腰椎下关节突的形态观测及其临床意义

通过对１００例成人Ｌ１～Ｌ５下关节突的基部宽,双侧下部外缘间距,长度及下关节突与椎弓根夹角的测量,对腰椎下关节突做了解剖学分型,并对其临床意义进行了讨论。为教学及临床应用提供详实的解剖学依据。     

腰椎弓根延长术截骨部位与神经根关系的解剖学研究

目的　观察腰椎弓根延长术截骨部位与其毗邻神经根的解剖关系,为腰椎弓根延长术离断椎弓根提供解剖数据。  方法　16例成人防腐脊柱标本, 自T12~S1去除软组织、棘突、椎板、关节突关节、横突, 充分暴露硬膜囊、神经根和腰椎弓根, 精细磨削椎弓根至椎弓根-椎体连接处,测量该部位椎弓根上缘至上位神经根下缘的间距(PSRD),椎弓根下缘至下位神经根上缘的间距(PIRD),椎弓根内缘至硬膜囊外缘或内侧神经根外缘的间距(PMRD),椎弓根外缘至外位神经根内缘的间距(PLRD),所有解剖参数都做双侧测量。  结果　腰椎弓根至上、下、内、外神经根的间距范围分别是4.9~8.6 mm,1.0~2.5 mm,0~1.6 mm,0.7~11.5 mm,左、右两侧数据无显著性差异(P>0.05),男、女之间数据无显著性差异(P>0.05)。  结论　腰椎弓根截骨延长时,截骨部位的内缘和下缘毗邻的神经根相对于上缘和外缘损伤可能性大,透视下对椎弓根内缘和下缘截骨时要十分小心。     

寰椎椎弓根解剖和CT测量在椎弓根螺钉固定中的意义

目的：确定寰椎后路椎弓根钉的进钉点和验证螺钉在寰椎侧块中的位置。方法：用40副干燥寰枢椎标本测量进钉点的最佳位置和相关数据，临床应用该置钉技术，CT测量6例术后病人钉在寰椎侧块中的位置和螺钉长度。结果：寰椎椎弓根平均宽度为7．78mm，进钉点在寰椎椎弓根中线外缘2．2mm，即枢椎下关节突中点的矢状线，CT测量螺钉均位于寰椎侧块内，螺钉长度为28--30mm。结论：寰椎椎弓根钉进钉点可用枢椎下关节突中点的矢状延长线来确定，螺钉长度28--30mm。     

枢椎椎弓根及峡部的临床解剖学观察

目的:明确枢椎椎弓根及峡部的解剖部位,指导枢椎后路螺钉的临床应用。方法:成人C2干燥骨标本30具,C3干燥骨标本10具,以横突孔周围结构为重点,进行枢椎形态比较学观察;测量枢椎椎弓根轴线在下关节突背侧的坐标点。结果:C2的下方结构与C3下方的表面解剖结构接近,枢椎上方结构与C3相比较,上关节突移向齿突的外下方,并使峡部拉长前移,其轴向角度为11.1°±2.4°;枢椎椎弓根轴向角度为42.6°±4.9°,椎弓根轴线-下关节突背侧关节突上缘的交点坐标O与下关节突上缘-中垂线交点O’基本重合。结论:枢椎上下关节突之间的部分,应为峡部和椎弓根的复合体,复合体的上部较为扁平的部分为峡部,其中下部分位于横突孔内后侧的半管柱状结构为椎弓根部,连接着椎体和下关节突。     

下颈椎椎动脉孔及其毗邻的解剖学和影像学观测

目的：为下颈椎前路手术预防椎动脉损伤提供解剖学数据。方法：(1)取20具尸体的C3～7段作为解剖标本,作两侧椎动脉孔内缘间距、椎体横、矢径、椎动脉孔内缘和椎弓根内缘间距、椎动脉孔内缘和椎体外缘间距、 椎动脉孔内缘和钩突关节内外缘间距、椎动脉孔前后缘与椎体前后缘的垂直距离、 椎动脉孔矢径的测量。(2)选30例已确诊为颈椎病患者和50例正常人作为检测对象,用CT测量上述数据。 结果： (1) C_3～7两侧横突孔内缘间距、椎体横径、椎体矢径、C_3～6椎动脉孔矢径逐渐增大。(2) 钩突内缘与椎动脉孔内缘间距在6 mm之内, C_3～6椎体外缘与椎动脉孔内缘间距不超过3 mm。(3) C_3～6 横突孔矢径和椎体矢径比值恒定(30.32%～31.86%), C_3～5 椎动脉孔前缘与椎体前缘距离逐渐减小,C_3～5椎动脉孔后缘与椎体后缘距离逐渐增加。结论：本文的测量数值与不同个体的椎动脉资料相结合,为预防椎动脉损伤提供了解剖学依据。     

枢椎椎弓根内固定的解剖学研究

目的通过标本测量,研究以下关节突中心点为入钉点,枢椎椎弓根螺钉的进钉方法及要点。方法50枚人尸体骨干骨标本,以下关节突中心点A为进针点,在枢椎腹侧测量椎弓根的内倾角α;在椎弓背侧,选择上关节突内缘C点为标志点,测量AC连线的冠状面内倾角β,探讨α与β的相关性。结果枢椎腹侧测量的椎弓根冠状面内倾角为43°±4°(左侧),45°±5°(右侧),均值44°±6°;枢椎背侧测量的下关节突中心点A与上关节面内缘点C的连线内倾角β为39°±5°(左侧),37°±6°(右侧),均值38°±7°;α,β差值平均为5°±2°。结论①椎椎弓根部的解剖特点决定了其椎弓根螺钉的进入方向必须非常精确,否则很容易穿出椎弓根内外壁,造成椎动脉或脊髓的损伤;②枢椎下关节中心点与上关节面内缘点的连线对于确定合理的钉道方向具有较好的参考价值。     

胸椎上关节突基底外1/3点为椎弓根进钉点的应用解剖

目的:研究胸椎上关节突基底外1/3点与椎弓根的解剖关系,为胸椎椎弓根穿钉提供一种新的定位方法。方法:选取45具成人干燥骨标本(男25具,女20具),测量胸椎上关节突基底外1/3点至相应椎弓根上缘、下缘、中轴线垂直距离,至内缘、外缘、中轴线水平距离,最适内倾角度、最适尾倾角度、最大内倾角度、最大尾倾角度。据测量结果设置穿钉参数,在5具尸体上模拟穿钉,CT评价螺钉位置。结果:各组长度、角度之性差比较无显著统计学意义(P>0.05)。胸椎上关节突基底外1/3点在椎弓根上缘、下缘、内缘、外缘所成框内,与椎弓根中轴线接近;最适内倾角度T1￣T3为25°,T4￣T10为15°,最适尾倾角度10°,据此参数在5具尸体上模拟穿钉均获成功。结论:胸椎上关节突基底外1/3点作胸椎椎弓根穿钉定位点,具有准确、可靠、简单实用等优点,是一良好的解剖定位标志。     

腰椎上关节突外缘与椎弓根中心关系的解剖学观测及其临床意义

目的 :探讨腰椎上关节突外缘的形态特点及其与椎弓根中心的关系。方法 :对 10 0套成人干燥腰椎骨标本上关节突乳突的形态特点及其外缘切线与椎弓根外侧骨皮质及中心进行了观测。结果 :L110 0 % ,L2 98.1% ,L396 .4% ,L4 4 5 .8% ,L58.1%上关节突外缘切线位于椎弓根中心的外侧。上关节突外缘切线距椎弓根外侧骨皮质的距离为L1(1.8± 0 .7)mm ,L2 (1.5± 0 .5 )mm ,L3(2 .3± 1.5 )mm。结论 :上关节突外缘多位于椎弓根中心的外侧 ,以它做为椎弓根螺钉进钉的定位标志过于偏外。     

腰椎椎弓根内部结构的解剖学研究

目的提供国人椎弓根内部结构的部分数据,探索椎弓根内部结构的规律,为临床应用提供参考依据。方法取10具成人尸体标本,取出L1~L5脊柱标本,螺旋CT扫描后进行多平面重建,测量椎弓根高度、宽度、内外缘、上下缘皮质厚度以及椎弓根内部松质骨的宽度和高度。结果L1~L5腰椎椎弓根高度平均为1.52cm,宽度为1.1cm,内缘皮质厚度为0.28cm,外缘皮质厚度为0.17cm,上缘皮质厚度为0.30cm,下缘皮质厚度为0.31cm,椎弓根内部松质骨宽度为0.65cm,高度为0.87cm。结论腰椎椎弓根外缘皮质厚度较内缘皮质厚度薄,上缘皮质厚度与下缘皮质厚度接近,椎弓根高度及宽度比内部松质骨的高度或宽度均更多0.5cm左右。     

胸腰椎横突副突和乳突的解剖学观测及其临床意义

目的：寻求椎弓根螺丝钉较便捷的进钉点。方法：观测２０具成年干燥Ｔ１１～Ｌ５共１４０块椎骨的横突副突、乳突，行穿针操作，椎骨Ｘ线拍片，用卡尺及角度测量仪测量。结果：腰椎横突副突、乳突及下关节突关节面外上缘连线，所形成的三角形顶角角分线中点与椎弓根长轴线相重合或极其接近，故此三角形的顶角角分线中点可作为椎弓根螺丝钉的进钉点。结论：通过１２例胸腰椎骨折病人临床应用证明是一种简捷、确实可行的椎弓根螺丝钉进钉点的定位方法。     

Pain and Effusion and Quadriceps Activation and Strength

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 injury^1,2 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, researchers^8,9 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,^10–12 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 al^13,14 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,^16–18 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.^16–18 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.     

即早基因c-fos与脑血管病及学习记忆

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.     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

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.