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1.
生理曲度变直与正常的颈椎有限元建模与分析   总被引:1,自引:0,他引:1  
建立生理曲度变直和曲度正常的颈椎全节段有限元模型,进行对比与分析.选取颈椎曲度变直患者采集CT数据,采用专用生物力学有限元软件构建高质量颈椎全节段模型,然后采用基于离散微分属性的体网格变形技术,将变直模型映射生成曲度正常模型,在进行有限元模型的验证后,用相同边界条件进行对比分析.结果表明,曲度变直模型活动度范围比正常范围减少16%~28%,应力增加4%~90%,C3-C4和C4-C5小关节、钩突关节、椎间盘容易出现应力集中,表明容易出现损伤和退化.通过使用新型建模软件和体网格变形技术,能方便构建生理曲度变直和正常模型,分析结果对临床诊断有指导意义.  相似文献   

2.
基于CT图像数据结合图像处理软件建立人体下颈椎C3-C7活动节段的三维有限元模型,并验证模型的有效性。选取一名健康志愿者颈椎CT数据,建立包括椎体、后部结构、终板、椎间盘、韧带和关节突等部分的下颈椎C3-C7三维有限元模型,赋予颈椎组织不同成分的材料属性,模拟人体颈椎在正常生理状态下承受扭矩载荷时,前屈、后伸、侧弯和旋转等运动情况下颈椎椎体、椎间盘和小关节的生物力学特性。颈椎C3-C7活动节段在四种工况下的活动范围与前人离体实验和有限元分析的研究结果基本吻合,颈椎椎体、椎间盘和小关节的应力分布符合其生物力学特性。下颈椎C3-C7活动节段的模拟结果符合人体的真实运动规律,为临床颈椎的生理、病理研究以及植入器械的力学性能分析奠定理论基础。  相似文献   

3.
选取下颈椎C4-C6活动节段的CT图像数据建立三维模型,其中包括颈椎C4-C6节段完整的各节椎体、椎间盘、终板、关节和5种韧带等结构模型。模拟前屈、后伸、左右侧弯、左右轴向旋转6种工况下的生物力学特性,经与离体实验和有限元结果对比分析证明,验证模型的可靠性。相同条件下,模型的关节活动度和应力分布特征与他人研究结果相似。该有限元模型可以分析颈椎生物力学特性,并为下颈椎临床诊断和植入物的力学性能研究奠定良好的基础。  相似文献   

4.
目的 利用Simpleware软件构建全颈椎三维有限元模型,并对模型进行验证和分析,为探讨颈椎损伤机制提供可靠模型。方法 基于CT断层扫描图像,利用医学图像处理软件Simpleware、逆向工程软件Geomagic建立C1~7全颈椎三维实体模型,导入Hypermesh进行颈椎网格划分、添加韧带并引入小关节突接触关系等,建立C1~7全颈椎有限元模型,在ANSYS中模拟前屈、后伸、侧弯和轴向旋转工况下颈椎的生物力学性能。结果 建立的模型准确可靠,在前屈、后伸、侧弯和轴向旋转时,活动范围与文献中离体实验和有限元分析结果相近。椎间盘应力集中在椎体受压侧,C4/5最易产生应力集中。结论 建立的C1~7全颈椎有限元模型能够有效模拟颈椎的生物力学特性,为后续颈椎挥鞭样损伤的生物力学研究奠定良好的基础。  相似文献   

5.
目的 研究以有限元分析为目标的使用Mimics软件三维重建颈椎的方法。 方法 导入CT断层图像到Mimics软件,选取合适的灰度阈值,确定仅含C3~6四个颈椎整体的断层图像,使用单象素编辑擦除工具区分相邻椎骨的间隙,采用三维重建命令建立各个颈椎模型。 结果 C3~6三维模型中椎体和椎体之间的间隙呈现出前后低、中间高的特征,两两相邻椎骨的关节突间隙为一个象素甚至为零,4个颈椎三角片数量为78 300,节点数量为39 133,所获得颈椎C3~6模型边界清晰、关节突间距微小适合进行有限元网格划分和分析。 结论 在Mimics中先包含整体然后区分相邻颈椎边界的方法所建立的颈椎模型其边界清晰且间距微小,适合进行有限元网格划分和分析。  相似文献   

6.
研究上颈椎C0-C3活动节段在不同载荷作用下前屈、后伸、侧屈和旋转时椎体应力、关节活动度(range of motion,ROM)及椎间盘的应力分布情况,探讨载荷改变对上颈椎生物力学特性的影响。基于CT图像数据建立人体上颈椎有限元模型,模型包括皮质骨、松质骨、纤维环、髓核、关节软骨、终板及韧带等结构,根据解剖特征赋予不同部位的材料属性,计算分析上颈椎C0-C3各节段在不同力矩作用下屈伸旋转时颈椎ROM、椎体应力和椎间盘最大应力变化趋势,与前人离体试验和有限元结果进行对比验证。人体上颈椎C0-C3节段在40 N和1.5 N·m载荷作用下,前屈时ROM最小,C0-C1、 C1-C2、C2-C3各节段ROM分别为1.88°、2.16°和1.59°;后伸时ROM大于前屈,最大相差幅度为2.32°;侧屈时ROM大于前屈,增幅分别为2.57°、2.41°和0.49°;轴向旋转时ROM最大,相对于侧屈ROM分别增加了247.64%、282.71%和-43.27%。当施加40 N预载荷和1.0、1.5、2.0、2.5 N·m力矩时,随着力矩等值增大,上颈椎C0-C3节段整体ROM呈非线性增加,变化特征为前屈时最小,旋转时最大;椎间盘最大应力值呈非线性增加(前屈和侧屈)和减少(后伸和旋转),ROM和应力分布趋势和前人研究结果一致。上颈椎三维有限元模型在不同载荷下数值分析的结果符合正常人体颈椎生理活动范围和生物力学特性,为临床颈椎病理和生理的生物力学研究提供理论依据。  相似文献   

7.
本文目的是精确建立复杂性腰椎管狭窄症(LSS)的退变腰椎有限元模型和减压手术模型,与正常模型进行对比与分析。首先,选取复杂性LSS患者采集CT数据,采用专用生物力学软件建立退变腰椎全节段模型,同时构建正常材质模型和减压手术模型,用相同边界条件进行对比分析。结果表明:复杂性LSS腰椎的活动度范围比正常模型要小,而减压模型的活动度变大。在应力方面,退变椎间盘L4-L5和邻近上位椎间盘L3-L4的终板、髓核和维环基质应力分布趋向四周边缘集中,而减压手术模型的应力进一步出现较大增加。仿真显示单纯的减压手术虽然可以减缓神经疼痛,但是很可能进一步造成腰椎稳定性的破坏,加速腰椎退变。  相似文献   

8.
目的 改善目前国内上颈椎有限元模型质量,建立具有详细解剖结构的上颈椎三维非线性六面体网格有限元模型并验证其有效性,以期应用于临床相关生物力学研究.方法 对一名健康成年男性志愿者,采用16排螺旋CT机进行0.5 mm薄层扫描,获得枕骨底C0到C3的体层图像数据并以Dicom格式保存.将数据导入Mimics 10.01软件,进行上颈椎三维几何模型重建,利用ICEM软件对C0~ C3三维重建模型进行六面体网格划分,关节软骨面间隙为0.5 mm,终板厚0.2 mm,关节软骨面定义为滑动接触,摩擦系数设为0.1.再运用Hypermesh V10.0调整网格质量,加载韧带,初步建立上颈椎(C0~ C3)三维六面体单元有限元模型.随后进行材料赋值、边界约束,模拟模型产生前屈、后伸、旋转、侧屈运动,将数据导入有限元软件ABAQUS 6.11进行各椎体三维运动的计算分析.最后将模型的三维活动度(ROM)及各工况下的应力云图与体外实验及其他模型文献数据进行有效性对比验证.结果 建立了具有详细解剖结构的上颈椎三维非线性六面体有限元模型,整个模型共30 550个节点和41 909个单元,模型运动范围及应力分布与文献数据相符合.结论 建立的上颈椎有限元模型具有较高的真实性,可应用于临床相关生物力学研究.  相似文献   

9.
本研究基于计算机断层扫描(CT)图像数据建立并验证正常人颈椎C4~7三维有限元模型,为研究中医手法治疗颈椎慢性疾病的生物力学机制提供模型平台。基于受试者颈部CT图像,依次运用Mimics 17.0、Geomagic12.0及Abaqus 6.13等软件创建正常人C4~7节段有限元模型。在模型上分别模拟前屈、后伸、左右侧弯和左右旋转工况,计算椎体间相对动度(ROM),将计算的结果与文献结果进行对比分析,并观察模型在1Nm载荷下6种工况下模型的主要应力分布情况。本研究成功建立了正常人颈椎C4~7三维有限元模型,共包含591 459单元、121 446节点,模拟了椎体、椎间盘、韧带、关节等几何结构与材料特性。模型在前后屈伸、左右侧弯和左右旋转6种工况下的ROM与实验研究数据基本一致,在1Nm扭矩或弯矩载荷下,模型主要应力分布基本反映了正常人颈椎生理活动时的主要应力分布情况。本研究建立的正常人颈椎C4~7三维有限元模型精确逼真,符合颈椎的生物力学特性,可用于研究中医手法治疗颈椎慢性疾病的生物力学分析。  相似文献   

10.
目的建立颈椎(C4-C6)三维有限元模型,研究钩突切除前后对颈椎稳定性的影响。方法根据健康志愿者的颈椎断层CT扫描序列图像,采用Mimics13.1和Solid Works2012软件进行三维重建和造型,利用ANSYS15.0软件,对颈椎及周围组织赋予不同的材料属性,建立颈椎(C4-C6)三维有限元模型。在建立的模型上加载,模拟脊柱的前屈、后伸、左右侧曲、左右旋转6种工况下的生理活动,获取位移、应力等数值云图,并进行分析验证。在C5节段左侧钩突上分别切除钩突高度的25%、50%和60%,获得不同范围钩突切除时的左侧弯状态下颈椎各部位的位移、应力等数值云图,分析不同范围钩突切除对颈椎稳定性的影响。结果本研究建立了三个椎体运动节段的三维有限元模型,模型高度模拟颈椎结构与材料特性,研究了不同范围钩突切除后,颈椎稳定性受到的影响。钩突切除高度的25%后的左侧弯状态与未切除时对比分析,位移云图变化不大,最大等效应力减小。钩突切除高度的50%、60%后的左侧弯状态下的位移继续增大,最大等效应力逐渐减小。结论切除钩突高度的25%时对颈椎稳定性影响不大,随着切除钩突范围的增加,颈椎的稳定性逐渐降低。  相似文献   

11.

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

  • Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
  • The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
  • To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.
Quadriceps weakness is a common consequence of traumatic knee joint injury1,2 and chronic degenerative knee joint conditions.3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.5 The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,6 biomechanical deficits,7 and possibly reinjury.5 Furthermore, researchers8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,1012 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators15 have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,7 produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,1618 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.5 The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.19 Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.1618 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.20 Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.  相似文献   

12.
13.
即早基因c-fos与脑血管病及学习记忆   总被引:6,自引:1,他引:5  
即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.  相似文献   

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OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.  相似文献   

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