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PubMed1995

Rheumatic manifestations of disorders of the central and peripheral nervous system.

Many inflammatory rheumatic conditions may result, in part, from local release of sensory neuropeptides; substance P is currently the best studied of these. Various neurologic diseases that result in movement disorders continue to come to the attention of rheumatologists, primarily because of the pain and stiffness associated with them, and they are often misdiagnosed. Neuroarthropathies remain the most distinctive of the joint disorders that appear to result directly from neurologic injury, but little new information concerning these disorders has been generated in the past year.

Arthritis↗
PubMed2001

Expression and distribution of transcription factor NF-kappaB and inhibitor IkappaB in the inflamed peripheral nervous system.

The NF-kappaB family of transcription factors is critically involved in the immune response. The activity of these proteins is under strict control of an inhibitory molecule called IkappaB. The present study investigated the expression and distribution pattern of NF-kappaB and IkappaB in sural nerve biopsies obtained from patients with Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy, and various non-inflammatory neuropathies. In inflammatory demyelinating as well as non-inflammatory neuropathies, NF-kappaB was primarily expressed by macrophages, as determined by immunohistochemistry. IkappaB, however, could be localized to macrophages as well as T cells in inflammatory demyelinating neuropathies, whereas in non-inflammatory controls Schwann cells were found to be the primary cell type expressing this inhibitor. Quantitation of immunoreactivity revealed a statistically significant increase of NF-kappaB expression in inflammatory demyelinating cases compared to controls. Our results suggest an important function of the NF-kappaB pool in the genesis of inflammatory demyelination in the peripheral nervous system.

Guillain-Barre Syndrome↗
PubMed1992

Cytomegalovirus and the peripheral nervous system in AIDS.

Cytomegalovirus (CMV) has been associated with a spectrum of peripheral nerve syndromes in patients with AIDS. Lumbosacral polyradiculopathy, a rapidly progressive syndrome occurring in about 1% of AIDS patients, is characterized by low back pain, sphincter disturbance, progressive flaccid paraparesis, and neutrophil cerebrospinal fluid pleocytosis. CMV has been found consistently in the lumbosacral roots in association with inflammation, demyelination, and axonal loss. Anti-CMV therapy has been reported in open studies to prolong survival and may lead to improvement of the neurologic deficit. A few patients with mononeuritis multiplex have been found to have CMV inclusions associated with inflammation and axonal loss in the peripheral nerve. The diagnosis, dependent on finding CMV in a biopsy sample, has been made too infrequently to estimate the incidence and prognosis or response to treatment. Painful distal symmetrical peripheral neuropathy, the most frequent neuropathy in AIDS, is characterized by subacute onset of pain in the feet, with associated findings including mild sensory signs and fiber degeneration axonal atrophy on sural nerve biopsy. A prospective study found an association of this syndrome with CMV disease of other organs, and CMV has been found in the dorsal root ganglion in a single case. Anti-CMV therapy might be of benefit in these peripheral nerve syndromes; however, the effect of such treatment needs to be assessed in controlled studies.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Anti-GQ1b ganglioside antibody in peripheral nervous system disorders: pathophysiologic role and clinical relevance.

The recent literature about autoimmune peripheral neuropathies has been dominated by the discovery of antibodies to a variety of glycosphingolipids. Gangliosides are important carbohydrate determinants for autoimmune activity, and several studies have suggested that serum antibodies against gangliosides are responsible for some forms of acute and chronic neuropathy syndromes. However, this view is disputable, and despite substantial progress in understanding the potential pathogenic effects of antiganglioside antibodies, many central issues remain unresolved across the whole pathogenic process. Miller Fisher syndrome has been classified as a variant of Guillain-Barré syndrome that comprises the clinical triad of ataxia, areflexia, and ophthalmoplegia. It has been considered the archetypal antiganglioside antibody-mediated human neuropathy because anti-GQ1b ganglioside antibody is detected in most patients with Miller Fisher syndrome, decays rapidly with clinical recovery, and is not found in normal and disease control serum samples. The only other case in which this antibody is found is in patients with related conditions, which might share the same pathogenic mechanism, such as Bickerstaff brainstem encephalitis. The strength of this close serologic-clinical association is such that measurement of anti-GQ1b antibody in suspected cases of Miller Fisher syndrome is a useful diagnostic marker for clinicians. This article reviews the occurrence, the pathophysiologic role, and the clinical background of anti-GQ1b ganglioside antibody in Miller Fisher syndrome and related disorders.

Animals↗
PubMed1999

Immunohistochemical detection of somatostatin sst2a receptors in the lymphatic, smooth muscular, and peripheral nervous systems of the human gastrointestinal tract: facts and artifacts.

The cellular distribution of the somatostatin sst2A receptor protein was investigated in the lymphatic, smooth muscular, and nervous components of the human gastrointestinal tract using subtype-specific antibody R2-88 for immunohistochemical staining of cryostat and formalin-fixed, paraffin-embedded tissue sections. Germinal centers of intestinal lymphatic follicles were immunostained, exhibiting a predominantly plasma membrane localization of the receptor. Similarly, nerve fibers and cells in the submucosal and myenteric plexus were stained for sst2A. Antibody preabsorption with 100 nmol/L antigen peptide abolished staining in all of these tissues, and immunohistochemical staining correlated with the labeling observed after receptor autoradiography using the sst2-preferring radioligand 125I-[Tyr3]octreotide. Cytoplasmic immunostaining was detected in gastrointestinal smooth muscle cells and was inhibited by antibody pre-absorption with antigen peptide. However, 125I-[Tyr3]octreotide autoradiography was negative, and Western blots showed no band at the usual 70-90 kDa location for sst2A. Instead, a band was observed at 205 kDa. This band comigrated with the rabbit myosin standard, which was also stained with R2-88, although antibody sensitivity for myosin was less than 0.002% of that for the sst2A receptor. Rigorous computer-based sequence analysis demonstrated the peptide sequence chosen for antibody production was unique. Moreover, standard sequence alignment protocols were unable to identify the sequences in myosin responsible for the observed reactivity with the R2-88 antiserum. The observed cross-reactivity emphasizes the need for extensive controls to prove the specificity of immunostaining for such low abundance proteins as receptors even when the peptide sequence chosen for antibody production is unique. This study demonstrates for the first time the presence of specific sst2A receptor protein by immunohistochemistry in the human gastrointestinal lymphatic and nervous components, but not in gastrointestinal circular and longitudinal smooth muscle.

Animals↗
PubMed1999

Vascular endothelial growth factor has neurotrophic activity and stimulates axonal outgrowth, enhancing cell survival and Schwann cell proliferation in the peripheral nervous system.

Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells, and it promotes angiogenesis in vivo. Here we report that VEGF(165) has neurotrophic actions on cultured adult mouse superior cervical ganglia (SCG) and dorsal root ganglia (DRG), measured as axonal outgrowth. Maximal effect was observed at 10-50 ng/ml for SCG and 100 ng/ml for DRG. VEGF-induced axonal outgrowth was inhibited by the mitogen-activated protein kinase kinase inhibitor PD 98059 but not by the protein kinase inhibitor K252a. VEGF also increased survival of both neurons and satellite cells and the number of proliferating Schwann cells. Immunocytochemistry and immunoblotting revealed that VEGF was expressed in virtually all nerve cells in the SCG but only in a population of small-diameter (<35 micrometers) neurons representing approximately 30% of the neurons in DRG. Immunostaining showed that the VEGF receptor fetal liver kinase receptor (flk-1) was found on nerve cell bodies in DRG and to a lesser extent on neurons in SCG. Growth cones of regenerating axons from both types of ganglia exhibited flk-1 immunoreactivity, as did Schwann cells. We conclude that VEGF has both neurotrophic and mitogenic activity on cells in the peripheral nervous system.

Animals↗
PubMedDate not supplied

Peptidergic peripheral nervous systems in the mammalian pineal gland.

The distribution and density of tyrosine hydroxylase (TH) and neuropeptide Y (NPY)-immunoreactive, sympathetic fibers and calcitonin gene-related peptide (CGRP)-, substance P (SP)-, and vasoactive intestinal polypeptide (VIP)-immunoreactive, non-sympathetic fibers in the pineal gland, the effects of superior cervical ganglionectomy (SCGX) on these fibers, and the location of their terminals in the pineal gland were compared between rodents and non-rodents. A dense network of TH/NPY-positive fibers is present all over the pineal gland. A less dense network of CGRP/SP- or VIP-positive fibers occurs in the whole pineal gland of non-rodents, but these fibers are usually confined to the superficial pineal gland in rodents. After SCGX, some TH/NPY-fibers remain only in the deep pineal gland in rodents, whereas considerable numbers of these fibers persist throughout the gland in non-rodents. Thus, the remaining fibers, probably originating from the brain, may be more numerous in non-rodents. Since CGRP-, SP- or VIP-immunoreactive fibers in the pineal capsule can be traced to those in the gland, and since these fibers are ensheathed by Schwann cells, it is concluded that these fibers belong to the peripheral nervous system. However, the existence of SP-positive central fibers cannot be denied in some species. In the superficial pineal gland of rodents, sympathetic terminals are mostly localized in perivascular spaces, whereas the parenchymal innervation by sympathetic fibers in the pineal gland is more dense in non-rodents than in rodents. Synapses between sympathetic nerve terminals and pinealocytes occur occasionally in non-rodents, but only rarely in the superficial pineal gland of rodents. The occurrence of the synapses may depend on the frequency of intraparenchymal sympathetic terminals.

Adrenergic Fibers↗
PubMed1981

Axonal elongation into peripheral nervous system "bridges" after central nervous system injury in adult rats.

The origin, termination, and length of axonal growth after focal central nervous system injury was examined in adult rats by means of a new experimental model. When peripheral nerve segments were used as "bridges" between the medulla and spinal cord, axons from neurons at both these levels grew approximately 30 millimeters. The regenerative potential of these central neurons seems to be expressed when the central nervous system glial environment is changed to that of the peripheral nervous system.

Animals↗
PubMed2003

Transcriptional profile of the human peripheral nervous system by serial analysis of gene expression.

The peripheral nerve contains both nonmyelinating and myelinating Schwann cells. The interactions between axons, surrounding myelin, and Schwann cells are thought to be important for the correct functioning of the nervous system. To get insight into the genes involved in human myelination and maintenance of the myelin sheath and nerve, we performed a serial analysis of gene expression of human sciatic nerve and cultured Schwann cells. In the sciatic nerve library, we found high expression of genes encoding proteins related to lipid metabolism, the complement system, and the cell cycle, while cultured Schwann cells showed mainly high expression of genes encoding extracellular matrix proteins. The results of our study will assist in the identification of genes involved in maintenance of myelin and peripheral nerve and of genes involved in inherited peripheral neuropathies.

Blotting, Northern↗
PubMed2004

The peripheral nervous system and the pathogenesis of prion diseases.

Prion diseases are inevitably fatal neurodegenerative conditions which affect humans and a wide variety of animals. Unlike other protein aggregation diseases such as Alzheimer's, Parkinson's, and polyglutamine repeat diseases, prion diseases are unique in that they are transmissible. Therefore, prion diseases are also called transmissible spongiform encephalopathies. A number of prion diseases are caused by peripheral uptake of the infectious agent. In order to reach their target, the central nervous system, prions enter their host, accumulate and replicate in lymphoid organs, and eventually spread to the central nervous system via peripheral nerves. Once the agent has reached the central nervous system, disease progression is rapid, resulting in neurodegeneration and death. In this article, we review the state of knowledge on the routes of neuroinvasion used by the infectious agent in order to gain access to the central nervous system upon entry into extracerebral sites.

Animals↗
PubMed1988

Serotoninlike immunoreactivity in the central and peripheral nervous system of the scale worm Harmothoe imbricata (Polychaeta).

The distribution of serotoninergic neurons in the nervous system of the scale worm Harmothoe imbricata was visualized in the anterior half of the body by the peroxidase-antiperoxidase (PAP) immunohistochemical method with a specific antiserotonin antibody. Immunoreactive neuronal somata were localized in discrete ganglion cell masses of the dorsally situated cerebral ganglion and in segmental ganglia of the ventral nerve cord. They also make up the majority of neurons present in the parapodial ganglia. Large and small varicose fibers stained in the neuropile of all the above-mentioned ganglia but also in interganglionic connectives and segmental nerves. On the basis of soma size and location and of fiber distribution, the reactive neurons were identified as primarily interneuronal with a few motoneurons and presumptive afferent neurons. The presence of a motor component was substantiated by observations of several reactive varicose fibers spread over longitudinal muscle layers of the trunk. In addition, neurites of the subepidermal nerve plexus and enterochromaffinlike cells of the gut epithelium reacted with the serotonin antibody. It is concluded that serotoninergic pathways are ubiquitous elements in the organization of the central and peripheral nervous system of this polychaete. The significance of these findings in relation to other annelid groups and to the physiological role of serotonin is discussed.

Animals↗