L4 dural membranes from 5 fresh (immediately after extraction of organs for transplantation), male patients declared brain dead, ages 23, 46, 48, 55, and 60 years, were excised by anterior laminectomy. Morphologic orientation of the membrane and normal pH were maintained with an apparatus designed for this purpose. One hundred punctures (20 on each sample) at 90-degree angles were done with a new needle each time, 50 with 25-gauge Whitacre and 50 with 25-gauge Quincke needles. Half of the punctures with the Quincke needles were done with the bevel in parallel direction to the axis of the spinal cord, and the rest with the bevel perpendicular to it. Fixation in solutions of 2.5% glutaraldehyde phosphate buffer, followed by dehydration with acetone, was done 15 minutes after the punctures. After acetone was removed at ideal conditions of temperature and pressure, the specimens were then metallized with carbon followed by gold and inspected under a scanning electron microscope.
Twenty-five of the Whitacre and 23 of the Quincke punctures were found for evaluation. There were no differences in the cross-sectional area of the punctures produced by the Whitacre or Quincke needles on the dura. The area of the dural lesions produced by 25-gauge Quincke needles, 15 minutes after they have been withdrawn, was 0.023 mm2 (confidence interval [CI] 95%, 0.015 to 0.027) in the external aspect (epidural surface) and 0.034 mm2 (CI 95%, 0.018 to 0.051) in the internal aspect (arachnoid surface) of the dural sac. The area of the lesions produced by the 25-gauge Whitacre needles was 0.026 mm2 (CI 95%, 0.019 to 0.032) and 0.030 mm2 (CI 95%, 0.025 to 0.036) in the external and internal surfaces of the dural sac, respectively. There were no significant differences in the cross-sectional areas of the punctures produced by the 25-gauge Whitacre or 25-gauge Quincke needles. Moreover, with Quincke needles the dural lesions closed in an 88.3% (CI 95%, 86.3 to 92.4) and 82.7% (CI 95%, 74.1 to 90.9) of their original sizes in the epidural and arachnoid surfaces, respectively. With Whitacre needles, the closure occurred in an 86.8% (CI 95%, 83.8 to 90.3) and 84.8% (CI 95% 81.7 to 87.3) in the dural and arachnoid surfaces, respectively. However, there were differences in the morphology of the lesions. The Whitacre needles produced coarse lesions with significant destruction in the dura's fibers while the Quincke needles produced a 'U'-shaped lesion (flap) that mimics the opened lid of a tin can, regardless of the tip's direction.
The needles produced lesions in the dura with different morphology and characteristics. Lesions with the Quincke needles resulted in a clean-cut opening in the dural membrane while the Whitacre needle produced a more traumatic opening with tearing and severe disruption of the collagen fibers. Thus, we hypothesized that the lower incidence of PDPH seen with the Whitacre needles may be explained, in part, by the inflammatory reaction produced by the tearing of the collagen fibers after dural penetration. This inflammatory reaction may result in a significant edema which may act as a plug limiting the leakage of cerebrospinal fluid.
Regional Anesthesia and Pain Medicine 01/2000; 25(4):393-402. DOI:10.1053/rapm.2000.7622 · 2.12 Impact Factor