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PubMed2004

[Vasculitis and diseases of the peripheral nervous system].

Vasculitis commonly induces peripheral neuropathies. Neuropathy is isolated in one third of the cases or participates in a multisystemic disorder. The pathological mechanism is tissular ischaemia induced by inflammation and lesions of vessel walls. Pathophysiological classification of vasculitis is mainly based on the size of affected vessels but other approaches may be proposed such as immunological classification considering the presence or absence of immunological markers. The diagnosis is supported by neuropathological examination of muscle and nerve biopsies, but electrophysiological testing may contribute to establish the diagnosis and the prognosis of the disease by showing the highly suggestive pattern of multitroncular involvement and by evaluating the extent of the neuropathy and of axonal loss. In most cases, treatment with steroids and other immunosuppressive agents result in good but partial improvement.

Electrophysiology↗
PubMed1979

Ganglia formation of the peripheral nervous system.

Embryologic studies have shown that the ganglions of the peripheral nervous system are formed by the neuroblasts from the central nervous system. The histotopography of the neurons and their segmental communications with the central nervous system are established experimentally (segmental section of the ventral roots and resection of the spinal nodes: 100 experiments). It is proved that the neurons, which communicate with the definite segment of the spinal cord, are diffusely distributed in the ganglion mass.

Animals↗
PubMed1989

Neuron- and myelin-specific monoclonal antibodies recognizing cell-surface antigens of the central and peripheral nervous system.

Immunohistochemical screening of monoclonal antibodies raised against Triton X-114-treated synaptic membranes revealed two monoclonal antibodies, namely BM88 and BM72, with characteristic binding specificities in the central and peripheral nervous systems of the pig. Monoclonal antibody BM88 was exclusively associated with neuronal elements while BM72 was myelin-specific. Thus, in the central nervous system, immunostaining with BM88 was observed throughout the gray matter of all regions of the forebrain and spinal cord tested. In the peripheral nervous system, BM88 strongly labelled the perikarya and processes of dorsal root ganglion neurons as well as the myelinated and unmyelinated neuronal processes of the dorsal roots; BM88 immunoreactivity was also detected in neuronal cell bodies and fibres of the enteric ganglia. In addition, BM88 immunolabelled the cell-surface of cultured neurons derived from brain. In mixed cultures the staining was uniformly distributed on the perikarya and along the neurites of these cells. However, in neuron-enriched cultures where 95% of the cells were immunochemically identified as neurons, the staining of the neuronal surface membrane was patchy. This phenomenon was independent of days in culture and suggested that the distribution of the BM88 antigen on the cell surface of neurons may be regulated by neuron glia interactions. By Western blotting, the antigen recognized by BM88 in brain membrane fractions which had undergone reducing sodium dodecyl sulphate/polyacrylamide gel electrophoresis was shown to be a 22,000 mol. wt polypeptide. When extracted with Triton X-114 this polypeptide partitioned into the detergent-rich phase, a property typical of an amphipathic membrane protein. In non-reducing conditions BM88 bound to a band with a molecular weight of 43,000. These results show that the BM88 antigen is composed of two polypeptide chains of equal molecular weight linked by disulphide bridges. Monoclonal antibody BM72 recognized a myelin-associated antigen in the central and peripheral nervous system. Immunohistochemical evidence suggested a cell-surface location for this antigen. By solid phase radioimmunoassay, monoclonal antibody BM88 was shown to cross-react with brain membrane fractions from pig, rabbit and rat while BM72 recognized only a pig membrane antigen. Both monoclonal antibodies BM88 and BM72 may be used as specific cellular markers in the nervous system.

Animals↗
PubMed1977

Cannabis and the peripheral nervous system.

The possible ill-effects of cannabis on the peripheral nervous system were examined in 27 male subjects with respect to their motor and sensory nerve conduction. They were classified by their previous cannabis use into casual and heavy users. The nerve conduction studies were done after a baseline period of five days and then repeated after a three-week period during which the subjects could acquire and smoke standardized cannabis cigarettes. The casual users smoked a mean of 54-3 and the heavy users a mean of 109-5 cigarettes during the smoking period. No deterioration of peripheral nerve function could be demonstrated.

Adult↗
PubMed1993

Lithium and peripheral nervous system function in manic-depressive patients.

INTRODUCTION: Lithium salts are widely used in treatment of affective disorders, but lithium may cause electrophysiologically detectable changes in peripheral nervous system even with lithium concentrations within recommended therapeutic limits. The risk of lithium treatment against other risks to peripheral nervous system in psychiatric patients with affective psychoses was tested in our study. MATERIAL AND METHOD: Electrophysiologic parameters of motor and sensory peripheral nerve fibre function were measured in two age-matched groups of psychiatric patients (20 lithium-treated and 20 affective psychotic patients without lithium treatment) and a group of 20 healthy age-matched volunteers. RESULTS: Lower amplitudes of M waves (p < 0.015) and sensory nerve action potentials (p < 0.020) on stimulation of the median nerve have been found in both groups of patients. On peroneal nerve stimulation lower M wave amplitudes have been found only in the group of lithium-treated patients (p < 0.055). No significant differences in conduction parameters of motor and sensory fibres were demonstrated. CONCLUSION: Our results demonstrate subclinical involvement of motor and sensory axons in affective-psychotic patients, which is only slightly more pronounced in lithium-treated patients. We suggest that lithium (within therapeutic plasma concentrations) is just one among the factors leading towards minor axonopathy in psychiatric patients.

Adult↗
PubMed2004

BDNF overexpression produces a long-term increase in myelin formation in the peripheral nervous system.

The neurotrophin brain-derived neurotrophic factor (BDNF) is an endogenous regulator of the myelination process during development in the peripheral nervous system. Enhancement of myelin formation by BDNF is mediated by the neurotrophin receptor p75(NTR). Although this neurotrophin is a positive modulator of myelination during early development, the final effects of BDNF on myelin sheaths after active myelination is completed are largely unknown. Using BDNF transgenic mice, we examined the long-term effects of BDNF on myelination of the peripheral nervous system in vivo. Elevation of BDNF levels in the transgenic mice produced an increase in both the rate and extent of the myelination process. BDNF enhanced and accelerated myelin formation during early development and this increase in myelin content and thickness was maintained in adulthood. Besides enhanced myelination, BDNF also influenced axon caliber size but to a lesser extent. This lagging increase in axon caliber compared to myelin suggests that the axon size is not the only determinant of myelin thickness.

Animals↗
PubMed2007

Phylogenetic preservation of alpha3 Na+,K+-ATPase distribution in vertebrate peripheral nervous systems.

The alpha(3) isoform of Na(+),K(+)-ATPase is uniquely expressed in afferent and efferent neurons innervating muscle spindles in the peripheral nervous system (PNS) of adult rats, but the distribution pattern of this isoform in other species has not been investigated. We compared expression of alpha(3) Na(+),K(+)-ATPase in lumbar dorsal root ganglia (DRG), spinal roots, and skeletal muscle samples of amphibian (frog), reptilian (turtle), avian (pigeon and chicken), and mammalian (mouse and human) species. In all species studied, the alpha(3) Na(+),K(+)-ATPase isoform was nonuniformly expressed in peripheral ganglia and nerves. In spinal ganglia, only 5-20% of neurons expressed this isoform, and, in avian and mammalian species, these alpha(3) Na(+),K(+)-ATPase-expressing neurons belonged to a subpopulation of large DRG neurons. In ventral root fibers of pigeons, mice, and humans, the alpha(3) Na(+),K(+)-ATPase was abundantly expressed predominantly in small myelinated axons. In skeletal muscle samples from turtles, pigeons, mice, and humans, alpha(3) Na(+),K(+)-ATPase was detected in intramuscular myelinated axons and in profiles of nerve terminals associated with the equatorial and polar regions of muscle spindle intrafusal fibers. These results show that the expression profiles for alpha(3) Na(+),K(+)-ATPase in the peripheral nervous system of a wide variety of vertebrate species are similar to the profile of rats and suggest that stretch receptor-associated expression of alpha(3) Na(+),K(+)-ATPase is preserved through vertebrate evolution.

Animals↗
PubMed2006

Neuroanatomy of the brachial plexus: the missing link in the continuity between the central and peripheral nervous systems.

The brachial plexus is a complex network of nerves which extends from the neck to the axilla and which supplies motor, sensory, and sympathetic fibers to the upper extremity. Generally it is formed by the union of the ventral primary rami of the spinal nerves, C5-C8 and T1, the so-called "roots" of the brachial plexus. The goal here is to examine the neural architecture of the brachial plexus. The most constant arrangement of nerve fibers will be delineated, and then the predominant variations in neural architecture will be defined, particularly the prefixed and postfixed plexus, as well as the microanatomy and anatomy of the major terminal branches of the plexus. Multiple tracts connect many parts of the nervous system, and multiple ascending and descending tracts connect the peripheral nervous system (PNS) and lower spinal centers with the brain. This reflects that the nervous system is able to extract different pieces of sensory information from its surroundings and encode them separately, and that it is able to control specific aspects of motor behavior using different sets of neurons. Examination of the major sensory or motor pathways reveals a highly and tightly organized nervous system. In particular, at each of many levels, we see fairly exact maps of the world within the brain. In an effort to understand the functional neuroanatomy of the brachial plexus, this paper will focus briefly on the nervous connections of the nerves of the upper extremity with the brain. The goal here is to better understand "what the brain sees" after nerve injury and repair.

Afferent Pathways↗
PubMed2003

[The role of the peripheral nervous system damage in clinical picture of multiple sclerosis].

Multiple sclerosis (MS) was believed to be an autoimmune disease of central nervous system (CNS). Recently, several studies showing early involvement of peripheral nervous system (PNS) in MS pathological process have been published. This review own analyzer and published clinical and paraclinical data on PNS pathology in MS patients and CNS damage in patients with chronic inflammatory demyelinating polyneuropathy. Different mechanisms of the damage of PNS may explain different clinical manifestation of PNS involvement in MS.

Adjuvants, Immunologic↗
PubMed1998

Pathogenesis of Lyme neuroborreliosis in the rhesus monkey: the early disseminated and chronic phases of disease in the peripheral nervous system.

The histopathologic and immunohistochemical features of early and late neuroborreliosis of the peripheral nervous system were investigated in rhesus macaques infected with the JD1 strain of Borrelia burgdorferi. Infection was proven by culture or polymerase chain reaction analysis of skin biopsies and indirectly by Western blot analysis. Three months after infection, neuritis involving multiple nerves was the most consistent neurologic manifestation. Both macrophages and B lymphocytes but not T lymphocytes were present in the cellular infiltrates. Axonal structures surrounding infiltrates had changes consisting of demyelination and axonal phagocytosis. Some of the Schwann cells in lesions stained with anti-nitrotyrosine and anti-tumor necrosis factor-alpha antibodies. B. burgdorferi, or antigens thereof, were visualized immunohistochemically within macrophages. Forty-six months after infection, the most common changes were regenerative, whereas neuritis was infrequent. Aberrant axonal regeneration, irregularly sized myelinated fibers, and fibrosis were frequently observed. Possible mechanisms to explain the appearance and subsidence of Lyme neuritis are discussed.

Animals↗
PubMed1994

[A case of acute disseminated encephalomyelitis with pathologically-proven acute demyelinating lesion in the peripheral nervous system].

We present a case of acute severe demyelination affecting both CNS and PNS with pathological evidence. A 62-year-old man presented with acute onset of coma preceded by common cold-like symptoms. He was diagnosed as acute disseminated encephalomyelopathy (ADEM), and died of brain herniation in two weeks. At autopsy, in addition to severe demyelination of the white matter of the central nervous system, there was widespread acute demyelinating process in the peripheral nervous system. Myelin destruction by macrophage was most conspicuous in the spinal nerve root with preservation of the axon cylinder. So far the association of hypertrophic demyelinating neuropathy was reported in cases of multiple sclerosis. However, there have not been any papers in which substantial involvement of both CNS and PNS in cases of ADEM except for the clinical report by Amit. Antigenic cross-reactivity between CNS and PNS against myelin proteins or other antigens like glycolipid may elicit similar immune responses producing demyelination.

Acute Disease↗
PubMed1997

Experimental autoimmune encephalomyelitis: the antigen specificity of T lymphocytes determines the topography of lesions in the central and peripheral nervous system.

Recent studies on autoimmune encephalomyelitis and neuritis reveal that many different antigens of the central (CNS) and peripheral nervous system may become targets of an encephalitogenic T-cell response. The aim of this study was to determine the influence of T-cell specificity on the pathology of autoimmune-mediated inflammation in the nervous system. Autoimmune encephalomyelitis was induced by the adoptive transfer of CD4+ T-line cells specific for either myelin basic protein, myelin oligodendrocyte glycoprotein (MOG), myelin-associated glycoprotein, S100 beta, or glial fibrillary acidic protein. The severity of the inflammatory response was antigen- and dose-dependent. With the exception of MOG-specific T-line cells, all autoreactive T-cell lines induced inflammation in the CNS and peripheral nervous system. In the myelin-basic-protein-mediated model, the spinal cord was most severely affected with only minor inflammation in the forebrain. In contrast, both MOG- and myelin-associated-glycoprotein-specific T cells induced a far higher density of lesions in the periventricular and cerebellar white matter. S100 beta- and glial-fibrillary-acidic-protein-specific T cells mediated particularly severe inflammation in the gray matter. In addition to these topographic differences, antigen specificity also influenced the extent of both parenchymal inflammation and macrophage activation in the CNS. However, irrespective of the specificity or number of T cells transferred, the major neuropathologic correlate with disease severity was the absolute number of activated macrophages recruited into the CNS parenchyma (r = 0.9; p < 0.0001). This study suggests that differences in lesion distribution in multiple sclerosis patients may reflect differences in the antigen specificity of an encephalitogenic T-cell response.

Amino Acid Sequence↗
PubMed2006

Expression of doublecortin in tumours of the central and peripheral nervous system and in human non-neuronal tissues.

Doublecortin is a microtubule-associated phosphoprotein involved in neuronal migration and differentiation expressed in migrating neuroblasts in the central nervous system. We systematically analysed doublecortin expression in 179 tumours of the central and 65 tumours of peripheral nervous system as well as in 74 different non-neuronal tissues to evaluate the specificity of doublecortin as a marker for neuronal differentiation in glioneuronal tumours. Glioneuronal tumours and oligodendrogliomas grade II and III uniformly showed a high intensity and frequency of doublecortin staining, whereas intermediate doublecortin expression was observed in astrocytic tumours of grade II-IV. In pilocytic astrocytomas and ependymomas only scattered doublecortin positive cells were detected. In the peripheral nervous system, doublecortin expression was found in neurofibroma but was absent in schwannoma. Double staining of tumour tissue revealed co-expression of doublecortin and neurofilament in cells of gangliocytomas and gangliogliomas and co-expression of doublecortin with S100 protein or GFAP in glial tumours, respectively. In a tissue array comprised of 74 different normal non-neuronal human tissues, doublecortin expression was demonstrated in epithelia of the kidney, liver, salivary glands and duodenum among others. Interestingly, doublecortin expression could not be shown in brain metastases of tumours originating from these tissues. Immunohistochemical data was further corroborated by Western blot analysis and reverse transcription polymerase chain reaction. In conclusion, doublecortin can be regarded as specific neuronal marker only in normal developing brain, but lacks specificity in glioneuronal and glial tumours and other non-neuronal human tissues where it is expressed in a wide variety of tumours and tissues.

Biomarkers, Tumor↗