顾建文教授,解放军306医院 颅咽管瘤是发生在颅内鞍上区累及下丘脑的良性肿瘤,手术切除后可达到完全性治愈。但是由于肿瘤多是侵蚀垂体柄、漏斗、灰结节、乳头体和视交叉等下丘脑结构,使手术切除肿瘤困难,术后下丘脑损害合并症如尿崩症、高热和昏迷等,严重影响病人愈后,因之对颅咽管瘤的治疗效果是神经外科水平的标志之一。 颅咽管瘤的发病率北美报告约占人口0.13/10万;占欧洲人颅内肿瘤发病率2.7%~4.9%;国内报道约占颅内肿瘤发病率3.5~5%,其中儿童为5%,成人为3.5%。治疗方法常见的有外放疗、间质内放疗和化疗、手术切除。由于肿瘤呈良性生长,可伴有囊性变和钙化,对放疗和化疗不敏感,不能很好地解除对下丘脑神经结构的压迫,同时也有引起放射性损伤的危险,如早期视力障碍加重、多饮多尿,晚期可有下丘脑功能低下和智力减退等。手术切除由于死亡率高,合并症严重,以往多采取部分切除肿瘤,再结合外放疗来延缓病情的发展。 1990颅咽管瘤是发生在颅内鞍上区累及下丘脑的良性肿瘤,手术切除后可达到完全性治愈。但是由于肿瘤多是侵蚀垂体柄、漏斗、灰结节、乳头体和视交叉等下丘脑结构,使手术切除肿瘤困难,术后下丘脑损害合并症如尿崩症、高热和昏迷等,严重影响病人愈后,因之对颅咽管瘤的治疗效果是神经外科水平的标志之一。 颅咽管瘤的发病率北美报告约年,瑞士Yasargil首先报道肿瘤手术全切除率在90%,术后死亡率16%;1992年,美国Hoffman等人报道肿瘤的手术全切除率在60%,术后死亡率20%;并提示,其疗效与手术方法、肿瘤切除率、术中下丘脑神经结构的保护密切相关。此后人们开始探索积极的肿瘤 全切除术,其理由为:1)全切除可达到完全治愈的效果;2)部分切除肿瘤没有肯定的疗效,并可使手术区解剖结构紊乱和肿瘤与周围结构粘连,使二次手术困难,更难以作到肿瘤全切除;3)目前对大部分肿瘤没有其它好的治疗方法。从文献资料来看,肿瘤全切除的术后死亡率由1990年以前的20%,下降到1995年的10%以下,到2000年报道术后死亡率为5%以下。 下丘脑神经结构和功能的保护是关键;把三脑室前部下丘脑结构分为五个部分;依椐颅咽管瘤的发生部位将其分为下丘脑下型和下丘脑上型。对下丘脑下型的肿瘤,多采取纵裂前入路,对后者手术多采取翼点、额下和经蝶窦入路,利用神经血管间隙切除肿瘤,能从多个方位显露肿瘤,但术中操做使血管神经损伤和血管痉挛的危险性增加。 另外,手术保护下丘脑的显微穿通动脉对维护下丘脑的功能和防止术后并发症如记忆障碍、尿崩症、高热、昏迷和瘫痪十分重要。肿瘤全切除是指,手术显微镜下切除全部肿瘤,术后影像学证实肿瘤消失。目前来看,使肿瘤全切除困难的原因有:1)肿瘤钙化坚硬较大;2)肿瘤与下丘脑结构或穿通动脉粘连;3)肿瘤囊壁薄不能与周围结构分离;4)手术视野限制未能见到残留肿瘤,术后影像检查发现肿瘤未能全切。随访手术后10年内的患者,仍有10%肿瘤复发率。其主要原因:1)全切除仍有肿瘤细胞残留可能;2)手术过程造成肿瘤细胞移位生长;3)肿瘤与第三脑室底无蛛网膜分隔并在下丘脑呈侵润性生长。对于肿瘤复发有占位效应患者,可进行二次手术切除肿瘤。对于远离神经结构的复发实性肿瘤,可采用r-刀或其它立体放射治疗。约50%~80%患者全切除后可发生术后下丘脑和垂体功能障碍并发症。手术早期神经垂体并发症有抗利尿激素(ADH)缺乏引起的尿崩症(DI),患者主要表现为口渴、多饮和多尿;抗利尿激素分泌异常综合征(SIADH),患者除有多饮和多尿外,以低血钠为特征,严重时引起脑水肿,患者出现头痛、恶心、呕吐和抽搐,即脑耗盐综合征(CWS)。还有视上垂体束、视上核和室旁核损伤,患者觅水功能障碍,无口渴感。血钠升高,全身乏力和轻度尿崩症,也称脑盐潴留综合征(CSRS)。腺垂体前叶激素缺乏是颅咽管瘤切除术后需长期治疗的并发症,方法包括发育呆小和迟缓儿童的生长素(GH)的代替治疗;雄性、雌性激素缺乏引起的性发育障碍患者的性腺激素的代替治疗,及其下丘脑功能低下的糖皮质激素代替治疗和甲状腺功能低下的甲状腺素的代替治疗。虽然已有多种人工合成激素代替下丘脑和垂体激素的治疗,但下丘脑和垂体激素的功能并不仅仅是单纯 给予激素代替方法。而是系统的、全面的生理和临床的治疗。从我们术后随访资料来看,青春发育前的患者,下丘脑功能受累不严重,在肿瘤全切除后下丘脑得到良好保护者,患者仍可恢复身体生长和性功能发育。
解放军306医院,顾建文教授 一患者脑袋怕震,怕环境噪声,发现为三叉神经鞘瘤,经过手术切除恢复良好。 三叉神经鞘瘤约占脑瘤的0.2%~1%。可起源于三叉神经的任何节段,但以美克尔(Meckel)囊内为多。属良性肿瘤,生长缓慢。按部位分为颅中窝型、颅后窝型及哑铃型3种。 临床表现主要有三叉神经本身和邻近结构受累的症状和颅内压增高症状。根据肿瘤位置的不同,临床表现如下: 1、颅中窝型:早期多以三叉神经本身受累的症状为主,其表现类似原发性三叉神经痛者约占1/3,为发作性剧痛。三叉神经分布区感觉减退者较多,但有时仅有角膜反射减弱,不可忽略。运动根受累者甚少,或至晚期方始出现。当肿瘤累及邻近结构,特别是肿瘤发展至海绵窦及眶上裂等部位,则出现其它脑神经受累症状,如病侧眼球运动障碍、复视、眼球突出及视力、视野改变等。其中以展神经和动眼神经瘫比较明显,瞳孔常有散大,光反射迟钝。眼球突出约占1/3至1/2,可能系海绵窦受压,影响眼静脉回流,或肿瘤直接经眶上裂突入眶内的结果,眼底静脉常有淤血。若肿瘤向前发展压迫视神经和视交叉时,则有视神经原发性萎缩、视力减退和视野缺损甚至失明。此型颅内压增高症状出现较晚亦较轻。有时肿瘤如鸭蛋大小并无颅内压增高症状。 2、颅后窝型:肿瘤多起源于三叉神经根。运动根受累的症状多较突出,如颞肌及咀嚼肌无力、萎缩等。临床表现为三叉神经痛者极少,但感觉减退可早期出现,且多系第1、2、3支同时受累,也可能仅有角膜感觉减退。肿瘤压迫第7、8对脑神经时,可引起面肌抽搐、周围性面瘫、耳鸣、听力减退,前庭功能亦受累。肿瘤靠近小脑幕者,有第9、10、11对脑神经受损的症状。小脑受压时,多有共济失调。如脑干受压或移位,常出现对侧或同侧锥体束征。一般颅内压增高症状出现较早且较明显。 3、哑铃型:肿瘤跨居中颅窝与后颅窝之间,可由中颅窝向下或由后颅窝向上生长,临床症状兼有上述两型的症状特点。 该例患者术前影像: 该例术后影像
顾建文教授,解放军306医院 Glioblastoma vasculature and vascular mimicry Introduction Glioblastoma (GB) is the most common intracranial malignancy with an annual incidence of approximately 3 – 5 cases per 100,000 individuals. In terms of overall cancer burden GB is uncommon, however, the combination of brain localization, invasiveness, and extremely poor prognosis make it one of the most feared of all cancer diagnosis. Glioblastoma currently has an overall median survival time of 12 – 15 months despite maximally combined therapy of neurosurgery, radiation, and combination thermotherapy. It is interesting to note that the extremely slow development of effective therapy/treatment lies in stark contrast to the rapidly expanding foundation of knowledge regarding the molecular pathogenesis of this disease. The vast majority of research in the field of neuro-oncology has been published in the last 20-30 years, largely driven by a greater understanding of brain tumor genetics. More recent molecular classification has provided the basis for the existence of four distinct types of high-grade primary glioblastoma: classical, mesenchymal, neural, and pro-neural subtypes. These subtypes are differentiated molecularly based upon various proteomic features, signature mutations, methylation features, and currently identified tranional regulators. The comprehensive molecular classification of high-grade gliomas is just now starting to transform current classification, which currently follows the consensus WHO histopathological criteria. Despite sophisticated molecular classification schemes, a relatively high percentage of gliomas remain difficult to reproducibly categorize due to considerable histological overlap. Phenotypically, the tumor displays marked hypercellularity, serpiginous areas of necrosis, and expansive endothelial cell proliferation with tumor vasculature being torturous, disorganized, and highly permeable. Grade IV neoplasms exhibit extremely aggressive proliferation of endothelial cells as compared to Grade II and Grade III tumors. The increased vascular permeability compounds the issue by leading to increased cerebral edema and inflammation. Abnormalities in the endothelial walls, pericyte coverage, and basement membrane also result in loss of structure and function of the critical blood brain barrier. Glioma vasculature formation occurs through at least three distinct processes. 1) Angiogenesis; the process of generating new blood vessels from rerouting and remodeling of pre-existing vessels, 2) Vasculogenesis; classically considered an embryonic process, but has since been identified in tumors as thede novoformation of primitive blood vessels by the differentiation of circulating bone marrow-derived endothelial progenitor cells, and 3) Vascular Mimicry (VM); recently identified to provide a contribution to tumor vasculature by trans-differentiation of glioma cells into tumor-derived endothelial cells (TDECs). Molecular pathways It is said that cancer metastases, regardless of the primary tumor, play by a different set of rules from the primary tumor, and cancer deaths primarily result from invasion and metastases that are resistant to conventional therapies that may otherwise effectively treat the primary tumor. Tumor survival is dependent upon a rich blood supply needed to sustain tumor growth and further metastasis. Malignant gliomas, like other neoplasms, require angiogenesis to establish a source of nutrients/oxygen and to eliminate cellular waste products. The tumor vasculature also creates a localized “niche” microvascular environment within which the tumor-initiating cells may be able to effectively resist therapy. Angiogenesis is a key pathologic event and necessary for the progression of a solitary localized neoplasm to a highly aggressive tumor. This critical tenant subsequently ignited the field of neoplastic angiogenesis research, which has focused on targeting endothelial cells forming the neovasculature of growing tumors and served as the major organizing principle for drug development of various clinical trials. Because GB is one of the most vascular rich tumors and VEGF (vascular endothelial growth factor) is produced by tumor cells, anti-VEGF antibody (bevacizumab/Avastin) has been used in clinical trials. The results of clinical trials are disappointing to say the least, more than half of patients with GB only transiently respond to combination treatment of Avastin andIrinotecan. Mechanisms proposed ot explain resistance to anti-VEGF therapy include 1) Activation of other pro-angiogenic signaling pathways 2) Recruitment of bone marrow (BM)-derived myeloid cells that protect and nurture vascular cells and/or 3) Protection of blood vessels by increased pericyte coverage. In GBs, the antitumor effect of the antiangiogenic therapies is likely due to normalization of vasculature, which also decreases edema. The disappointing results of the angiogenesis inhibitor trials, together with new evidence generated from molecular and animal research on human GB tumor progression, have given insights into the molecular mechanisms underlying the perfusion of tumors, particularly those expressing an aggressiveinvasivephenotypes such as GB. In tumor angiogenesis, bone marrow-derived endothelial cell precursors (ECPs) have historically been known to be the main source of the vascular endothelial cells. However, recently it was shown that BM-derived endothelial precursor cells did not solely contribute to the vascular endothelium, and it is now understood that TDECs in GB transdifferentiated from neuroectoderm and that tumor cells themselves can be involved in tumor angiogenesis. This more recent evidence suggests an alternative mechanism, one whereby tumor microvasculature is derived directly from tumor cells, and this process is called Vascular mimicry (VM). VM describes the functional plasticity of aggressive cancer cells formingde novovascular networks, providing perfusion pathways for expanding tumors, transporting fluid from leaky vessels, and/or connecting to endothelial-lined vasculature. VM evidence suggests that this blood-perfused microvasculature plays a critical role in tumor development and is independent of endothelial cell angiogenesis. Interestingly, VM networks have also been shown to exhibit anticoagulant properties through local expression of anticoagulant molecules with the overall goal to facilitate the flow of blood into and among aggressive tumors. The original study describing VM was based on evidence that showed transport of injected fluorescent dye throughout VM networks. Subsequent experimental evidence has shown real-timein vivophysiologic perfusion of blood between endothelial-lined mouse vasculature and VM networks in human tumor xenografts using Doppler imaging of microbead circulation. This study went on to show that aggressive melanoma cells are capable of de novo three-dimensional vascular structure formation, this finding was subsequently validated by high resolution Electron Microscopy showing the morphological/structural details of the tumor-formed vessels and similarities in ultrastructure between VM and traditional endothelial-lined vasculature. Melanoma studies also showed tumor cells may co-express endothelial, embryonic/stem cell, and tumor cell markers. A really interesting study that describes hypoxia as a catalyst of VM phenotype was demonstrated with the transplanatation of human metastatic melanoma cells into an ischemic mouse limb, which resulted in the formation of a blended vasculature composed of human melanoma and mouse endothelial cells. After blood flow to the limb was sectored, the melanoma cells formed a large tumor, this study demonstrates the amazing influence of the microenvironment on the transendothelial differentiation of melanoma cells, which reverted to a more tumorigenic phenotype as the environmental cues changed. Transdifferentiation of GB stem cells (GSCs) into mural-like (vascular smooth muscle/pericyte-like) tumor cells highlights the plasticity of GSCs. The plasticity of GSCs is further displayed by the multi-potency of neuronal stem cells that are capable of differentiating into several cell lineages (i.e., astrocytes, neurons, and oligodendrocytes); and into a variety of cells such as blood cells, muscle cells, and vascular endothelial cells. Many molecular details underlying VM have been deciphered, but as with any other topic of scientific research, there are still many more questions than answers. However, it is known that critical VM-modulating genes are associated with vascular (VE-cadherin, EphA2, VEGF1) embryonic and /or stem cells (Nodal, Notch4), and hypoxia related (HIF, Twist1) signaling pathways. A few selected common genes and pathways will be discussed briefly in this article. 1)Notch and Nodal signaling pathwaysare tow pathways that have been shown to be critical both for embryonic stem cell regulation and tumor cell behavior; interestingly, crosstalk between these pathways regulates tumor cell behavior, aggressiveness, and VM network formation. Nodal signaling modulates vertebrate embryogenesis functioning in left-right asymmetry determination and stem cell pluripotency; generally absent in adult tissues but is known to become reactivated in aggressive cancer. Noteworthy is the fact that aggressive cancers reactivate Nodal, but not its regulatory protein Lefty, therefore Nodal signaling proceeds unchecked and is able to promote aggressive tumor cell behavior. Notch signaling is important in stem cell differentiation and self-renewal and is expressed in various embryonic and adult tissues. 2) Hypoxia-Inducible-Factor (HIF) complex is a key regulator of oxygen homeostasis in both physiological and pathological environments. HIF can modulate and cross talk with both Notch and Nodal signaling pathways. HIF over-expression in cancer induces the expression of gene products involved in angiogenesis (i.e., VEGF). It is important to note that hypoxia has been shown to induce both Notch and Nodal pathways via HIF1-alpha/2-alpha and HRE signaling. There is significant cross-talk between HIF1-alpha and Notch-signaling, overall working within tumor cells to promote an undifferentiated cellular state. This is how it becomes conceivable that therapeutic usage of antiangiogenic agents may counterintuitively promote tumor plasticity and metastatic/invasive progression. Genetic analysis of individual ECs via microdissection followed by genetic analysis of GB ECs showed that 50-90% of ECs in the GB tumors carry the genetic abnormalities found in the tumor cells themselves, suggesting a common origin. Furthermore, mouse experimentation has revealed that the tumor-derived endothelial cells originated form tumor-initiating cells and did not result from the cell fusion of ECs and tumor cells. Anin vitrodifferentiation assay in the same study suggested that hypoxia was the critically important factor in the differentiation of GB tumor cells to ECs and is independent of VEGF. Tumor derived endothelial cell (TDEC) formation was not only resistant to anti-VEGF receptor inhibitor, but it led to an increase in their frequency. It can be surmised that that TDECs make an important contribution to the resistance of GB to anti-VEGF therapy, and it can therefore also be a potential target for GB therapy. By and large, tumor cell VM nicely illustrates the functional plasticity of the aggressive cancer phenotypes and serves as a selective advantage for rapidly growing tumors in need of perfusion. VM can provide one of several sources for a tumor blood supply that can directly or indirectly interact with other vasculature. The literature is in agreement what the underlying induction of VM seems to be related to hypoxia, which in turn activates a variety of genetic alterations as previously described that then directly promote the transendothelial phenotype of tumor cells capable of VM. Treatment Obstacles As previously mentioned, the detailed and precise deion of the molecular biology of glioblastoma lies in stark contrast to the lack of advances in therapy. With a currently expanding knowledge of molecular biology, more potential targets have been identified and the key will be to develop potent inhibitors and effectively use combinations of them in an appropriate and targeted manner. A major limitation to targeted drug delivery is that migrating primary tumor GB cells blend in with normal tissue, are difficult to identify and target, and do not elicit an angiogenesis response. Additional therapeutic obstacles include 1) No effective agonists/antagonists against identified targets, 2) Therapeutic molecules must pass BBB in order to reach invading cells, including those located at a distance from the central part of tumor. Varying degrees of BBB dysregulation exist within a given GB tumor, by itself, the BBB is known to present a challenge to effective transit of therapeutic molecules to the brain, and continued study of BBB in tumor setting s is needed to lend insight into effective drug delivery in GB, and 3) currently lack ideal animal model for GB treatment studies. Combined antivascular therapy aiming at both mural-like tumor cells and endothelial cells, in addition to cytotoxic drugs targeting tumor cells may hold promise. It seems plausible that the most efficient way to target tumor cell plasticity is to inhibit multiple signaling pathways simultaneously. The molecular pathways that have been experimentally identified as critically involved in VM. The molecular pathways that have been experimentally identified as critically involved in VM, along with failed clinical trial data should serve as a strategic roadmap for drug development with goal being to overcome tumor cell plasticity, drug resistance, neoplastic angiogenesis, invasion and metastasis. The emerging data on embryonic pathways, Notch and Nodal, which are reactivated in aggressive tumor cells, may provide valuable therapeutic targets that exploit the convergence of embryonic and tumorigenic signaling. Suppression of these pathways results in the inhibition of VM, tumorigenicity, and the reversion of the stem cell-like phenotype to that of a differentiated cell type. Simultaneous targeting of the Notch and VEGF pathways may perhaps provide a more viable combination approach to target cancer stem cells with anti-VEGF therapy. Conclusion and Future Work Several centuries of research have shown the high degree of plasticity associated with aggressive neoplasms. With the recent addition of sophisticated molecular tools, the exact mechanisms, etiology, and implications of tumor cell pathobiology have been further elucidated. During this time, research has demonstrated that the presence of a small population of GSCs is closely associated with resistance to radiotherapy and anti-angiogenic therapy. However, clinical treatment using an anti-VEGF therapy alone has routinely failed to significantly affect patient survival and clinical outcomes. It is logical to speculate that as part of its ability to survive in the presence of anti-angiogenic agents and reemerge from dormant primary tumors, GSCs may undergo an alternative vascularization that develops mural-like cell-associated networks and nourishes the bulk of the growing tumor cells. From the literature within the field of neoplastic angiogenesis, it is now appreciated that the tumor vasculature is highly complex and can be derived from a variety of sources, including angiogenic vessels, cooption of preexisting vessels, mosaic vessels lined by both tumor cells and endothelium, and postnatal vasculogenesis. Furthermore, recent studies have shown the tumor origin of endothelial-like cells, vascular mimicry, in specific cancers, further complicating the strategies for targeting a genetically unstable and heterogeneous vasculature. The commitment to genomic characterization of GB has fueled substantial progress in understanding of this cancer, particularly within the past 5-10 years. Extensive genomic characterization has provided a high-resolution image of the various molecular alterations underlying GB, and suggests that indeed this disease represents several histologically similar, yet molecularly heterogeneous diseases. The heterogeneous nature of this neoplasm, both within and across tumors, underscores the difficulty in developing efficacious treatment and provides a challenge both to annotate tumors and to stratify patients for trials and treatment. Despite tremendous progress in understanding of the genetic basis of glioblastoma, targeted therapeutic approaches based on known genomic alterations have yet to be proven efficacious. The morphological heterogeneity that prompted the original deion of high-grade glioma as, “multiforme”, has indeed extended to the molecular level. It is likely that intratumoral heterogeneity and target cooperativity conspire to create a multiple dependency state whereby single-target inhibitors are not sufficient to significantly attenuate tumor growth. There is also an incomplete understanding of the functional consequences of many of the mutated genes in GB. Research is just now beginning to understand how this molecular heterogeneity is manifested and what exactly the functional consequences of these genetic alterations are. It is also not clear if these intermingled cell populations with unique genomic alterations behave as independent tumors or are interdependent with each other. In addition to understanding the molecular basis of GB heterogeneity, it will also be important to consider the contributions and phenotypes of the diverse non-tumor cell types, like stromal and inflammatory cells that also populate the glioma microenvironment. Further work is indeed necessary to fully understand GB biology and will require integrated studies, including genomic, animal models of disease, and as always a careful study of human tissue.
顾建文教授,手术经验,解放军306医院 枕大孔腹侧肿瘤的外科治疗要求对手术入路的暴露、术中椎动脉及神经根的处理很严格。临床多常见与脑膜瘤。表现多以颈项部不适起病,渐出现声嘶、音调低沉、吞咽困难、呛咳,胸部束带感,四肢无力。体检发现:咽反射减退或消失,发音障碍,悬雍垂偏移,胸锁乳突肌、斜方肌无力,伸舌偏移,单肢或四肢肌力减退,肩带肌及上肢肌萎缩,T2-5平面以下浅感觉减退。经MRI检查并确立诊断。 术前显示肿瘤位于颅底脑干前方 切除的肿瘤 术后复查肿瘤消失 手术方法 患者侧卧位,头部略前旋。取耳后“C”型切口,起于耳廓上缘后方,弧形延向后下,再转向前下,止于胸锁乳突肌中点上方。皮肤切开,将斜方肌、头夹肌、颈夹肌、肩胛提肌自枕骨离断、翻向前下方,显露头后大直肌、下斜肌和上斜肌围成的枕下三角。在此三角内可扪及下方走行的椎动脉。从枕骨上切断头后大直肌的附着点,将其游离、翻向后下;在C1横突上离断下斜肌附着点,将其游离、翻向后下;离断上斜肌在枕骨的附着点,翻向前下。此时可见从C1横突孔穿出的椎动脉,被静脉丛包绕并向后走行于椎动脉沟内约2cm,折向内、穿过硬脑膜入颅。骨膜下沿椎动脉沟将椎动脉推开,游离并咬除C1半侧后弓,咬除枕骨鳞部,打开枕大孔。切开寰枕关节囊,咬除、磨除C1外侧块及枕骨髁后部约1cm。如肿瘤主体达桥脑水平,还应切除部分乳突,显露乙状窦及其前部。“Y”剪开并悬吊硬脑膜,将硬脊膜连同椎动脉一起向前方牵开,充分暴露枕大孔区肿瘤。锐性切开肿瘤和神经表面的蛛网膜,可见CN及C1神经根常常走行于肿瘤的外表面。用神经剥离子游离神经后,铲除肿瘤附着于硬脑膜上的基底,离断血供后,分块或整块切除肿瘤。 既往枕大孔区病变的手术常用一侧枕下乙状窦后入路及颈椎后入路,此入路对于显露枕大孔腹侧具有较大的局限性,特别当病变为脑膜瘤、位于枕大孔腹侧并向双外侧生长时,上述两种入路难以充分暴露病变,而且同侧颈神经、Ⅸ、Ⅹ、Ⅺ、Ⅻ颅神经及椎A颅内段大多位于肿瘤的表面且面对术者,手术不仅难以首先铲除肿瘤基底、离断血供,出血多而且容易造成上述神经、血管的损伤。采用远外侧入路暴露后,术者可从下脑干外侧呈切线直视枕大孔腹侧及对侧区域,病变暴露充分,可以比枕下乙状窦后入路缩短手术路径约2~3Cm,至少增加视角15~20o,术野明显扩大。椎A颅内段及同侧颈神经、Ⅸ、Ⅹ、Ⅺ、Ⅻ颅神经基本可以直视,可以直视下直接铲除肿瘤基底,从而离断肿瘤血供,便于肿瘤手术切除,同时避免和减少神经、血管损伤,即使出现损伤亦有条件术中行吻合或修复。采用远外侧入路行肿瘤切除,除走行肿瘤表面的副神经因影响手术操作被牺牲外,无其他医源性神经损伤,患者手术疗效好,术前症状均明显改善或消失。 远外侧入路通过磨除枕骨髁和外侧块的方法,可以扩大术野、增加暴露。特别是肿瘤较大并长至对侧时,此入路的优点可以充分体现。枕骨髁长度约为30+/-4毫米,每磨除枕骨髁1毫米,可以向腹侧扩大视角大约2.4o,磨除枕骨髁1/3,可增大视角15.9o,磨除1/2可增大19.9o。当肿瘤前后径比较大、脑干被向后推压明显时,术野可操作空间较大,枕骨髁磨除范围可以相对减小,反之磨除范围应相对扩大。磨除前先打开寰枕关节囊,可先将枕骨髁内部磨空,然后再用咬骨钳将皮质部分切除,操作需谨慎细致,避免误伤,磨除过程常常会碰到髁后静脉出血,可以采用明胶海绵填塞或骨腊封闭处理之。由于磨除枕骨髁和C1外侧块破坏了寰枕关节,影响颅枕交界区稳定性,所以既要考虑磨除,增加肿瘤的暴露,又要慎重,以免导致稳定性问题。当磨除枕骨髁超过1/2时,需行植骨、固定。本组病例磨除范围均在1cm以内,未超过枕骨髁长度的1/2,我们认为已经能够较好地暴露肿瘤,满足手术需要,所有病人均未植骨,术后病人恢复良好,未出现稳定性问题。 手术过程中椎动脉的处理至关重要。椎动脉出横突孔到穿入硬膜的平均距离 22+/-3毫米,椎动脉穿过硬膜到发出小脑后下动脉分支的平均距离17+/-8毫米,显露此段椎动脉须尽量减少损伤。暴露、游离颅外段椎动脉时,首先要识别由头后大直肌、上斜肌、下斜肌构成的枕下三角,椎动脉在此三角下方走行,可通过扪诊的方法辨清其方向,注意避免使用电刀直接损伤。分离位于椎动脉沟内部分时,应自后向前在骨膜下进行,将骨膜和椎动脉一并向内上推开即可。椎动脉的颅外段常常被静脉丛包绕,显露时过程中常会引起比较麻烦的静脉丛出血,可用明胶海绵压迫和双极电凝止血。除非必须,亦可将椎动脉连同静脉丛一起分离,不必打开静脉丛从而减少手术出血;椎动脉颅内段的识别与处理非常重要,当肿瘤较小时,常可以看到椎动脉被脑膜瘤推向后外侧,然后向内上走行。可以循椎动脉走行,锐性分离肿瘤与椎动脉之间的蛛网膜,游离椎动脉。当肿瘤较大、向后外生长并将椎动脉包绕时,可以通过椎动脉从硬膜外穿入硬脑膜的部位推断其进入硬膜下起始处,然后分别从起始处的头端和尾端铲除基底,当接近椎动脉时,可以循椎动脉的大致走行在其背侧锐性切开肿瘤,首先显露并游离椎动脉背侧,然后分别自头端和尾端绕过椎动脉、铲除其腹侧的肿瘤,游离椎动脉腹侧部分。在到达对侧时,需谨防伤及对侧椎动脉。在涉及椎动脉的操作过程中,须仔细、慎重,如有破裂不要惊慌,即刻行妥善修复。 脑膜瘤多为膨胀、压迫性生长,与周围的神经根、延髓、颈髓边界清楚。即使因为长期压迫,局部出现粘连,只要严格循蛛网膜界面操作,多能将肿瘤与神经组织分离。本组病例在切除肿瘤前,先锐性剪开肿瘤表面的蛛网膜,将肿瘤表面的神经根游离、向内侧牵开,副神经脊髓支或C1神经的感觉根经上述操作仍明显影响手术者,可考虑切断。如后组颅神经在穿出硬脑膜处被肿瘤包绕或向后方推压,可采用分别从头端和尾端切除肿瘤,然后“掏空”神经腹侧肿瘤的方法,从而达到保护神经的目的。肿瘤与脑干或颈髓界面的分离,应在颅内压较低的状态下进行。如肿瘤较大,可采用术前行腰穿、术中放液的方法,分块或瘤内切除肿瘤,肿瘤“囊内压”降低后,将瘤皮牵向外侧就能显露肿瘤与脑干、颈髓的蛛网膜界面,锐性切开,便可顺利游离、切除肿瘤,同时保护脑干、颈髓完好。 手术结束时须严密缝合硬脑膜。如难以缝合,可应用自体筋膜或生物膜修补,并用生物胶涂敷,减少脑脊液漏出。因本入路切开/断肌肉组织较多,如硬脑膜缝合不够严密,局部积液,容易引起感染,需慎重对待。
顾建文教授,综述,解放军306医院近年来受激拉曼散射显微成像的技术成为热点。被称为受激拉曼散射显微成像的技术帮助外科医生在手术过程中更好的区分患者脑内的癌组织和正常组织,这可能会提高该类手术的安全性和
作者,顾建文教授,解放军第306医院 一、鞍隔脑膜瘤的影像学诊断意义 目前, 临床及影像学仍将起源于鞍结节、鞍隔、蝶骨平台, 解剖范围直径不超过3 cm以内的脑膜瘤统称为鞍上脑膜瘤。鞍隔脑膜瘤是指自鞍隔脑膜的蛛网膜颗粒生长的脑膜瘤, 较为罕见, 国内仅见25例报道。以往影像学缺乏对鞍隔脑膜瘤的认识, 容易误诊为垂体瘤者, 神经外科多采用经口、鼻、蝶窦入路鞍底行鞍内肿瘤切除术。 由于鞍隔脑膜瘤位于垂体腺上方, 经此入路手术,切除肿瘤难度大, 时常不可避免地损伤垂体腺, 较难全部切除肿瘤, 容易残留肿瘤组织, 术后易复发,术中损伤垂体严重, 可出现或加重视力障碍、失明、内分泌功能失调等并发症。CT、MRI可清楚显示颅内解剖结构, 准确提供病变部位及侵及范围、毗邻关系等资料。既往将鞍隔脑膜瘤笼统地称为鞍上或鞍结节脑膜瘤显然不妥。因此, 影像学应采用鞍隔脑膜瘤诊断名称,对神经外科提高鞍隔脑膜瘤手术治愈率以及其降低手术并发症均具有十分重要的意义。 典型鞍隔脑膜瘤影像 不典型鞍隔脑膜瘤影像 二、鞍隔脑膜瘤CT及MRI诊断 鞍隔脑膜瘤术前CT表现为肿瘤向鞍内生长压迫垂体腺或肿瘤向鞍上、鞍旁生长,CT较难分辨肿瘤与垂体腺等解剖结构,易误诊为垂体瘤等肿瘤。MRI检查鞍隔脑膜瘤向鞍上、鞍内生长压迫垂体腺使之变扁,肿瘤信号酷似垂体瘤等肿瘤,也易误诊为垂体瘤。 有以下表现者应考虑脑膜瘤:CT上表现为鞍上圆形、类圆形均匀或略均匀的稍高密度或等密度影,亦可伴有钙化, 增强明显; MRI在冠状面或矢状面上表现为正常垂体腺之上的圆形或类圆形影,T1WI上呈较均匀等信号,增强明显, 边缘清楚, T2WI上呈略均匀高信号区;临床上结合病人视力障碍及头痛表现,无内分泌紊乱,以及生长激素和泌乳素正常等资料。MRI在冠状面或矢状面上显示正常垂体腺呈均匀类圆形信号,与脑干相仿, 可见垂体柄, 垂体后部呈点状脂肪信号为特征性表现。 由于垂体腺在肿瘤下方, 二者境界较清楚,容易鉴别, 故MRI对诊断鞍隔脑膜瘤有其独道之处。CT 诊断价值不如MRI, 而且CT很难分辨出鞍隔脑膜瘤与垂体腺, 但CT 在显示脑膜瘤伴钙化时比MRI优越。 鞍隔脑膜瘤主要应与垂体腺瘤、颅咽管瘤相鉴别。(1)垂体腺瘤:CT表现为由鞍内向鞍上及鞍旁生长的类圆形、哑铃形肿块,呈均匀或略均匀等密度或稍高密度影,增强明显;MRI T1WI呈等信号或混杂信号, T2WI呈混杂信号或不均匀高信号。由于垂体腺瘤常伴有组织坏死及囊性变, 显示长T1、长T2信号, 结合蝶鞍 X线平片,如蝶鞍扩大、鞍底下陷, 前后床突上翘及骨质变尖细等,临床上病人有内分泌紊乱等表现, 对垂体腺瘤诊断不难。(2)颅咽管瘤 :CT表现为鞍上或突入第 3脑室的圆形、类圆形的囊性低密度区伴囊壁蛋壳样钙化, 诊断不难。但对等密度或高密度颅咽管瘤, 单凭CT较难与鞍隔脑膜瘤鉴别 ,应配合MRI检查。由于颅咽管瘤的瘤内容物含胆固醇角化物、蛋白、正铁血红蛋白、钙化等, 故T1WI上呈混杂信号 (低信号与高信号混杂), 或不均匀低信号; T2WI上呈不均匀高信号或混杂信号;结合病人有内分泌紊乱等表现, 对大多数颅咽管瘤诊断不难。
术者:顾建文教授,解放军306医院 附:一例巨大恶性脑膜瘤切除手术,患者70岁,头痛很久没有在医院检查,直到晚期。手术很顺利,肿瘤侵犯颅骨,顺利切除肿瘤。(手术完成时间2006年8月 ,术者, 顾建
作者,顾建文教授,解放军第306医院 脑积水是因颅内疾病引起的脑脊液分泌过多或(和)循环、吸收障碍而致颅内脑脊液存量增加。临床小儿多见头颅增大、囟门扩大、紧张饱满、颅缝开裂愈期不合、落日目、呕吐、抽搐、语言及运动障碍,智力低下;成人多见间断性头痛、头胀、头沉、头晕、耳鸣耳堵、视力下降、四肢无力等。 理论上讲脑积水(hydrocephalus)是脑室和脑池(蛛网膜下腔)内脑脊液总量增多,颅内压力增高,继而引起脑室扩张及脑池、脑沟、脑裂等处的蛛网膜下腔增宽。儿童由于颅缝尚未闭合,脑积水必然会引起头围增加。 (一)分类 脑积水根据发病机制不同分为:①非交通性或梗阻性脑积水,脑室内液体因梗阻不能进入蛛网膜下腔。②交通性脑积水是发生在蛛网膜下腔即脑室外的梗阻或回流障碍,也包括蛛网膜颗粒吸收回流脑脊液障碍。③分泌亢进性脑积水,原因是脑脊液分泌过多,这种类型相当少,是否应看作一种单独的类型,尚有不同的看法。病因是各种各样的:梗阻性脑积水的原因常是先天畸形如导水管狭窄,小脑扁桃体疝(Arnold-Chiari畸形),第四脑室囊肿(Dandy-Woalker综合征)和其它脊椎闭合不全,但也可继发于其它占位性囊肿和肿瘤。胎儿子宫内的感染如弓形体、风疹、巨细胞病毒等感染以及围产期颅内出血也能引起脑积水。交通性脑积水的病因是脑膜炎引起的粘连或外伤性蛛网膜下腔和硬膜下出血。分泌亢进引起的脑积水发生于脉络丛乳头状瘤。 (二)临床症状 头颅异常增大,增长迅速。前囟宽大。额骨前突,前颅凹颅底向下移位。眼球向下倾斜(落日征),患儿精神及体格发育迟缓,肌肉痉挛,偶有抽搐。 (三)CT表现 1.梗阻性脑积水正常第三脑室横径6mm,第四脑室前后径15mm;两侧室最大横径与同一水平颅腔横径之比小于22%~32%(evans指数),脑积水时大于40%,脑室明显扩张,变为圆钝。借助脑室扩张的分布类型确定阻塞部位。单侧或双侧室间孔梗阻导致单侧或双侧侧脑室扩张,而三、四脑室正常。导水管狭窄是先天性脑积水最常见的原因,表现双侧脑室及三脑室扩张,而四脑室正常,偶尔或导水管近端也扩张。四脑室中孔和侧孔(Magendie and Luschka)阻塞,引起所有脑室(包括四脑室)扩张。 2.交通性脑积水CT显示脑室呈球形扩张,程度较轻,第四脑室扩张程度最小。基底池往往扩张,两侧半球也能见到因为脑脊液蓄积引起的脑沟增宽。交通性脑积水有时难以与脑萎缩鉴别。鉴别困难的病例可以在短期后随访复查以除外进行性(亦即活动性)脑积水。 3.活动性(active)脑积水脑室体积进行性增加与所谓静止性(static)或代偿性脑积水不同。活动性脑积水临床症状显著,CT随访检查有进展。较早的CT片上有下列表现:①脑室周围密度减低晕:脑脊液经长期压迫损伤的室管膜进入周围实质,在脑室周围形成带状密度减低区,尤以额角和颞角显著,脑室轮廓由于水肿而变得模糊。②枕角扩张显著,原因是脑白质比较脑神经核团更易受水肿的损害,额角、侧室体部近基底神经节而枕角周围是白质,故枕角扩张显著。另一些作者认为枕部头颅骨生长较快。 4.经治疗的脑积水置入导管可引流侧室脑脊液至右心或腹膜腔。CT可以显示导管尖的位置,但正确的位置并不一定指示正常的功能。如引流好,脑室体积明显减小,数日或数月后脑结构也逐渐恢复正常。这种脑组织体积迅速增加可能是由于引流后原先被压迫伸长的神经纤维重新排列的缘故。引流后往往后遗脑萎缩,脑池、脑沟增宽。CT还可显示由引流引起的合并症:①单侧或双侧硬膜下水瘤:偶尔见于外科引流术后,CT显示贴近颅骨的镰刀状或带状脑脊液密度病变。②硬膜下血肿:如硬膜下水瘤体积过大,导致静脉过度牵引以至撕裂,产生硬膜下血肿。CT显示硬膜下高密度镰刀形血肿影像或血肿下沉在水瘤的底部。③脑内血肿是导管引流术较少引起的伤害血管的合并症。有时能见到沿导管平行分布的出血影像,侧室内也可有出血。④脑室萎缩:常常是由于强有力的引流,引起脑室迅速变小以致脑室壁相互接近,CT上的脑室呈缝隙样。很少的情况下,此种萎缩还可合并脑室炎症、粘连及室管膜下纤维化,由于脑室不扩张,如发生引流障碍则很难诊断。即所谓裂隙脑室综合征(slit-ventricle syndrome),颅内压增加,但脑室狭窄,裂隙状,此时诊断引流不充分主要是根据临床症状而不是CT表现。⑤引流管阻塞,随后CT表现脑室容积增加,脑室周围密度减低,脑室增大不成比例,常常枕角扩张更显著,但若脑室粘连闭塞则例外。⑥脑室限局扩张(Dilatation of isolated sections of a ventricle):导水管狭窄,四室中孔或侧孔闭塞,尽管幕上引流功能正常,但四室仍然扩张,假如其余的脑室相互之间不是自由相通的话,某个部位也可能限局性扩张。在这些情况下就需要同时做几处的引流,治疗脑积水。⑦脑室炎:室管膜和室管膜周围充血,CT显示沿室管壁有明显增强。慢性脑室炎,胶质增生可引起脑室边缘轻度密度增高,即使未用造影剂时也是如此。 (四)MRI特点 除表现脑室扩大外,在梗阻性脑积水,脑脊液可经室管膜渗入脑室周围,脑室周围间质性水肿,在质子密度加权像上表现为脑室周围有一圈高信号,很有特点。 正常压力脑积水,MRI可以显示导水管有流空现象,邻近的第三和第四脑室也可见到流空现象,而没有显著的脑脊液流空被认为是弥漫性脑萎缩的表现(Bradllty,1986,1991),如合并有其它交通性脑积水的MR征象时,有显著的脑脊液信号流空征象则适合作脑室引流手术。 (五)外部性脑积水(external hydrocephalus) 这种患儿也表现头围逐渐缓慢增大,颅缝分离,但不表现脑室扩大,而是基底池、侧裂、纵裂池以及大脑皮质脑沟增宽。有人认为这可能是交通性脑积水的早期阶段,因为有报告这类患者日后发生脑室扩大,需要引流治疗。但也有人认为外部性脑积水是一种良性的、自限的蛛网膜下腔扩大,引流治疗可能会减慢头围的增长,但对临床症状是否有改善也缺乏证据。 值得指出的是1~2岁的婴幼儿、脑发育与颅骨生长的比较,相对缓慢,因而脑沟、裂、池相对较宽。脑表面蛛网膜下腔可以宽达4mm,纵裂池6mm,侧裂池10mm,都属于正常范围。18个月~2岁以后,脑发育加快,脑沟变窄。因此2岁以前不能单凭蛛网膜下腔稍宽,就轻率诊断为脑萎缩或外部性脑积水。必须参照头颅大小以及是否有进行性头围增大两个条件。只有在头围明显增大,头生长加快时才能诊断脑积水(图)。 (六)脑积水和脑萎缩的鉴别 脑实质破坏萎缩也可以引起脑室扩大(中央性萎缩)或脑沟增宽,蛛网膜下腔、脑裂、脑池增大(周围性萎缩),或二者兼而有之(弥漫性萎缩)。在影像上与脑积水相似。 脑积水为颅腔内脑脊液增多,原因是脑脊液动力学异常,引起颅内压力增高。当婴幼儿颅缝尚未闭合时,必然会引起头颅扩大,头围增加。而脑萎缩,脑生长缓慢,其结果是小头畸形(microcephaly),脑萎缩虽然也引起脑沟增宽、脑室扩大,其原因是脑体积减少。因此比较脑与头颅骨的大小有助于诊断脑萎缩。但是如果颅骨也生长缓慢,脑与颅骨没有明显差别,则认识脑萎缩比较困难。所以诊断脑积水必须同时具备脑室扩大,脑沟增宽和头围进行性增大两个条件。而诊断脑萎缩必须确实有脑组织减少的证据,即脑沟、脑室增大伴有头颅外形减小(小头)。不过,也有少数患者脑萎缩与脑积水合并存在,这时单凭影像学,诊断就很困难了。 治疗 1.非手术治疗 适用于早期或病情较轻,发展缓慢者,其方法:①应用利尿剂或脱水剂,如乙酰唑胺、双氢克尿塞、速尿、甘露醇等。②经前囱或腰椎反复穿刺放液。 2.手术疗法 对于重度脑积水,智能低下已失明、瘫痪,且脑实质明显萎缩,大脑皮质厚度小于1cm者,均不适宜手术。手术治疗对进行性脑积水,头颅明显增大,且大脑皮质厚度超过1cm者,可采取手术治疗。 (1)减少脑脊液分泌的手术 脉络丛切除术后灼烧术,现已少用。 (2)解除脑室梗阻病因手术 如大脑导水管形成术或扩张术,正中孔切开术及颅内占位病变摘除术等。 (3)脑脊液分流术 手术目的是建立脑脊液循环通路,解除脑脊液的积蓄,兼用于交通性或非交通性脑积水。常用的分流术有侧脑室-小脑延髓池分流术,第三脑室造瘘术,侧脑室-腹腔、上矢状窦、心房、颈外静脉等分流术等。 3.微创分流术 目前治疗脑积水最普及的疗法是脑室-腹腔分流术,也称微创分流术,并被认为是比较有效的治疗手段之一。微创分流术把微创外科新技术应用到脑室-腹腔分流术中,具有创伤小、对腹腔干扰少,减少腹腔粘连甚至能够松解轻微腹腔粘连,术后瘢痕不明显且隐蔽,疼痛轻、恢复快等诸多优点。术后意识不清、胡言乱语等症状全部消失,生活质量可得到极大改善和提高。
顾建文教授,解放军第306医院 (中国专利:CN2489732,2002-05-08.)垂体腺瘤扫描片均应达到能观察A正侧位蝶窦的大小、壁厚、气化程度,B蝶窦中隔的数量、位置,C蝶鞍的大小、鞍底是否侵蚀、前床突及鞍背的移位程度,D肿瘤与蝶鞍的关系,E鼻中隔是否偏移、前鼻棘清晰、犁状骨规则。 定位方法:眉弓中点、鼻棘-鞍、鼻棘夹角定位法:术前在CT中线矢状位断层扫描片上测量鞍底中点(A)与前鼻棘(B)连线长度和眉弓中点(C)与前鼻棘的夹角,该长度为5~8cm,平均为6.8cm,夹角为56°~64°,平均为60°,术中依据A-B-C夹角及长度剪裁好相应的胶片,即可引导手术入路的角度和深度。 解剖学标志定位法:鼻中隔及犁状骨确定中线结构:术前根据冠状位CT,确定鼻中隔及犁状骨居中情况,严格沿鼻中隔分离鼻粘膜至犁状骨,可保证入路不偏移中线。蝶窦开口与犁状骨体为蝶窦前壁的标志:蝶窦开口一般为蝶窦前壁的上限,犁状骨体部为气化的蝶窦,当手术分离至犁状骨时,上述标志可准确引导切开蝶窦前壁。蝶窦中隔为进一步矫正鞍底中点的重要标志:蝶窦中隔数量及位置不一,提前测量中隔偏移距离,可提示鞍底的中点的准确位置。鞍底的形态提供鞍底中点的标志:鞍底一般在蝶窦腔内呈弓状隆起,其最高点为鞍底的中点。其上往往附着有蝶窦中隔骨质突起,对定位有进一步指导作用。鞍区的骨质破坏提供定位标志:术前仔细研究鞍区受破坏的颅底CT、X线片,将破损区与鞍底的关系测量清楚,术中暴露破损区域时即可找出相应鞍底的位置。 经唇下-鼻中隔-蝶窦入路是经蝶入路鞍区肿瘤切除术的最常用的类型。自1907年始,Cushing采用该术式效果不佳,死亡率高,照明器械不佳及抗生素缺乏,并且对鞍隔上肿瘤暴露不足。故一度停滞发展。后来随着电视X线透视机、显微镜的应用,解决了手术中一些精细操作的问题,使该项手术又呈现了新的生命。但至今为止X线侧位片及电视X光机仍为定位入路所必需的方法,能否直接定位,我们进行了一定的尝试。我们根据Guiot等人对肿瘤对鞍底破坏方式所作的分级,严格选择适应症1-4级及O,A,E级肿瘤122例,行经唇下-鼻中隔-蝶窦入路显微切除术,手术采用我们自行归纳总结的非X线综合定位法,使得手术时间较X线定位法时间明显缩短。应用A-B-C夹角测量鞍底的位置及深度的方法,因A-B,B-C连线长度均为6~8cm,实际测量两线的夹角较为准确,但手术中铺盖无菌单及Cushing氏牵开器的阻挡,妨碍实际的测量,需估测B-C线,有一定的误差。将解剖学标志定位法结合起来,包括手术入路所经途中的一系列标志(鼻中隔定位中线结构、蝶窦开口及犁状骨体提示蝶窦前壁的位置、鞍底的形态及破坏程度和蝶窦中隔的位置可决定鞍底的位置)结合起来综合判断,则能够达到准确判定鞍底位置的目的。总结该方法的经验,要求我们充分利用影像学的资料,仔细分析可能与定位有关的一切信息,在手术过程中加以利用即可得到良好的效果。同时避免选择蝶窦气化不良及蝶窦过大病例。该方法经临床验证,有一定的使用价值。
玄璿,解放军306医院神经内科 绝大多数人在一生中都会有头痛的经历。可你是否知道,有一种头痛是致命的。 56岁的王女士在与丈夫吵了一架后,突然出现剧烈头痛,颈部强直并伴有恶心、呕吐,持续不缓解,后由家人送至解放军306医院。急诊CT检查发现患者为蛛网膜下腔出血(见下图)。神经内科的专家们立即行无创头颈部动脉CTA检查,发现患者前交通动脉动脉瘤,原来,蛛网膜下腔出血的祸根是动脉瘤破裂。全脑血管造影及前交通动脉瘤栓塞手术挽救了王女士的生命。因此脖子硬的头痛是致命的。 颅脑CT检查提示蛛网膜下腔出血 全脑血管造影检查提示前交通动脉动脉瘤(箭头所示) 前交通动脉动脉瘤栓塞术后(箭头所示) 在306医院神经内科蔡艺灵副院长及其团队的积极抢救治疗下,患者被从死亡线上拉了回来,病情得到了控制。住院治疗20天后,患者头痛症状完全消失,未遗留任何神经系统后遗症,顺利出院。 解放军306医院神经内科介入团队在积极进行术前准备 蔡艺灵副院长及其团队在全力救治患者 蛛网膜下腔出血相关知识 蛛网膜下腔出血分为原发性和继发性。原发性蛛网膜下腔出血是指脑底部或脑表面血管破裂后,血液流入蛛网膜下腔引起相应临床症状的一种脑卒中。在脑血管意外中,其仅次于脑血栓和高血压脑出血,位居第三。颅内动脉瘤是导致蛛网膜下腔出血的最常见病因,约占50%~85%。颅内动脉瘤一般病程较为隐匿,但起病突然,一旦发病,致死及致残率极高,因而被称为颅内的“不定时炸弹”,是最危险的脑血管病之一。颅内动脉瘤是威胁人类生命和健康的最常见的重大疾病。 究竟怎样会引起动脉瘤,并导致动脉瘤破裂出血呢? 颅内动脉瘤可能由动脉壁先天性肌层缺陷或后天获得性内弹力层变性或二者的联合作用所致。动脉瘤的发生存在一定程度的遗传倾向和家族聚集性,如在有动脉粥样硬化、动脉瘤家族史及多囊肾患者中,动脉瘤患病率增高。但颅内动脉瘤不完全是先天性遗传,相当一部分是在后天长期生活中发展起来的。随着年龄增长,动脉壁弹性逐渐减弱,薄弱的管壁在血流冲击等因素影响下向外突出形成囊状动脉瘤。病变血管可自发破裂,或因血压突然增高或其他不明显的诱因而导致血管破裂,血液进入蛛网膜下腔,通过围绕在脑和脊髓周围的脑脊液迅速播散,刺激脑膜,引起头痛,颈部强直。长期吸烟、未得到控制的高血压、过量饮酒,都是导致颅内动脉瘤破裂出血的主要危险因素。因此,平时对危险因素加以控制,才有可能在一定程度上降低动脉瘤的发生。也可以通过脑血管造影的影像学手段,来及早发现未破裂动脉瘤的存在,以便能在动脉瘤破裂出血之前给予恰当的治疗。