Eye movement quantitative evaluation before and after high-dose 6-methylprednisolone in multiple sclerosis

We studied saccadic and smooth pursuit eye movements in 24 patients suffering from multiple sclerosis during disease worsening, before and after high-dose 6-methylprednisolone infusions. Quantitative evaluation of saccades was based on amplitude/duration and amplitude/peak velocity relationships, precision (i.e. the ratio of actual to desired saccade amplitude) and the latency, whereas smooth pursuit eye movements were studied using target velocity/performance index relationship. At basal recordings, 22/24 (91.7%) of the patients showed at lest one abnormality. Eleven of the 24 patients (45.8%) showed modification of one or several parameters: improvement in 6 patients, worsening in 2, coexistence of both trends in 3. Latency improvement was the only significant modification when patients were considered as a group. Neurophysiological modifications did not correspond to clinical changes.     

Autoimmune reactions in patients with M-component and peripheral neuropathy.

A study of 17 patients with autoimmune axonal or demyelinating peripheral neuropathy in combination with M-component is described. The M-component was associated with MGUS (monoclonal gammopathy of undetermined significance) in 12 patients, CLL in one patient, WaldenstrÖm's disease in one patient, and myeloma in three patients. Immunohistological examination with direct and indirect fluorescence showed binding of antibodies to nerve structures of the same class and light chain as seen in the M-component. In five cases of IgM M-component, the demyelinating neuropathy was caused by binding of the IgM M-protein and complement C3b to myelin-associated glycoproteins (MAG). In 12 cases with axonal neuropathy, binding of IgG to the connective tissue of the peri- and endoneurium was found in 50% of cases, IgM in five cases, and IgD in one case. None of the patients had central nervous system (CNS) symptoms. The clinical and therapeutic difficulties are discussed; only two patients with an acute course responded to immunosuppression. A marked co-expression of other autoimmune phenomena is interpreted in the light of cross-reactions between the autoantibody and similar tissue autoantigens.     

Lymphoid tissues induce NGF-dependent and NGF-independent neurite outgrowth from rat superior cervical ganglia explants in culture

Induction of neurite outgrowth from superior cervical ganglia (SCG) by rat lymphoid tissues was studied using a tissue culture model. Neonatal rat SCG were cultured with 6–12-week-old rat thymus, spleen, or mesenteric lymph node (MLN) explants in a Martrigel layer, in defined culture medium without exogenous nerve growth factor (NGF). SCG were also co-cultured with neonatal rat heart (as positive control) or spinal cord (SC; as negative control). To determine whether inflammation affects the ability of lymphoid tissues to induce neurite outgrowth, we also examined MLN at various times after infecting rats with Nippostrongylus brasiliensis (Nb-MLN). In one series of experiments, a single lymphoid tissue explant was surrounded by four SCG at a distance of 1 mm. The extent of neurite outgrowth was determinded by counting the number of neurites 0.5 mm away from each ganglion at several time points. Adult thymus and, to a lesser extent, spleen had strong stimulatory effects on neurite outgrowth from SCG after 12 hr or more in culture. For thymus tissue, this was similar to the positive control heart explants. MLN from normal rats had minimal effect on neurite outgrowth; however, Nb-MLN showed a time-dependent enhancement of the neurite outgrowth, maximal at 3 weeks after infection. The relative efficacy of neurite outgrowth induction (heart ≥ thymus ≥ Nb-MLN ≥ spleen ≥ MLN ≥ SC) was confirmed in a second series of experiments where one SCG was surrounded by three different tissue explants. We then examined the role of 2.5S NGF, a well-known trophic factor for sympathetic nerves, in the lymphoid tissue-induced neurite outgrowth. Anti-NGF treatment of co-cultures of SCG and heart almost completely blocked the neurite outgrowth. Anti-NGF also significantly inhibited thymus- and spleen-induced neurite outgrowth, but not as effectively as heart-induced neuritogenesis (93,80, and 77% inhibition at 24 hr; 86,70, and 68% inhibition at 48 hr for heart, thymus, and spleen, respectively). On the other hand, anti-NGF inhibited only 8% of neurite outgrowth induced by 3-week post-infection Nb-MLN at 24 hr, and 41% at 48 hr. These data show that several adult rat lymphoid tissues exert neurotrophic/tropic effects. The predominant growth factor in thymus and spleen is NGF, while Nb-MLN produces factor(s) which is (are) immunologically distinguishable from NGF. These neurotrophic/tropic factors are produced during the reactive lymphoid hyperplasia that forms part of the inflammatory response against the nematode, N. brasiliensis. This suggests the possibility that cytokines produced by lymphocytes or other inflammatory cells may stimulate sympathetic neurite outgrowth in vivo. © 1994 Wiley-Liss, Inc.     

动脉韧带与左喉返神经的解剖研究

本文用30例成人尸体观察了动脉韧带和左喉返神经,动脉韧带长1.2.97±4.53mm,圆索状动脉韧带23例(77％),直径为3.92±1.12mm。动脉韧带的主动脉端附着于主动脉弓(80％)或降主动脉(20％),肺动脉端附着于左肺动脉,6例肺动脉端位于心包内。19例(63％)左喉返神经绕主动脉弓,11例(37％)绕动脉韧带的主动脉端。     

Ascending general visceral pathways within the brainstems of two teleost fishes: Ictalurus punctatus and Carassius auratus.

The primary general visceral nucleus in goldfish (Carassius auratus) and catfish (Ictalurus punctatus) is located at the ventroposterior boundary of the vagal gustatory lobe and receives coelomic visceral, but not gustatory inputs. The neuronal tracer horseradish peroxidase (HRP) was employed to visualize sources of input to and ascending projections from the primary general visceral nucleus in these species. In addition, immunocytochemical techniques were utilized to define the cytological divisions within the pontine gustatory-visceral complex. The pontine secondary visceral nuclei in both catfish and goldfish contains numerous somata and fibers immunoreactive for calcitonin gene-related peptide (CGRP). In contrast, the secondary gustatory nuclei are devoid of fibers and cells immunoreactive for CGRP. In both the goldfish and the channel catfish, the primary general visceral nucleus receives input from the vagal gustatory lobe, as well as the medullary reticular formation. In the channel catfish, the primary general visceral nucleus projects bilaterally to the secondary visceral nucleus, which lies rostrolateral to the secondary gustatory nucleus in the dorsal pons. Fibers cross the midline via the rostral part of the isthmic commissure. Injection of HRP into the primary general visceral nucleus of a goldfish labels ascending fibers that project to a secondary visceral nucleus situated ventral, lateral, and rostral to the secondary gustatory complex. In general, the results indicate that general visceral systems ascend in parallel to gustatory systems within the brainstem, and that general visceral but not gustatory nuclei are immunoreactive for the peptide CGRP.     

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.     

Peptidergic neurons in the snail Helix pomatia: Distribution of neurons in the central and peripheral nervous systems that react with an Antibody raised to the insect neuropeptide,leucokinin I

In this study, antiserum raised against an insect myotropic peptide, leucokinin I (DPAFNSWGamide), was: used for mapping leucokinin-like immunoreactive (LK-LI) neurons in the gastropod mollusc, Helix pomatia. Immunocytochemistry performed on both whole-mounts and cryostat sections demonstrated LK-LI neurons in all ganglia of the central nervous system (CNS), except the visceral ganglion. Altogether about 700 immunolabelled neurons have been found, with nearly one-half (46%) in the cerebral ganglia. A large proportion of the LK-LI neurons have small cell bodies and are likely to be interneurons. The most prominent LK-LI cell group is represented by the entire neuron population of the mesocerebri, which is the major source of a thick fiber bundle system, encircling and innervating the whole CNS. One single LK-LI giant neuron was found, which is located in the left pedal ganglion and is termed GLPdLKC (giant left pedal leucokinin immunoreactive cell). This cell has not been identified previously. The ganglion neuropils are heavily innervated by varicose LK-LI fiber arborizations. Some integrative centers, such as the medullary neuropil of the procerebri, reveal an extreme density of LK-LI innervation. All major peripheral nerves contain a large number of LK-LI axons, and LK-LI innervation is found in the musculature of different peripheral organs (buccal mass, lip, tentacles, oviduct, intestine). Among the peripheral organs investigated, the intestine contains a rich varicose LK-LI network, composed of both intrinsic and extrinsic elements. Radioimmunoassay (RIA) demonstrates a very high content of LK-LI material in Helix ganglion extracts (about 50 pmol/CNS). This is the first report on the occurrence of a substance resembling the myotropic neuropeptide leucokinin I in a phylum outside arthropods. Based on our immunocytochemical observations, a role for leucokinin-like peptides in both central and peripheral regulatory processes in Helix is suggested. According to double-labelling experiments, only a small number of the LK-LI neurons are labelled with an antibody to the vertebrate tachykinin substance P.     

正常人眼筛板的结缔组织纤维结构

采用组化特染，透射电镜和图象分析仪观察了３５只正常人眼筛板结缔组织的纤维成分和结构形态，根据生物力学原理分析了筛束的力学性质和筛板的结构特征，探讨了筛板的损害形式和在眼压与视神经损害间的中介作用及其影响因素。结果显示，筛束含有细胞间质所有三种纤维，具有弹性、塑性和刚性三重复合性质，筛板纵向椭圆、筛束行径和密度象限性差异及筛板厚度个体性差异等与筛板抗损害性能有关。眼压对筛板作用有两种途径，筛板损害是     

A 4-year controlled clinical study into the use of a ceramic hydroxylapatite implant material for the treatment of periodontal bone defects

10 patients with chronic adult periodontitis who had greater than 1 tooth with infra-bony pockets were treated at the test defects by periodontal flap procedures with implantation of hydroxylapatite particles; the control defects were treated by the same surgical procedures but without the implant. A total of 58 test defects and 59 control defects were treated. Each defect had measurements carried out at given sites on the involved tooth surfaces, the sites being considered for subsequent tabulation purposes under the category of shallow (less than 3 mm) moderate (3-6 mm) and deep (greater than 6 mm) initial pocket depths. There were 146 and 152 shallow sites, 216 and 241 moderate sites and 140 and 133 deep sites, at test and control sites, respectively. Measurements of recession, probing pocket depths and probing attachment levels were made at 6 months and 1, 2, 3 and 4 years. At all sites over the period of the study, for the moderate and deep initial pockets there was a significant reduction in probing depths and an increase in the probing attachment levels. At the 4th year of assessment for the initially deep pockets, the reduction in probing depths was significantly greater for the sites treated with the implant material. In view of the difficult clinical problem posed by the treatment of teeth with deeper periodontal bone defects, further research using either this type of implant material or similar material should be considered.     

Axonal swellings in human intramuscular nerves.

The presence, morphology, distribution, and abundance of axonal swellings in intramuscular nerves were evaluated. Axonal swellings were present in intramuscular nerves in 42% of 127 muscle biopsies from patients with a variety of conditions. The incidence was highest in muscle from patients with peripheral neuropathy, but swellings were present in muscle from patients with motor neuron disease, primary muscle diseases, and some individuals without clinical or histological evidence of neuromuscular disease. The greatest number of swellings in intramuscular nerves was in muscle from patients with chronic inflammatory demyelinating neuropathy. Swellings were spherical or elliptical, 4-20 microns in diameter, 5-30 microns in length, and composed of neurofilaments. Swellings were present only in myelinated axons of intramuscular nerves, proximal to nodes of Ranvier or in internodal regions. Swellings were not associated with axonal degeneration. They were probably not transported. The formation or accumulation of swellings may reflect altered axonal dynamics common to a number of disease processes.