The fine structures of the VIP-Like immunoreactive neurons in the cat hypothalamus

The fine structures of the VIP-like immunoreactive neurons in the suprachiasmatic nucleus (SCN) and the arcuate nucleus ( ARN ) of the cat hypothalamus were investigated by electron microscopic immunocytochemistry. The VIP-like immunoreactive soma and fibers could be successfully visualized by a modified PAP method. VIP-like immunoreactive neurons in both nuclei contained immunoreactive rER, Golgi complexes and many immunoreactive granules, as well as well developed mitochondria. VIP-like immunoreactive synaptic endings with synaptic membrane specialization of Gray's type I and II were found in the SCN. Moreover VIP-like immunoreactive preterminal elements that made synaptic contact with VIP-like immunoreactive neuronal soma were also detected. On the other hand, it was difficult to detect typical preterminal endings with immunoreactivity in the ARN ; however, VIP-like immunoreactive processes in contact with the basement membrane of the capillaries were observed. These observations indicate that VIP-like immunoreactive neurons in the SCN act as intrinsic neurons and are involved in neuroendocrine function in ARN .     

Proctolin-like immunoreactive neurons in the blowfly central nervous system

The pentapeptide proctolin (H-Arg-Tyr-Leu-Pro-Thr-OH) is a well-studied bioactive substance in insects. With an antiserum against proctolin we have mapped proctolinlike-immunoreactive (PLI) neurons in the nervous system of the blowfly Calliphora erythrocephala. In the brain, including the suboesophageal ganglia, 80-90 neurons were found to be PLI. A further 200-250 PLI neurons innervate the lobula of the optic lobe. The thoracic ganglia contain 100-130, and the abdominal ca. 60 PLI neurons. In the brain and ventral ganglia the immunoreactive neurons are of different types: interneurons, efferents (possibly some motorneurons), and neurosecretory cells. Some of these neurons are individually identifiable; others can be identified collectively as clusters. Identifiable neurons innervate protocerebral neuropil associated with the pars intercerebralis and the beta-lobes of the mushroom bodies as well as tritocerebral neuropil. Some of the prominent clusters innervate the central body of the protocerebrum, tritocerebrum, and possibly leg motor neurons. One abdominal cluster is of special interest because it consist of efferent neurons with processes in the lateral abdominal nerves. Some of these processes are located in the neural sheath in neurohaemal regions, and electron microscopy demonstrates that their terminals are outside the blood-brain barrier. The PLI processes in the protocerebrum contain large granular vesicles and form chemical synapses with different kinds of nonimmunoreactive neural elements. Thus, in Calliphora the proctolinlike substance may be used as a central transmitter/modulator, a neuromuscular transmitter, and a neurohormone released into the circulation.     

Autoimmune maintenance and neuroprotection of the central nervous system

The genesis of immune privilege high in the evolutionary tree suggests that immune privilege is necessary, if not advantageous for the progressive development of the CNS. Upon reaching a certain degree of complexity, it seems as if the CNS was obliged to restrain the immune system from penetrating the blood-brain barrier. CNS autoimmunity against myelin proteins is known to be a contributory factor in the pathophysiology of multiple sclerosis and in the animal model of experimental autoimmune encephalomyelitis (EAE) (Wekerle, 1993). Such autoimmunity has therefore been regarded as detrimental and hence obviously undesirable. However, recent findings in our laboratory suggest that T-cell autoimmunity to CNS self-antigens (Moalem et al., 1999), if expressed at the right time and the right place, can do much good in the CNS. We shall review the experiments briefly, and then discuss their implications for our understanding of immune privilege and CNS maintenance after injury.     

Localization of immunoreactive alpha-bag-cell peptide in the central nervous system of Aplysia

The bag cells of the marine mollusc Aplysia are well-characterized neuroendocrine cells that initiate egg laying, but the natural stimulus triggering bag-cell activity has not been determined. As a first step toward identifying central neurons that might provide synaptic or neurohormonal input onto the bag-cell network, antibodies specific for alpha-bag-cell peptide (alpha-BCP) were generated. This peptide belongs to a small family of structurally related peptides that can elicit bag-cell activity in vitro. Antibody specificity was established by immunodot assay and preabsorption studies: immunocytochemical labeling was abolished in each ganglion when the antibodies were preincubated with either alpha-BCP-thyroglobulin conjugate or alpha-BCP-(1-8) but was not affected by preincubation with thyroglobulin or thyroglobulin-thyroglobulin conjugate. The antibodies specifically labeled the bag cells in the abdominal ganglion and ectopic bag cells in both the abdominal and right pleural ganglia. The ectopic bag cells were similar to conventional bag cells in size and morphology, but varied in number and location among preparations. In the cerebral ganglion, the antibodies labeled a bilaterally symmetrical pair of cell clusters, containing approximately ten cells each, on the dorsal surface of the ganglion. The cerebral cells were smaller than bag cells, were constant in location, and sent their processes into the neuropil rather than the connective tissue sheath. Immunoreactive processes were observed in the neuropils of the cerebral, pleural, and pedal ganglia and among the axons of the cerebropedal, cerebropleural, and pleurovisceral connectives. No immunoreactive cell bodies were observed in the buccal or pedal ganglia. Identical patterns of labeling were observed in Aplysia californica, A. brasiliana, and A. dactylomela. The distribution of immunoreactive cell bodies within the circumesophageal ganglia of all three species thus parallels the distribution of receptive sites for the in vitro induction of bag-cell activity by atrial gland peptide B, a peptide structurally related to alpha-BCP. These observations suggest that the immunoreactive cells identified in these studies, or a subset of them, may be involved in the physiological induction of bag-cell activity. Since low doses of alpha-BCP have additional inhibitory actions on the bag cells, however, it is possible that the identified cells could play a more complex role in the regulation of bag-cell activity.     

Morphology of demyelination in the human central nervous system

The principles of the neuropathological classification of disorders of central nervous system myelin are recalled. They are illustrated by a few selected examples. Dysmyelination is characterized by the production of an abnormal and unstable myelin sheath; it is often associated with hypomyelination (paucity of myelin formation) and is due to metabolic disorders. It is the main process in leukodystrophies. Storage of different lipids (e.g. sulfatides, long-chain fatty acids) or associated pathology of various cell types (in Alexander's disease, for example) are used for classifying these disorders. Biochemical and genetic characterizations are presently ongoing. Demyelination is the destruction of apparently normal myelin. It is often followed by remyelination. Our present knowledge on the neuropathology of multiple sclerosis, the most common demyelinating disease, is summarized. Cell-mediated demyelination affects the myelin sheaths for an obscure reason. The causes of the multifocal and sharply demarcated plaques, and of the fading of the remyelination process at the edge of some plaques, are not clear. A few examples of demyelinating diseases of known etiology and of various mechanisms are given. The similarities between acute disseminated leukoencephalitis and experimental autoimmune encephalitis are stressed. In progressive multifocal leukoencephalopathy, chronic infection of oligodendrocytes by JC virus induces poorly defined areas of demyelination. In AIDS, the pathogenesis of the myelin change is unclear. Macrophages may be responsible. Toxic and vascular disorders provide also good models for the understanding of mechanisms of demyelination.     

脊椎动物中枢神经系统CTGF免疫反应阳性细胞的比较发育

采用免疫组织化学方法研究了鲢、蛙、蛇、鸡、牛、犬和大鼠中枢神经系统（ＣＮＳ）结缔组织生长因子（ＣＴＧＦ）免疫反应阳性细胞的分布和发育规律。低等脊椎动物链、蛙和蛇ＣＮＳ仅有少量ＣＴＧＦ免疫反应阳性神经元,分布于脊髓灰质腹侧角、延髓的一些核团、丘脑前核、下丘脑背侧核、下丘脑腹侧核。鸡ＣＮＳ的ＣＴＧＦ免疫反应阳性神经元除广泛分布于脊髓和脑干外,小脑、间脑和大脑纹状体的多数脑区阳性神经元亦较多。哺乳动物牛     

Ultrastructural morphometric analysis of somatostatin-like immunoreactive neurones in the rat central nervous system after labelling with colloidal gold

Nerve terminals of the rat median eminence, arcuate nucleus and spinal cord were examined in the electron microscope after post-embedding, colloidal gold labelling of immunoreactivity to somatostatin. Strong immunostaining was thus obtained together with adequate morphological preservation. Reactive boutons showed clusters of gold particles essentially confined to dense-cored vesicles. In the median eminence, the positive varicosities made up more than half of all terminals and averaged 735 nm in diameter. Those in the arcuate nucleus and spinal cord were much less numerous and generally smaller (575 nm). The labelled vesicles had mean external diameters of 109, 95 and 79 nm in the median eminence, arcuate nucleus and spinal cord, respectively. Calculations of the likely amounts of somatostatin within the vesicles of the median eminence and arcuate nucleus yielded values of 0.7 and 1.4 mM, corresponding to 190 and 230 molecules of the peptide, respectively. These data support a neurotransmitter or modulator role for somatostatin in the central nervous system.     

中枢神经系统淋巴瘤MRI表现

目的：探讨中枢神经系统淋巴瘤的影像学特征。方法：对１９例经手术及病理证实的中枢神经系统淋巴瘤的影像学表现，特别是ＭＲ表现进行分析。结果：单发肿瘤１５例，位于幕上１３例，幕下２例。多发肿瘤４例。多数病灶位于深部白质，１４例病灶邻近脑室。肿瘤平均最大径超过３ｃｍ。Ｔ１像１４例信号较低，５例等信号。Ｔ２像５例低信号，余为等信号。肿瘤水肿相对较轻。注射造影剂后，肿瘤多数均匀强化。病理均为ＮＨＬ恶性淋巴瘤。结论：中枢神经系统淋巴瘤的影像学表现与某些中枢神经系统病变有类似及重叠之处。通过认真的影像分析并结合活检结果，有利于治疗方法的选择。     

Viral infections of the central nervous system

Viral infections of the central nervous system in the tropical countries of Asia and the Indian subcontinent are different from those of the Western and developed world. Many of the endemic and epidemic encephalitides that are prevalent in these regions, such as Japanese encephalitis, have characteristic findings on imaging, especially on magnetic resonance imaging, allowing a rapid diagnosis and differentiation from clinically similar syndromes. Other emerging viral infections in the region in recent years have posed new challenges. The contribution of neuroimaging to the management of these emerging infections is also discussed.     

Distribution of measles virus in the central nervous system of HIV-seropositive children

In an autopsy study the distribution of measles virus (MV) in the central nervous system (CNS) of 18 measles-infected children (13 HIV seropositive, 5 HIV seronegative), in Abidjan, Ivory Coast was examined using immunocytochemistry and in situ hybridization. Of these children 17 died from measles giant cell pneumonia. In 3 of the 13 HIV-seropositive patients MV antigens and genomic RNA was detected in the CNS. One of these positive patients had an MV encephalitis with abundant virus throughout most of the CNS. MV was not detected in the CNS of any of the 5 HIV-seronegative patients. These findings, albeit in a small number of cases, would suggest there may be an increased susceptibility to infection of the CNS with MV in HIV-positive children. In this respect entry and growth of MV in the CNS in HIV-seropositive individuals may be similar to the occurrence of measles inclusion body encephalitis in immunocompromised individuals. Furthermore, comparison of the HIV-MV encephalitis patient with two patients with subacute sclerosing panencephalitis (SSPE) demonstrated a paucity of virus in neuronal processes in the HIV-MV encephalitis. Unlike in SSPE, MV maturation by budding through the plasma membrane may occur, thereby minimizing build up of and intracellular movement of incomplete virus. Received: 6 March 1998 / Revised, accepted: 2 June 1998     

中枢神经系统肿瘤相关炎症研究进展

19世纪Rudolf Virchow在肿瘤组织中第一次发现了炎症细胞,肿瘤与炎症免疫之间的关系便成为人们研究肿瘤的一个重要途径[1].炎症在肿瘤的发生、发展过程中的重要作用已逐步为人们所认识[2].     

Primary Burkitt-type lymphoma of the central nervous system

Summary A primary Burkitt-type lymphoma of the central nervous system (CNS) is presented. The right temporoparietal tumor in a woman of 55 was diagnosed histologically as a Burkitt-type lymphoma. Primary Burkitt-type lymphoma of the CNS is extremely rare and has been reported previously only four times. This is the first case reported in Eastern Asia.     

中枢神经系统结核误诊分析(附35例临床病理报告)

目的探讨中枢神经系统结核诊断及误诊原因.方法分析了35例生前被误诊、尸解病理证实的中枢神经系统结核.结果误诊为化脓性脑膜炎9例,病毒性脑炎7例,乙型脑炎4例,脑肿瘤及脑积水各3例,视神经脊髓炎、脑脓肿、败血症各2例,麻疹、多发性脑脊髓瘤、淋巴瘤各1例.临床表现除脑膜刺激征、颅高压外,可有中枢神经系统局灶损害症状.脑脊液改变为压力升高,细胞计数与蛋白含量增高,糖与氯化物降低.尸检发现脑膜病变为主,脑实质、脑室、脑血管、脊髓均有结核病变.结论中枢神经系统结核临床表现与结核病变性质、部位密切相关,认识其病理类型、临床症状多样性以及动态脑脊液观察有助于提高诊断率.     

中枢神经系统海绵状血管畸形的免疫组化染色研究

目的 应用免疫组化染色观察不同类型中枢神经系统海绵状血管畸形的内皮细胞标记物、血管生成和增殖活性,探讨病变出血的分子基础. 方法 以自2004年4月至2008年8月南方医院神经外科经显微手术切除的97例中枢神经系统轴内海绵状血管畸形的病理标本为观察对象,根据患者MRI表现分类及其与术中病理形态的比较将所有患者分为出血组(47例)和非出血组50例;另设正常对照组20例,标本来自颅脑外伤患者切除的脑组织.将3组病理标本进行CD34、α-平滑肌肌动蛋白(α-SMA)及血管内皮生长因子(VEGF)免疫组化染色并比较. 结果 海绵状血管畸形内皮层中,CD34呈不同程度的表达,有明显的不连续性;管腔小的病变血管中.CD34染色层较厚;而在管腔大的病变血管中,CD34染色层却较薄,且常不连续.α-SMA表现为阴性或弱阳性(-)～(++).弥散地分布于内皮下层.VEGF有较明显的表达(-)～(++),主要弥散地位于内皮层、内皮下层以及病变血管之间的纤维结缔组织中.正常对照组、出血组与非出血组之间CD34、α-SMA及VEGF免疫组化染色经Kruskal-Wallis H检验示差异均有统计学意义(P＜0.05).所有标本Ki-67染色均呈阴性. 结论 血管结构上缺乏平滑肌可能是部分海绵状血管畸形容易出血的原因之一;VEGF弥散性的表达增多,可能与出血诱导的非特异上调有关;Ki-67染色呈阴性表明至少在标本取得时不存在增殖状态.     

中枢神经系统血管母细胞瘤的显微外科治疗

目的探讨中枢神经系统血管母细胞瘤的临床特征、诊断和鉴别诊断．以及外科手术治疗特点。方法对1999年2月-2006年5月施行手术治疗的21例中枢神经系统血管母细胞瘤患者（肿瘤位于小脑半球者14例，第四脑室内延髓背侧2例，延髓下部1例和脊髓内4例）的临床资料进行回顾性总结与分析。结果手术全切除肿瘤患者14例，次全切除7例，其中2例于手术前施行微导管超选择性肿瘤供血动脉栓塞术。手术后神经系统症状明显改善18例，2例因脑积水症状未改善行侧脑室．腹腔分流术，1例手术后并发出血，再次手术。12例患者平均随访25个月，9例恢复正常工作和生活，1例遗留小脑性共济失调，2例肿瘤复发（1例再次手术全切除肿瘤；1例多部位复发而行γ-刀治疗。随访7个月肿瘤无增大）。本组无死亡病例。结论 中枢神经系统血管母细胞瘤为良性肿瘤，肿瘤全切除可获得根治。应用显微外科技术、手术前供血动脉栓塞以及立体定向放射外科等综合措施可提高疗效。     

原发性中枢神经系统非霍奇金淋巴瘤临床分析

目的探讨原发性中枢神经系统非霍奇金淋巴瘤(PCNSNHL)的早期诊断、治疗方法及预后。方法回顾性分析86例术后经病理证实为PCNSNHL的临床特征、影像学特点、治疗方法及预后。结果术前早期诊断12例。随访63例,死亡48例,平均生存期13.74个月。术后行放、化疗组,平均生存期14.68个月(最长达5年);未行放、化疗组,平均生存期仅2个月。结论PCNSNHL术前早期诊断有可探讨之规律,尤其是影像学特征;采用包括手术和放、化疗在内的综合治疗是提高疗效的关键。     

仅累及中枢神经系统血管炎相关分析

目的初步探讨仅累及中枢神经系统血管炎的临床特点、检查及治疗方法。方法对诊治的11例仅累及神经系统血管炎的患者进行相关分析。结果患者多年轻化,临床表现多样化,磁共振表现无特征性,免疫系统相关检查阴性,大多对激素治疗有效。结论年轻患者,反复脑血管病,而无脑血管病危险因素,即使免疫相关检查正常,也要高度警惕仅累及中枢神经系统血管炎可能,及早完善DSA,尽早激素干预治疗。     

大鼠脑挫伤后Nogo-A mRNA表达水平变化的实验研究

目的观察大鼠脑挫伤后Nogo-AmRNA在神经组织表达量的变化。方法取35只SD大鼠,随机分为7组,每组各5只。1组设为正常对照组,其余6组分别在脑挫伤(自由落体打击脑损伤)后12、24h及3、9、15、21d处死,取脑组织提取RNA,采用半定量RT-PCR法,检测正常及各损伤组Nogo-AmRNA的相对水平。结果脑组织中Nogo-AmRNA表达量在损伤后12h开始出现明显升高(0.1373±0.0009),24h表达稍有下降(0.1067±0.0008),3d后再次上升(0.1220±0.0010),至第9天达到高峰(0.1762±0.0007)并维持于较高水平,至伤后15d(0.1397±0.0005)缓慢下降,伤后21d(0.0129±0.0002)恢复至伤前水平。结论中枢神经损伤后,Nogo-A在抑制神经再生过程中可能发挥着重要作用。     

Fetal central nervous system malformations on MR images

Sonography is the method of choice for prenatal malformation screening but it does not always provide sufficient information for correct diagnosis or adequate abnormality evaluation. Fetal magnetic resonance imaging (MRI) is considered as a valuable second line imaging tool for confirmation, completion and correction of sonographic findings. Fetal MRI has proven its value in the evaluation of central nervous system pathologies, especially of midline and posterior fossa malformations. The role of MRI is not only to confirm or exclude possible lesions but also to define their full extent, aiding in their characterization, and to demonstrate associated abnormalities. The authors describe the most common anomalies of CNS revealed by fetal MRI in a chronological way related to the age of pregnancy, with a review of own MR images and with reference to the literature and own experience.