32例椎管内神经鞘瘤的诊断及手术治疗

目的探讨椎管内神经鞘瘤的诊断和手术治疗。方法回顾性分析本科2007年1月~2014年12月32例椎管内神经鞘瘤的临床资料、手术情况。结果 32例均获得随访,随访时间19~72个月,平均25个月。32例均采用后正中入路,实施全椎板切除或半椎板切除减压联合肿瘤切除术,肿瘤均完整切除,术后5例出现脑脊液漏,对症保守治疗后愈合。根据术后疗效评价标准,优良率为90.6%。结论 MRI检查是确诊椎管内神经鞘瘤的最有价值的手段,详细的病史采集和体格检查是防止早期病例漏诊的基本措施。手术切除是处理此类肿瘤的有效手段,但是需注意术中操作技巧、避免医源性神经损害。     

单侧或双侧钉棒系统置入治疗椎管及椎间孔神经鞘瘤:脊椎稳定性评价

背景:神经鞘瘤切除方式的选择关系着瘤体能否切净、能否有效避免肿瘤切除过程中牵拉损伤脊髓神经,最终关系着治疗的预后。目的:分析椎管内、椎间孔区域神经鞘瘤行椎板关节突切除复合单侧或双侧钉棒系统置入内固定后的脊柱稳定性。方法:对颈、胸、腰不同部位椎管内、椎间孔区神经鞘瘤48例患者行椎板关节突切除复合钉棒系统置入内固定治疗,其中管内神经鞘瘤34例行双侧螺钉固定,椎间孔区域神经鞘瘤14例行单侧螺钉固定。结果与结论:内固定后3 d及内固定后3,6,12个月X射线复查结果示:内置物位置良好,植骨融合,无脊柱失稳、椎体滑脱现象。治疗后神经功能Bodford(1997)评分及生活质量评分均较治疗前显著提高(P0.01);治疗后Lovett分级评估肌力较治疗前显著提高(P0.01);治疗后疼痛程度分级(VRS)法疼痛较治疗前明显好转(P0.01)。48例患者神经鞘瘤均完全切除,内固定后有6例出现脑脊液漏,1例出现脑脊液感染,有1例因脑脊液感染行二次手术,3例因肿瘤侵蚀神经根行肿瘤神经根一并切除。表明对椎管内神经鞘瘤采用椎板切除双侧钉棒内固定、椎间孔区域神经鞘瘤采用部分椎板关节突切除单侧钉棒能够充分暴露肿瘤所在区域的视野,完整切除神经鞘瘤,有效避免损伤脊髓神经,更能有效维持脊柱稳定性,防止出现椎体滑脱、椎体失稳,其远期效果尚需进一步研究。     

巨大纵隔肿瘤影像学与手术病理

目的探讨巨大纵隔肿瘤影像学与手术难点及病理诊断. 方法分析了12例巨大纵隔肿瘤的术前临床影像诊断和手术治疗要点. 结果 12例中胸腺瘤4例,神经纤维瘤3例,畸胎瘤2例,神经鞘瘤1例,食管平滑肌瘤1例,脂肪肉瘤1例.12例均成功行肿瘤全切除术.术后出现复张性肺水肿7例.无手术死亡. 结论手术治疗是巨大纵隔肿瘤的主要治疗手段.术中行肿瘤分块切除或先行瘤内减张的方法,可提高手术的安全性和切除率.切除肿瘤后缓慢胀肺,并在术后24小时内行人工辅助通气对防治复张性肺水肿有重要意义.     

消化系统神经鞘瘤11例临床病理特征及预后

目的：探讨消化系统神经鞘瘤的临床病理学特征、诊断与鉴别诊断、治疗及预后。方法回顾性分析11例消化系统神经鞘瘤的临床资料,并复习相关文献。结果肿瘤位于胃部5例,腮腺、右颌下腺各2例,肛门、左腭各1例。5例表现为腹痛或腹胀,6例表现为病灶处包块。5例行CT检查示肿瘤均为边界清楚的圆形或椭圆形软组织结节影,未见囊性变和钙化,4例CT增强示肿瘤呈轻~中度均匀强化。肿瘤细胞以Antion A区为主,由梭形细胞组成,呈栅栏状或漩涡状排列,2例见淋巴细胞套,11例均未见Verocay小体。6例行免疫组化检测,6例肿瘤细胞S-100阳性,CD34、CD117、DOG1和SMA均阴性。11例均行手术切除,术后随访均未见神经鞘瘤相关的复发和转移。结论消化系统神经鞘瘤临床表现无特异性,确诊需依靠病理检查和(或)免疫组化检测,S-100蛋白是诊断消化系统神经鞘瘤的重要标志物。术前CT检查有助于术前诊断,手术完整切除肿瘤病灶预后良好。     

高颈段神经鞘瘤手术入路的选择

高颈段神经鞘瘤是起源于脊髓C_(1-4)节段神经根鞘膜组织的良性肿瘤,临床并不少见。随着MRI检查的广泛应用,诊断水平也已得到提高。手术切除肿瘤是其唯一有效的治疗方法,但有关手术入路的选择目前尚无定论。我院1995年10月～1999年9月共收治高颈段神经鞘瘤8例,回顾性分析手     

骶骨神经源性肿瘤临床病理分析

目的:探讨骶骨神经源性肿瘤的临床病理学特征、诊断及鉴别诊断.方法:收集21例发生在骶骨的神经源性肿瘤,通过光镜观察及免疫组织化学分析其临床、影像学、病理学特征、免疫表型、鉴别诊断及手术预后.结果:21例中女15例,男6例,平均年龄44.9岁.临床上以骶尾部疼痛为主,影像学上表现为骶骨或骶骨及骶前肿块.神经鞘瘤17例,其中经典型神经鞘瘤8例,富于细胞神经鞘瘤9例.神经纤维瘤3例,节细胞神经瘤1例.累及骶骨的肿块,多数有不同程度的骨质破坏.免疫表型:神经鞘瘤均弥漫强阳性表达S-100蛋白,不表达NF.神经纤维瘤和节细胞神经瘤表达NF.富于细胞神经鞘瘤有4例为复发病例,平均复发时间6.5年.经典型神经鞘瘤和神经纤维瘤各有1例为复发病例.结论:骶骨神经源性肿瘤是少见肿瘤,以良性多见.各病理类型及亚型在形态学和生长方式上有一定的差异,故诊断时应明确病理类型及亚型,以供临床随访、治疗.     

巨大纵隔肿瘤影像学与手术病理

目的 探讨巨大纵隔肿瘤影像学与手术难点及病理诊断。方法 分析了12例巨大纵隔肿瘤的术前临床影像诊断和手术治疗要点。结果 12例中胸腺瘤4例，神经纤维瘤3例，畸胎瘤2例，神经鞘瘤1例，食管平滑肌瘤1例，脂肪肉瘤1例，12例均成功行肿瘤全切除术，术后出现复张性肺水肿7例，无手术死亡，结论 手术治疗是巨大纵隔肿瘤的主要治疗手术，术中行肿瘤分块切除或先行瘤内减张的方法，可提高手术的安全性和切除率，切除肿瘤后缓慢胀肺，并在术后24小时内行人工辅助通气对防治复张性肺水肿有重要意义。     

胃肠间质细胞瘤12例分析

目的:探讨胃肠间质细胞瘤的诊断和治疗方法.方法:分析12例胃肠间质细胞瘤的临床表现、病理特点、诊断及治疗情况.结果:12例中,6例胃间质瘤,6例小肠间质瘤.主要症状为不规则腹痛、腹块、消化道出血.经胃镜、钡餐、CT检查发现.12例均行手术切除,病理证实诊断.9例随访,无复发,死亡.结论:胃肠间质细胞瘤大多为恶性或低度恶性,治疗以手术切除,术后严密随访.胃肠间质细胞瘤是指一类独立起源于胃肠道原始间质干细胞并呈非定向分化的间叶肿瘤[1].过去受病理诊断技术的限制,这类肿瘤多被诊断为平滑肌瘤、平滑肌肉瘤及神经纤维瘤.近年来随着病理诊断技术的进步,这类肿瘤被统一命名为胃肠道间质瘤(gastrointestinal stromal tumors,GLSTs).我科自1995年至今收治胃肠道间质瘤12例.报告如下.     

恶性外周神经鞘膜瘤和细胞性神经鞘瘤的形态学和免疫表型特征

细胞性神经鞘瘤较为少见,是一种公认的良性外周神经鞘膜肿瘤,可被误诊为恶性外周神经鞘膜瘤。为制定一个细胞性神经鞘瘤诊断共识标准,作者回顾性分析来自两家医学机构的115例恶性外周神经鞘膜瘤和26例细胞性神经鞘瘤的临床病理学特征。临床资料从电子医疗记录档案中获得,并对形态学特征、最高核分裂计数、Ki-67增殖指数和免疫表型(SOX10、SOX2、p75NTR、p16、p53、EGFR和NF)进行评估。结果提示以下几个特征可以区分细胞性神经鞘瘤和恶性外周神经鞘膜瘤：(1)与恶性外周神经鞘膜瘤患者相比,细胞性神经鞘瘤不发生远处转移或者死于该病。更具特征性的是5年无进展生存率细胞性神经鞘瘤为100%,恶性外周神经鞘膜瘤仅18%,5年疾病特异性生存率分别为100%和32%;(2)神经鞘漩涡：瘤周包膜,包膜下丰富的淋巴细胞、巨噬细胞的浸润,和缺乏束状生长模式等支持细胞性神经鞘瘤的诊断,而出现血管周围细胞密集,肿瘤突入血管腔内和坏死则支持恶性外周神经鞘膜瘤的诊断;(3)在恶性外周神经鞘瘤中SOX10、NF及p16表达完全缺失,而表达EGFR( P值均<0．001)。 p75NTR在80%的恶性外周神经鞘膜瘤中表达,在细胞性神经鞘瘤阳性率为31%( P<0．001);(4) Ki-67增殖指数在20%以上者高度提示恶性外周神经鞘膜瘤的可能,其敏感性为87%,特异性为96%。总之,结合组织病理学及免疫表型特征可以提供一些有用的具有较高敏感性和特异性的标准,以鉴别恶性外周神经鞘膜瘤和细胞性神经鞘瘤。     

丛状神经鞘瘤2例临床病理分析

目的探讨丛状神经鞘瘤的临床病理学特征、诊断及鉴别诊断。方法观察2例丛状神经鞘瘤的临床表现、组织学形态及免疫表型并复习相关文献。结果 2例患者中,男女各1例,年龄分别为16岁和31岁,肿瘤均位于躯干皮肤。镜下见肿瘤在皮下呈多结节状分布,结节内瘤组织以细胞致密区(Antoni A)为主,相对缺乏细胞疏松区(Antoni B)。瘤细胞长梭形或波浪状,呈栅栏状、漩涡状排列,可见verocay小体。免疫表型:肿瘤细胞S-100及vimentin均弥漫阳性,GFAP部分阳性,EMA、CD57及Ki-67均阴性。结论丛状神经鞘瘤是一种较少见的良性周围神经鞘膜瘤,需与丛状神经纤维瘤、丛状纤维组织细胞瘤、丛状恶性外周神经鞘膜瘤等相鉴别。     

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.