The last decade has seen a significant improvement in the understanding of spinal cerebrospinal fluid (CSF) leaks and the resulting syndrome of spontaneous intracranial hypotension (SIH). For the reader of Headache and those caring for patients with chronic refractory headaches, three novel concepts are emerging from accumulating data published here and elsewhere: (1) the majority of people with an imaging-proven CSF leak have normal opening pressure; (2) CSF–venous fistulas (CVFs) are a major, rather than rare, cause of SIH; and (3) there is a persistent headache syndrome that occurs at an alarmingly high frequency after unintended dural punctures during epidurals done for analgesia in the obstetric setting.

The first article in our virtual issue, “Spontaneous Intracranial Hypotension: 10 Myths and Misperceptions” by Kranz et al. begins with an excellent review of advances up to 2018. The clarity of writing and elucidation of the ways in which SIH can be misunderstood and missed led to it being voted the Members Choice Award winner for 2018. It should not be overlooked by those wanting a primer on the basics of SIH.¹ Their myth one: “SIH Is Defined by Low CSF Pressure” traces the history from early reports in which opening pressure was considered a key feature of SIH, to a modern understanding that only a minority of patients with a proven CSF leak have a low opening pressure. When Kranz et al. evaluated their own cohort of 106 symptomatic patients with SIH who underwent thorough imaging regardless of the measured opening pressure, they reported only 34% of patients with symptomatic and imaging-proven CSF leaks had low opening pressure. This has held up since and has been extended to CVFs. One recent cohort of 17 consecutive spinal CSF leaks of which 12 were CVFs reported that only 1 of 17 had low opening pressure.² In another multi-institution cohort of 48 CVF, only 2 had low opening pressure.³

However, in retrospect, the most impressive aspect of “Spontaneous Intracranial Hypotension: 10 Myths and Misperceptions” may have been its anticipation of the growing importance of CVFs. In fact, their article shows the first image in Headache of a CVF. Discovered accidentally in 2014, the true revolution of CVFs arguably began to unfold only after the publication of “Spontaneous Intracranial Hypotension: 10 Myths and Misperceptions,” and can be traced to the first report in 2019 that the frequency of detectable CVF dramatically increases when patients are imaged in the lateral decubitus position with dense intrathecal contrast layering over nerve root sleeves.^{4, 5}

Two papers in our virtual issue highlight different aspects of the emerging understanding of CVFs. “Headache Response after CT-Guided Fibrin Glue Occlusion of CSF-Venous Fistulas” by Mamlouk et al.⁶ described CVF as a major, rather than a rare, cause of SIH. Of 78 patients presenting to the authors’ institution with brain or clinical features suggesting SIH, 30 had traditional extradural fluid collections visible on spine magnetic resonance imaging (MRI), while 38 had a CVF that could only be detected with lateral decubitus myelography.⁶ A similar finding was described in a recent report of sequential patients with SIH in Olmsted County, Minnesota in which 7 of 14 (50%) were found to have CVF as the cause of SIH.⁷ Mamlouk et al. also demonstrated the utility of computed tomography (CT) imaging for the detection of CVF. Though CVFs were initially discovered using digital subtraction myelography (DSM), imaging following contrast injection—a technique usually reserved for catheter angiography—suites, Mamlouk et al. described that CVFs can be readily detected using decubitus CT imaging, a finding increasingly validated.⁸ Finally, this work demonstrated that CVFs can be treated effectively in some but not all patients with percutaneous fibrin injection, a finding which has been since reproduced in a multi-site study of more than 100 patients with CVF.⁹

“Spontaneous Spinal Cerebrospinal Fluid-Venous Fistulas in Patients with Orthostatic Headaches and Normal Conventional Brain and Spine Imaging” by Schievink et al. reports the findings when lateral decubitus DSM was offered to 60 patients with orthostatic headache in whom brain and spine MRI were normal—a group that until 2019 was thought to not have a CSF leak.¹⁰ When MRI–negative patients with orthostatic headache were evaluated for CVF, the rate of detectable CVF was 10% overall, but these were non-uniformly distributed. The CVFs were all concentrated in the 31 (52%) patients who had meningeal diverticula, a spinal imaging finding considered normal that has been reported to occur in up to 44% of healthy control patients.¹¹ Thus, the rate of an undetected CVF in patients with a negative MRI of the brain and full spine was 20% among the subset with a meningeal diverticula. In another reported cohort of patients examining the relationship of brain MRI findings and outcome of spinal imaging for CVF, among 24 patients with no pachymeningeal enhancement on brain MRI and no epidural collection on spine MRI, 8 patients (33%) were found to have a CVF.¹² These findings broadly validate the findings reported by Schievink et al. in this virtual issue. We anticipate that future work will continue to elucidate the true prevalence of detectable CVFs in patients with normal MRI of the brain and spine.

In light of these papers, the pre-2019 literature on SIH needs to be critically reappraised. For example, reports that MRI of the spine is 90% sensitive for detecting CSF leaks, largely based on its correlation with non-decubitus CT myelography, should now be understood to mislead more than inform.¹³ Such studies evaluated the performance of MRI for detecting CSF leaks by using conventional CT myelography as a gold standard for establishing the presence or absence of epidural fluid collections, but this is an intellectual framework now clearly undermined by CVF, in which no epidural collection is present.

Another important emerging trend in the field of spinal CSF leaks is the growing understanding that after an unintended dural puncture (such as a dural puncture occurring during a labor epidural), a significant number of patients will report new, or worsened, headaches that persist for years. Highlighted in this virtual issue, “Did She Have an Epidural? The Long-Term Consequences of Postdural Puncture Headache and the Role of Unintended dural Puncture” by Barad et al., the authors reviewed several studies which document that up to 30% of women experiencing an unintended dural puncture will go on to have a chronic headache syndrome.¹⁴ These data suggest that for some accidentally punctured patients, the large-bore, cutting tip Tuohy needle intended to facilitate threading of an epidural catheter outside the dura may form a uniquely devastating puncture when advanced unintentionally through the dura.

While much of these data come from retrospective case–control studies, also highlighted in this virtual issue is 2019's important prospective cohort study of the same phenomenon. In “Incidence of Persistent Headache at 18 Months Following Accidental Dural Puncture in the Obstetric Population: A Prospective Service Evaluation in 45 Patients” by Gauthama et al., the authors report that a third of such patients have new or worsened headache 18 months after an unintended dural puncture.¹⁵ This finding closely mirrors the rates of persistent headache suggested by retrospective case control data, and supports their conclusion that “post-dural puncture headache from an accidental dural puncture can no longer be considered a self-limiting condition.”

One might expect that the recognition and treatment of patients as having a headache from a CSF leak due to a known dural puncture would be straightforward; however, the data and publications in this virtual issue suggest otherwise. Even when patients report a new and persistent orthostatic headache that dates from the time of a recognized dural puncture, there is evidence that they are not receiving care directed toward a suspected CSF leak. Adding to the clinical confusion is the fact that as time persists, the classic orthostatic nature of the headache may dissipate.^{16, 17} In “Management and Outcomes of Persistent Headache after Accidental Dural Puncture in the Obstetric Population: A 9-Year Prospective Audit” by Niraj and Critchley, outcomes are described for a cohort of 54 patients with persistent headache dating from the time of a known unintended dural puncture.¹⁸ The authors report the longest-term follow-up to date for such patients with an average follow-up of 5.7 years post-puncture. Only half of those with ongoing chronic symptoms years after a known unintended dural puncture were ever treated with an epidural patch in the immediate postpartum period. Subsequently, even when it was clear that chronic symptoms had developed, only 9 of 54 were later offered an epidural blood patch. In the pain clinic where they were assessed and treated, their treatment was focused on palliative medical management and occipital nerve blocks—not escalating treatment for CSF leak. This might be partially accounted for by the fact that only 16 of 54 reported postural features. Furthermore, while 50 of 54 patients had a brain MRI, all were interpreted as normal and thus the potential diagnosis of CSF leak may have been inappropriately dismissed. Unfortunately, most patients with chronic post-puncture headache will have normal brain imaging, even when spine imaging is positive. Schievink et al. reported on 27 patients with chronic symptoms of CSF leak dating from a known dural puncture: only 3 of 27 had either pachymeningeal enhancement or any brain sagging to suggest radiographically that symptoms were related to a CSF leak.¹⁹ In contrast, nine had spine findings on imaging: five extradural collections, one had a CVF, and three had small pseudomeningoceles (blebs). Eight of these nine patients had complete resolution of symptoms with fibrin patching or surgery directed at these spinal imaging findings. Of the nine patients with symptoms starting at the time of a known puncture who also had confirmatory spine findings, only three had some brain imaging features associated with CSF leak. The high rate of negative imaging in these patients combined with the progressively less clear orthostatic nature of symptoms may erode confidence in the diagnosis. Indeed, Niraj and Critchley proposed an alternative hypothesis to ongoing CSF leak as the cause of persistent headache after an accidental dural puncture—that there is a period of sensitization that occurs in the peri-puncture period that contributes to long-term symptoms. This hypothesis is challenged by the high rate of clinical response years after a puncture when patching or surgery is used as treatment, as reported by Schievink et al., or Niraj and Critchley's own data that one third of these patients continue to report that their headache is postural. The readers are advised to attend to how these controversies unfold in the next several years, but the implications are enormous. Epidurals are ubiquitous, and accidental dural punctures are a regularly recurring experience for even the best practitioners.

Why would these post-puncture leaks become persistent? One reason is highlighted by a case report in this virtual issue. “A Causative Role for Remote Dural Puncture and Resultant Arachnoid Bleb in New Daily Persistent Headache: A Case Report.”²⁰ The images are informing and highlight the small pseudomeningoceles previously described by Schievink et al. above.¹⁹ Following a known dural puncture, the patient acquired a persistent structural alteration at the site of the puncture, a small pseudomeningocele or “bleb” predisposing to ongoing CSF leak. The subtle nature of the finding on the spine MRI is highlighted, and one look at the surgical images challenges our conception that a punctured dura will reliably heal in a way that restores its pre-puncture architecture. In cases such as the one presented in this virtual issue, it does not. These blebs, it seems, are also most visible on a thin cut (1 mm) axial or sagittal 3D acquired T2 fat-suppressed sequence and can be easily missed on the standard 2D T2 fat-suppressed sequences (e.g., STIR), which are most often acquired 3–5 mm apart. Both better imaging and perhaps a better appreciation of our existing imaging are needed.

Picking up this theme, in “Dinosaur Tail Sign: A Useful Spinal MRI Finding Indicative of Cerebrospinal Fluid Leakage” by Sakurai et al., the authors describe a spinal MRI sign few headache practitioners or neuroradiologists appreciate as an imaging feature suggesting a higher likelihood of an existing CSF leak: linear fluid intensity signal outlining the sagittal perimeter of the dorsal epidural space extending one or more segments on lumbosacral sagittal fat-suppressed T2-weighted MRI.²¹ This undulating T2 bright perimeter of the dorsal epidural space was imagined by the authors to resemble a dinosaur tail, hence the “dinosaur tail sign.” Seen in both iatrogenic and spontaneous CSF leaks, the fluid signal may represent epidural venous distension, free uncontained fluid, or both. In their study, among patients with CSF leak, there were an average of 3.8 spinal segments, while among the controls these were both uncommon and when present, exclusively limited to a single spinal segment. The reader should appreciate that this is a very different imaging finding than the characteristic one that neuroradiology trainees are educated on: a discrete epidural fluid collection. We suspect it is neither being noted nor interpreted as pathologic when seen as would be suggested by this single study. Hence, these findings require validation. The theme here is that whether looking for a bleb or a dinosaur tail sign, the critical spinal MRI findings are more subtle than an epidural collection and require a careful and up-to-date interpreter.

These issues highlight the importance of prevention. Two articles in our virtual issue point to the role of the neurologist and headache practitioner in that prevention: “The Effect of Needle Size on Cerebrospinal Fluid Collection Time and Post-Dural Puncture Headache: A Retrospective Cohort Study” and “Lower Incidence of Postdural Puncture Headache Using Whitacre Spinal Needles after Spinal Anesthesia: A Meta-Analysis.”^{22, 23} Both studies add to the compelling data that use of pencil-point (atraumatic) needles reduces the rate of early post-dural puncture headache (PDPH) without increasing patient discomfort. A large subsequent meta-analysis in the Lancet reported the same core findings: atraumatic needle use reduces PDPH by just over 50% without increasing the rate of failed procedures.²⁴ Given that at least one study has found that an early PDPH is a risk factor for persistent post-puncture headaches, it stands to reason that needle choice may not only affect the rate of acute PDPH but persistent headache syndromes as well.²⁵

Finally, the last articles highlight the still-surprising clinical heterogeneity of spinal CSF leaks. “Paradoxical Headache in a Case of Chronic Spontaneous Intracranial Hypotension and Multiple Perineural Cysts” highlights the previously reported and incompletely understood phenomena in which some patients with CSF leak report a reverse postural headache improved when upright and worse when flat.²⁶ Chow et al. described a case in which hemifacial spasm was the primary manifestation of SIH, while the aforementioned case of the post-puncture bleb presented initially as a new daily persistent headache a time long remote from the puncture.^{20, 27} In each case, the ability of SIH to appear as something other than the stereotypical orthostatic headache is highlighted.

In summary, SIH remains a condition that eludes detection, humbles the clinician, and remains the great deceiver, but the headache community is increasingly catching on to its tricks. The incredible advances made in the knowledge of CSF leaks over the past decade are inspiring, and we look forward to the future, where undoubtedly new discoveries await.

过去十年，人们对脊髓脑脊液（CSF）漏以及由此产生的自发性颅内低血压（SIH）综合征的认识有了显着提高。对于《Headache》的读者和那些护理慢性难治性头痛患者的人来说，从这里和其他地方发表的累积数据中浮现出三个新概念：（1）大多数经成像证实脑脊液漏的人具有正常的开放压力；(2) 脑脊液-静脉瘘 (CVF) 是 SIH 的主要原因，而非罕见；(3) 在产科环境中进行硬膜外镇痛期间意外刺穿硬膜后，会出现持续性头痛综合征，这种症状的发生频率高得惊人。

我们的虚拟期刊中的第一篇文章“自发性颅内低血压：10 个神话和误解”，作者：Kranz 等人。首先对 2018 年的进展进行了精彩回顾。文笔清晰，对 SIH 可能被误解和错过的方式进行了阐述，使其被评为 2018 年会员选择奖得主。对于那些希望获得会员选择奖的人来说，它不应该被忽视。 SIH 基础知识入门。¹他们的神话一：“SIH 是由低脑脊液压力定义的”，追溯了从早期报告（其中开放压力被认为是 SIH 的一个关键特征）到现代认识的历史，即只有少数已证实脑脊液漏的患者具有低脑脊液压力。开启压力。当克兰兹等人。他们对 106 名有症状的 SIH 患者进行了评估，无论测得的开放压如何，都接受了彻底的影像学检查，他们报告说，只有 34% 有症状且经影像学证实的脑脊液漏患者的开放压较低。此后这种情况一直存在，并已扩展到 CVF。最近的一组 17 例连续脊髓 CSF 漏（其中 12 例为 CVF）报告称，17 例中只有 1 例的开放压力较低。²在另一个由 48 名 CVF 组成的多机构队列中，只有 2 名的开启压力较低。³

然而，回想起来，《自发性颅内低血压：10 个神话和误解》最令人印象深刻的方面可能是它对 CVF 日益增长的重要性的预期。事实上，他们的文章展示了Headache of a CVF 中的第一张图像。CVF 于 2014 年被意外发现，可以说是在《自发性颅内低血压：10 个神话和误解》出版后才开始展开，并且可以追溯到 2019 年的第一份报告，即当患者以侧卧位成像，神经根套上有密集的鞘内造影剂分层。^{4, 5}

我们虚拟期刊中的两篇论文强调了对 CVF 新兴理解的不同方面。Mamlouk 等人的“CT 引导纤维蛋白胶闭塞脑脊液静脉瘘后的头痛反应”。⁶将 CVF 描述为 SIH 的主要而非罕见原因。在作者所在机构就诊的 78 名患者中，其脑部或临床特征提示 SIH，其中 30 名患者在脊柱磁共振成像 (MRI) 上可见传统硬膜外积液，而 38 名患者的 CVF 只能通过侧卧位脊髓造影检测到。⁶最近一份关于明尼苏达州奥姆斯特德县连续 SIH 患者的报告中描述了类似的发现，其中 14 名患者中的 7 名 (50%) 被发现因 CVF 而导致 SIH。⁷马姆卢克等人。还展示了计算机断层扫描 (CT) 成像在检测 CVF 中的实用性。尽管 CVF 最初是使用数字减影脊髓造影 (DSM) 发现的，但造影剂注射后成像（一种通常用于导管血管造影的技术）套件，Mamlouk 等人。描述了使用卧位 CT 成像可以轻松检测 CVF，这一发现日益得到验证。⁸最后，这项工作证明，经皮纤维蛋白注射可以有效治疗部分而非所有患者的 CVF，这一发现已在 100 多名 CVF 患者的多中心研究中得到重现。⁹

Schievink 等人的“直立性头痛和常规脑和脊柱成像正常的患者的自发性脊髓脑脊液静脉瘘”。报告了对 60 名脑部和脊柱 MRI 正常的直立性头痛患者进行侧卧位 DSM 治疗时的结果，直到 2019 年，这些患者被认为没有脑脊液漏。¹⁰当 MRI 阴性的直立性头痛患者接受 CVF 评估时，总体可检测到 CVF 的比例为 10%，但分布不均匀。CVF 全部集中在 31 名 (52%) 患有脑膜憩室的患者中，这是一种被认为正常的脊柱影像学发现，据报道，这种情况在高达 44% 的健康对照患者中出现。¹¹因此，在脑膜憩室亚组中，大脑和全脊柱 MRI 阴性的患者中，未检测到 CVF 的比例为 20%。在另一个报告的患者队列中，检查了脑部 MRI 结果与 CVF 脊柱成像结果之间的关系，在 24 名脑部 MRI 上没有硬脑膜增强且脊柱 MRI 上没有硬膜外收集的患者中，8 名患者 (33%) 被发现有CVF。¹²这些发现广泛验证了 Schievink 等人报告的发现。在这个虚拟问题中。我们预计未来的工作将继续阐明大脑和脊柱 MRI 正常的患者中可检测到的 CVF 的真实患病率。

鉴于这些论文，2019 年之前有关 SIH 的文献需要重新批判性地评估。例如，报告称脊柱 MRI 对于检测 CSF 漏的敏感性为 90%，主要是基于其与非褥疮 CT 脊髓造影的相关性，现在应该被理解为误导而不是告知。¹³这些研究通过使用传统 CT 脊髓造影作为确定是否存在硬膜外积液的黄金标准，评估了 MRI 检测脑脊液漏的性能，但这是一个现在明显受到 CVF 破坏的知识框架，其中不存在硬膜外积液。展示。

脊髓脑脊液漏领域的另一个重要的新兴趋势是，人们越来越认识到，在意外硬脑膜穿刺（例如硬膜外分娩过程中发生硬脑膜穿刺）后，大量患者会报告新的或恶化的头痛，并持续一段时间。年。本期虚拟期刊重点介绍了“她接受硬膜外麻醉了吗？” Barad 等人撰写的《硬脑膜穿刺后头痛的长期后果和意外硬脑膜穿刺的作用》一文中，作者回顾了几项研究，这些研究记录了高达 30% 的经历意外硬脑膜穿刺的女性会继续患有慢性头痛综合症。¹⁴这些数据表明，对于一些意外刺穿的患者，旨在促进将硬膜外导管穿入硬脑膜外的大口径、尖端切割的 Tuohy 针在无意中穿过硬脑膜时可能会形成独特的破坏性穿刺。

虽然这些数据大部分来自回顾性病例对照研究，但本期虚拟期刊还强调了 2019 年针对同一现象的重要前瞻性队列研究。Gauthama 等人在《产科人群意外硬脑膜穿刺后 18 个月内持续性头痛的发生率：对 45 名患者进行前瞻性服务评估》一文中，作者报告说，三分之一的此类患者在意外硬脑膜穿刺后 18 个月内出现新发头痛或头痛加重。意外的硬脑膜穿刺。¹⁵这一发现与回顾性病例对照数据显示的持续性头痛发生率密切相关，并支持他们的结论：“意外硬脑膜穿刺导致的硬脑膜穿刺后头痛不再被视为自限性疾病。”

人们可能会认为，由于已知的硬脑膜穿刺而导致脑脊液漏出而头痛的患者的识别和治疗会很简单；然而，本期虚拟期刊中的数据和出版物表明情况并非如此。即使患者报告自确认硬脑膜穿刺以来出现新的持续性直立性头痛，也有证据表明他们没有接受针对疑似脑脊液漏的治疗。更令人困惑的是，随着时间的推移，典型的直立性头痛可能会消失。^{16, 17}在 Niraj 和 Critchley 撰写的“产科人群意外硬脑膜穿刺后持续性头痛的管理和结果：9 年前瞻性审计”中，描述了 54 名持续性头痛患者的结果，该队列可追溯到已知的意外硬脑膜穿刺。¹⁸作者报告了迄今为止对此类患者的最长随访时间，穿刺后平均随访时间为 5.7 年。在已知的意外硬脑膜穿刺数年后出现持续慢性症状的患者中，只有一半在产后立即接受了硬膜外补片治疗。随后，即使很明显已经出现慢性症状，54 名患者中也只有 9 名后来接受了硬膜外血贴。在他们接受评估和治疗的疼痛诊所中，他们的治疗重点是姑息性医疗管理和枕神经阻滞，而不是针对脑脊液漏的升级治疗。部分原因可能是 54 人中只有 16 人报告了姿势特征。此外，虽然 54 名患者中有 50 名进行了脑部 MRI 检查，但所有患者都被解释为正常，因此可能不恰当地排除了脑脊液漏的潜在诊断。不幸的是，大多数患有慢性穿刺后头痛的患者即使脊柱成像呈阳性，其脑部成像也正常。希文克等人。报告了 27 名因已知硬脑膜穿刺而出现慢性脑脊液漏症状的患者：27 名患者中，只有 3 人有硬脑膜强化或任何脑下垂，从影像学上表明症状与脑脊液漏相关。¹⁹相比之下，9 例有脊柱影像学发现：5 例硬膜外积液，1 例有 CVF，3 例有小假性脑膜膨出（气泡）。这九名患者中的八名通过纤维蛋白修补或针对这些脊柱成像结果的手术完全缓解了症状。在 9 名在已知穿刺时出现症状且也有脊柱检查结果的患者中，只有 3 名患者具有与脑脊液漏相关的一些脑成像特征。这些患者的影像学阴性率很高，加上症状逐渐不太清楚的直立性，可能会削弱诊断的信心。事实上，Niraj 和 Critchley 提出了另一种假设，以替代持续的脑脊液渗漏作为意外硬脑膜穿刺后持续性头痛的原因，即在穿刺期间会出现一段致敏期，从而导致长期症状。这一假设受到了挑战，因为根据 Schievink 等人的报告，在穿刺数年后使用修补或手术作为治疗时，临床反应率很高，或者 Niraj 和 Critchley 自己的数据表明，这些患者中有三分之一继续报告他们的头痛是姿势。建议读者关注这些争议在未来几年将如何展开，但其影响是巨大的。硬膜外麻醉无处不在，即使对于最优秀的从业者来说，意外硬膜穿刺也是经常发生的经历。

为什么这些穿刺后泄漏会持续存在？本期虚拟期刊中的案例报告强调了其中一个原因。“远程硬脑膜穿刺和由此产生的蛛网膜泡在新发的日常持续性头痛中的致病作用：病例报告。” ²⁰这些图像告知并突出显示了 Schievink 等人先前描述的小型假性脑膜膨出。多于。¹⁹在一次已知的硬脑膜穿刺后，患者在穿刺部位发生了持续的结构改变，出现了一个小的假性脑膜膨出或“水泡”，容易导致持续的脑脊液漏。脊柱 MRI 发现的微妙性质得到了强调，一看手术图像就挑战了我们的观念，即刺穿的硬脑膜会以恢复其刺穿前结构的方式可靠地愈合。在本虚拟问题中提出的情况下，事实并非如此。这些气泡似乎在薄切 (1 mm) 轴向或矢状 3D 采集的 T2 脂肪抑制序列上也最明显，并且在标准 2D T2 脂肪抑制序列（例如 STIR）上很容易被忽略，这些序列是最常见的是间隔 3-5 毫米。需要更好的成像，或许还需要更好地理解我们现有的成像。

在 Sakurai 等人的《恐龙尾征：一种有用的脊髓 MRI 发现表明脑脊液渗漏》中，作者抓住了这个主题，描述了很少有头痛从业者或神经放射科医生欣赏的脊髓 MRI 征象，作为一种成像特征，表明脑脊液渗漏的可能性更高。现有的脑脊液漏：线性流体强度信号勾画出腰骶矢状脂肪抑制 T2 加权 MRI 上延伸一个或多个节段的背侧硬膜外腔矢状周界。²¹作者将背侧硬膜外腔的这种起伏的 T2 明亮周边想象成恐龙尾巴，因此称为“恐龙尾巴标志”。在医源性和自发性脑脊液漏中均可见，液体信号可能代表硬膜外静脉扩张、游离液体或两者。在他们的研究中，在脑脊液漏的患者中，平均有 3.8 个脊柱节段，而在对照组中，这些脊柱节段并不常见，而且当存在时，仅局限于单个脊柱节段。读者应该意识到，这是一种与神经放射学实习生所接受教育的特征性影像学发现截然不同的影像学发现：离散的硬膜外液体收集。我们怀疑它既没有被注意到，也没有被解释为病理性的，正如这项单一研究所暗示的那样。因此，这些发现需要验证。这里的主题是，无论是寻找水泡还是恐龙尾巴标志，关键的脊髓 MRI 发现都比硬膜外收集更微妙，需要仔细且最新的解释。

这些问题凸显了预防的重要性。我们虚拟期刊中的两篇文章指出了神经科医生和头痛治疗师在预防中的作用：“针头尺寸对脑脊液收集时间和硬膜穿刺后头痛的影响：回顾性队列研究”和“硬膜后穿刺发生率较低”脊髓麻醉后使用惠特克脊髓针治疗头痛：荟萃分析。” ^{22, 23}这两项研究都增加了令人信服的数据，即使用铅笔尖（无创伤）针可以降低早期硬膜穿刺后头痛 (PDPH) 的发生率，而不会增加患者的不适。《柳叶刀》随后进行的一项大型荟萃分析报告了相同的核心发现：无创针头使用可将 PDPH 降低 50% 以上，而不会增加手术失败率。²⁴鉴于至少一项研究发现早期 PDPH 是持续性穿刺后头痛的危险因素，因此针头的选择可能不仅会影响急性 PDPH 的发生率，还会影响持续性头痛综合征。²⁵

最后，最近的文章强调了脊髓脑脊液漏仍然令人惊讶的临床异质性。“慢性自发性颅内低血压和多发性神经周围囊肿病例中的矛盾性头痛”强调了先前报道的和不完全理解的现象，其中一些脑脊液漏患者报告反向体位性头痛在直立时有所改善，而在平躺时更严重。²⁶周等人。描述了一个病例，其中面肌痉挛是 SIH 的主要表现，而上述穿刺后疱疹病例最初表现为距穿刺很长时间后每天新出现的持续性头痛。^{20, 27}在每种情况下，SIH 都表现出不同于刻板的直立性头痛的能力。

总而言之，SIH 仍然是一种难以被发现的疾病，使临床医生感到羞愧，并且仍然是一个大骗子，但头痛界越来越多地认识到它的伎俩。过去十年来，在脑脊液泄漏知识方面取得的令人难以置信的进步令人鼓舞，我们期待着未来，毫无疑问，新的发现正在等待着我们。