Observation of the lesions themselves using the scanning E/M produces 2 very distinctly different pictures:
(1) Quincke: The bevels on Quincke-type spinal needles possess 2 distinct components: (a) a distal beveled tip that produces a small cutting lesion of the dura-arachnoid complex and (b) sharp-edged shoulders. As the tip advances, the sharp edges cut and distend the dura, favoring clean progression through the complex. Quincke spinal needles produce a precise, controlled cut, limiting damage of dura mater and arachnoid layer. The tip of the needle “folds” cut tissue inside the dura so that dural and arachnoid lesions produced by Quincke needles show a “crescent” shape resembling the letters “U” or “V,” not dissimilar to the lid of an opened can. The edges are clean cut, and tissue “loss” is minimized. Only a thin orifice remains “open” in lesions caused by beveled cutting spinal needle tips.
(2) Whitacre: Pencil-point tips produce greater tearing of tissue margins and folding at the edges of the lesion. The edges of dural and arachnoid lesions caused by pencil-point needles are jagged and irregular. The tissue margins are fragmented because the process of needle advancement is one of blunt tearing and avulsion.
There were significant differences between the dural and arachnoid lesion area in 27G Whitacre (P = 0.029) but not in perimeter length (P = 0.345).
There were no significant differences between the parallel and perpendicular bevel approach using the same 29G Quincke needle type on dural surface lesions (group 3 vs group 5: dural area, P = 0.880; dural perimeter, P = 0.910) or on arachnoid surface lesions (group 4 vs group 6: arachnoid area, P = 0.940; arachnoid perimeter, P = 0.640). There were no significant differences between the dural and arachnoid lesions in 29G Quincke needles using either parallel orientation (area, P = 0.142; perimeter, P = 0.377) or perpendicular alignment (area, P = 0.361; perimeter, P = 0.305).
There were significant differences between the size (area) of lesions produced by 27G Whitacre needle and overall 29G Quincke needle lesions on the arachnoid surface (area, P = 0.001; perimeter, P = 0.011) but not on dural surface (area, P = 0.181; perimeter, P = 0.234). Such difference in arachnoid layer area between 27G Whitacre needles and 29G Quincke needles was confirmed in both parallel alignments for area (P = 0.008) and perimeter (P = 0.024) and in perpendicular alignments in both area (P = 0.001) and perimeter (0.039). Dural lesions showed no differences between 27G Whitacre and 29G Quincke needles with either parallel alignment (area, P = 0.182; perimeter, P = 0.271) or with perpendicular orientation (area, P = 0.377; perimeter, P = 0.280).
This study demonstrates that (1) accepted theories of the etiology of PDPH need to be revised; (2) with 27G or smaller-size needles, the lesions produced by different needles are small—there is no difference between needle orientation in the nature of the lesions produced; (3) it is the arachnoid damage that contributes primarily to PDPH characteristics; (4) dural fibers tend to have sufficient “memory” to close back the hole created by a spinal needle, whereas arachnoid has diminished capacity to do so; (5) spurious theories regarding dural fiber orientation are incorrect—the distribution of “fibers” is not unidirectional but randomly laid out in concentric, independent layers, and theories based on fiber “splitting rather than cutting” are a little more than myth; (6) pencil-point needle injury wounds are “avulsion” lesions not “splitting” lesions; (7) once needles of less than 27G are selected by clinicians, other needle characteristics (eg, shaft rigidity, which determines the extent of deviation from the directional axis of entry; internal area of the hollow needle, which determines speed of CSF flashback) become more important priorities when compared with needle tip style, needle shoulder bevels, or tip orientation relative to spinal axis; (8) according to our studies, in vitro, the lesion produced by the 29G Quincke needle is smaller than that produced by the 27G Whitacre needle. Additional factors applicable to clinical practice may be evaluated in future studies; (9) even though PDPH is not recognized as a significant complication of spinal sac puncture with fine needles, the pathogenesis of PDPH and its resolution algorithm are a far more complex process that involves many more “stages” of development than hitherto imagined; (10) the arachnoid “barrier” and dura “superstructure frame” functions are emphasized, and (11) an improved, uniform, standardized, and universal electron microscopy methodology for the management and measurement of dura-arachnoid complex lesions has been used.
The “dural” hole obtained after a lumbar puncture consists of 2 components: (a) a dural lesion obtained by piercing several laminae of the dura mater and (b) an arachnoid layer puncture.
As a Quincke needle tip is advanced, the jagged fragments at the edge of the lesions tend to fold inward, after all dural and arachnoid layers are severed, and the edges of the lesion are displaced away from the needle tip. As soon as the spinal needle is withdrawn, the edges of the lesion tend to retract because of the viscoelastic properties of the affected dura mater. This may favor the return of the ragged edges to their original position, hastening the closure of the dural sac lesion.
Pencil-point spinal needles of Whitacre style have noncutting tips and tend to displace the dural sac before piercing the dural laminae during a lumbar puncture. Lack of sharp beveled tips produces a larger “tenting” indentation before the dura-arachnoid penetration.
Closure of the lesion produced by either needle is a complex phenomenon with many mechanisms at play. One could hypothesize that the more pronounced avulsion of fibers produced by pencil-point needles, when compared with the cleaner cut made by Quincke-type needles, could increase the local inflammatory reaction and associated edema in vivo, resulting in faster closure of the traumatic lesion.22 This hypothesis has never been confirmed.
It should be remembered that our study results reflect a snapshot of “closure” of the dural and arachnoid holes caused by the 2 different types of fine needles under very specific conditions and may therefore not reflect the entire process of damage and repair. For example, (1) examination of the closure process was arrested within approximately the first 20 minutes. Once the tissue samples were “fixed,” viscoelastic properties no longer apply so that the size and shape of the lesions could no longer change spontaneously; (2) once the samples were extracted, the effects of pressure from CSF pressing outward across the dural sac lesion and CSF flow past the edges of the lesion are removed. This could have an effect on the final rearrangement of the lesion edges around the zone of closure so that the in vitro conditions may not mimic entirely what actually happens in real time.
If these limitations are recognized and accepted and keeping in mind that observations are restricted to the structure of early lesions in the dura-arachnoid during lumbar spinal sac puncture with small-gauge needles, it is interesting to note that lesions observed are not circular and suffer a rearrangement process with approximation of edges. Approximation of edges of the puncture hole may also occur in vivo because of the dural viscoelastic properties. Indeed, each needle type and size exert a different stretching force or “tenting” effect.
Electron microscopy examination of the epidural or “outer” surface of the dural sac shows extent of closure of dural laminae within the dura mater, whereas observation of the intrathecal or “inner” surface of the dural sac permits study of the nature and early resealing of the hole in the arachnoid layer (Figs. 1–4). Furthermore, E/M examination through the “inner” arachnoid layer allows observation of partial or even complete closure of internal dural laminae (Figs. 2 and 4). A different degree of closure of each dural sheet lesion is possible because the dura mater is made up of multiple concentric dural laminae.20 Each lamina acts as an independent unit so that the mode and extent of closure, response to trauma, mechanisms for healing, and damage sustained at puncture are both similar and different for each structural and functional unit within the dura mater. These observations cast a novel light onto understanding how rearrangement of the edges of dural lesion affects the lesion's area parameter rather than simple measurement of the corresponding perimeters, that is, that both size of hole and perimeter characteristics, especially on the arachnoid “inner” surface, are important, we surmise, in establishing rate of dural CSF leak and lesion closure time. In contrast to the dura mater, the arachnoid layer is formed of arachnoid cells firmly attached by specialized membrane junctions (tight junctions and desmosomes) forming the major meningeal barrier of the dural sac. Images from our previous researches20,21 show such differences (Fig. 5). The arachnoid layer has no “directionality” of its components,19,21 so that it is now the perimeter characteristic of the arachnoid layer lesion that is of even greater importance.
The reduced hole area and “length” of perimeter in the dural laminae in 29G Quincke compared with 27G Whitacre needles in percentages are almost proportional to the diameter of needle used (Table 1). With small needles, the size of the lesion depends more on the diameter of the needle than on the design of the tip of the needle.
In clinical practice, Whitacre needles enjoy a marginally reduced incidence of PDPH, but they cannot be considered to be nontraumatic needles; the edges of the lesions produced are irregular when compared with the smooth margins of lesions caused by the sharp, beveled cutting Quincke needles.
A reduced perimeter length and area (size) of the lesion are produced by viscoelasticity, whereas perimeter length is affected mainly by tissue retraction; as it partly recovers its original position, the area is influenced by additional factors such as CSF pressure. Importantly, as shown in Table 1, it was observed that the size of dural lesion was reduced to 20% of the original hole size; that is, that dura mater recovered 80% of its distended, puncture position.
Interestingly, all the dural lesion images suggest that fiber damage, rather than fiber separation, occurs with spinal needles. This questions the commonly held intuitive belief that dural fiber separation, rather than fiber damage, occurs with pencil-point and bullet-head puncture needles. Because we demonstrate an irregular border of the lesion perimeter instead of a linear split, as would be expected if fiber separation were to occur, we conclude that attributing diminished PDPH to Whitacre pencil-point needles is probably only 1 aspect, probably rather minor, of the reasons for the desirability of using these needles preferentially. Dural fibers have neither a longitudinal distribution nor a parallel orientation; the fibers are randomly distributed.20,22 Favoring pencil-point spinal needles on the basis that they are less traumatic is not supported by our findings.
Likewise, the concept of “fiber separation” utilized until now to recommend aligning the bevel of Quincke-type needles in the axial plane is also not supported by this study.22,23
The 29G and 27G needles studied have external diameters ranging from 330 to 400 μm. These dimensions are orders of magnitude larger than collagen (0.1-μm diameter) or elastin (2-μm diameter) fiber ultrastructure within the dura mater.17,20 Such diameter difference, together with the shape of the observed lesions, suggests that fiber avulsion, rather than fiber separation, occurs. No needle, regardless of design type, can be considered “nontraumatic” or “atraumatic.”
When it comes to arachnoid layer ultrastructure, alignment of bevel of Quincke-type needles is even more irrelevant because arachnoid cells have neither longitudinal distribution nor parallel orientation and are much smaller than the elastin fibers.19,21 This study confirms that there were no significant differences in the size (area and perimeter) of lesions analyzed when the lumbar puncture was performed with the bevel of the 29G Quincke-type needle oriented parallel or perpendicular to the spinal axis.
Although counterintuitive, the finding that the dura-arachnoid lesions cannot be related to any “fiber splitting” mechanism applies, to varying degrees, to other needle sizes. Figure 6 compares the lesions produced by 27G Whitacre and 29G Quincke needles with those produced by 22G and 25G Quincke and 25G Whitacre needles, captured at the same magnification, from our previously published articles.22,23
Although superficially, there may seem to be a discrepancy between this study's E/M microanatomical findings and in vivo clinical experience; deeper examination of the clinical studies shows wide variability of results. To cite 2 simple examples where clinical practice does not mimic laboratory conditions, (a) each of our E/M images is for a single “clean” puncture, whereas in clinical practice, it is sometimes necessary to perform several puncture attempts before CSF is obtained. This “watering-can” multiple-hole array may exhibit totally different characteristics to a single hole; (b) our brand new, single-use needles were used once and discarded; in clinical practice, if the first attempt fails, the needle is technically “blunt” from deformation of the tip especially if osseous structures, for example, spinous process or vertebral lamina, are encountered. This effect is magnified in situations (eg, countries with limited resources) where spinal needles are resterilized and reused. Tip deformation is worst with Quincke-type needles and is virtually minimal with Whitacre pencil-point needles.24 Some insertion techniques could reduce vertebra impingement and consequent needle deformation.25
In our studies, we tested only single punctures using high-quality, “new,” pristine propriety needles of original design. Blunt, deformed, poor-quality, multiple-use, or poorly designed needles in multipuncture situations were not looked atm but we surmise that in such studies wounds will be larger, more jagged, and less likely to close and will only magnify our findings and render our conclusions even more relevant.
On the other hand, our in vitro studies were performed on specimens of isolated dural sacs that were not subjected to tensile forces that occur during changes of posture and position.
The etiology and pathogenesis of PDPH, especially, although less commonly encountered, with fine-gauge spinal needles, are not fully understood. It cannot be solely explained by the type and size of needle used. Many other factors contribute, so that the process initiated by the dural and arachnoid puncture leads to a complex interaction of factors and healing processes. The dural and arachnoid layers have entirely different structure and function and heal differently.26,27
This study analyzes lumbar punctures in ideal conditions with direct visualization of location of puncture using undamaged, undeformed needles in a single piercing at the first attempt. Nevertheless, these data contribute to new ideas and hypotheses, some of which do not support the currently espoused putative mechanisms in current clinical studies.
The Whitacre 27G suffers from other design deficiencies, as does the Quincke 29G. These extremely thin needles with low internal cross-sectional area are more likely to be deflected laterally away from the midline and have poor “flashback” time (delayed exit of CSF into the hub even when the distal needle aperture is intrathecal). Because internal radius drops dramatically as one goes from 27G to 29G, and area is a squared function of radius by the equation A = πr2, in practice most practitioners will opt for a 27G as opposed to a 29G needle. This study confirms that lesions produced by 27G Whitacre needles under laboratory conditions are greater than lesions produced by 29G needles, but theoretical advantages (less discomfort, lower PDPH incidence) are outweighed by other disadvantages (deflection, slow flashback, multiple attempts, failed puncture); that is, the risk-benefit ratio of 29G needles becomes vanishingly low.
A very relevant aspect of these studies is that the lesion produced within the arachnoid layer is at least as important as the dura mater hole on subsequent genesis of CSF loss because the dura, unlike the arachnoid, lacks cellular tight junctions. Closure of the dura mater whose fibers lack spatial orientation would not, alone, prevent further CSF leakage until the subjacent arachnoid layer had been completely restored. This phenomenon does not diminish the importance of the dural layer in the healing process because dura provides the lattice superstructure along which the arachnoid can seal the gap.
There is no benefit in adopting a specific needle-tip type or alignment of sharp beveled tips given the rectangular shape of arachnoid cells and the absence of a specific spatial orientation.
In summary, lesions produced by fine spinal needles are small. While the dura mater's viscoelastic property has a much better initial capacity to reduce hole size and CSF leak than the arachnoid layer, it is synergistic arachnoid healing that completely stops CSF leakage. This study underpins the importance of further studying the arachnoid layer in the etiology of PDPH. While this study does not give a definitive answer as to the origin and progression of PDPH, the results contribute to a better understanding of its etiology and dismiss some myths relating to possible containment and harm-reduction strategies.
The authors thank Alfredo Fernández Larios, Alfonso Rodríguez Muñoz, and Ana Vicente Montaña, from the National Center for Electron Microscopy ICTS, Madrid, for their technical assistance in the use of scanning E/M.
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