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PubMedDate not supplied

Peripheral nervous system involvement in Klippel-Trenaunay syndrome.

Klippel-Trenaunay syndrome (KTS) is a rare congenital malformation of unknown etiology characterized by cutaneous hemangiomas, venous varicosities and bony and soft tissues hypertrophy usually affecting one limb. Several complex anomalies involving various organs and systems have been described, whereas involvement of the peripheral nervous system has rarely been reported in KTS. We describe the case of a 67-year-old woman with KTS and peripheral neuropathy related to the presence of epineurial microscopic arteriovenous anastomoses (AVA) and endoneurial vascular coils in sural nerve biopsy from both hypertrophic and non-hypertrophic limb. The maintenance of AVA has been proposed to be the cause of the hypertrophy. The observation in our patient of AVA in non-hypertrophic limb contrasts with this hypothesis.

Aged↗
PubMed2002

Post-infectious central and peripheral nervous system diseases complicating Mycoplasma pneumoniae infection. Report of three cases and review of the literature.

Three patients with a central and peripheral nervous system disease complicating a Mycoplasma pneumoniae (M. pn.) infection are presented. Patient 1 suffered from bilateral optic neuritis as well as acute Guillain-Barré syndrome recovering after plasmapheresis. The two other patients suffered from severe haemorrhagic leukoencephalitis (Hurst) which only could be contained by aggressive decompressive craniectomy with duraplasty. All three illnesses were clearly shown to be associated with M. pn. infection. Our three patients represent the full scale of central nervous (CNS) (cerebral and myelitic) as well as peripheral nervous system (PNS) (GBS, optic neuritis) manifestation of a disease caused by the same pathogenetic - post-infectious - mechanism; pathogenic CNS and PNS epitopes might be shared in post-infectious neurological disease following M. pn. infection.

Adolescent↗
PubMed1986

Antibodies to glycolipids in demyelinating diseases of the human peripheral nervous system.

Antibodies to complex glycolipids occur in patients with a variety of diseases of the peripheral nervous system. Many patients with demyelinating neuropathy occurring in association with IgM paraproteinemia have a monoclonal antibody that reacts with a carbohydrate determinant shared between sulfate-3-glucuronyl paragloboside (SGPG), the myelin-associated glycoprotein and other glycoproteins of peripheral nerve. Other patients with neuropathy in association with IgM paraproteinemia have monoclonal antibodies reacting with carbohydrate determinants on various gangliosides. More than 80% of the IgM monoclonal antibodies from patients of this type that have been screened in our laboratory react with SGPG or ganglioside antigens. High levels of antibodies reacting with ganglioside antigens are also found in some patients with inflammatory neuropathies such as Guillain-Barré Syndrome and chronic relapsing inflammatory polyneuropathy. The pathogenetic significance of these antibodies reacting with acidic sphingoglycolipids remains to be established.

Antibodies↗
PubMed2004

A perfused rat brain model maintaining the connection between the central and peripheral nervous systems.

We have developed a new perfused brain model in rats. In this model, the cerebral circulation is separated from the systemic circulation, while the connections between the central and peripheral nervous systems are preserved. After bilateral common carotid, external carotid and vertebral artery ligation, bilateral common carotid arteries were cannulated to infuse rinsed human type O red blood cells mixed with modified Ringer's solution. To drain cerebral venous blood, external jugular veins were cannulated. Normal electrocortical activities were observed on electroencephalograms (EEGs) for more than 1h after the beginning of the perfusion. Somatosensory evoked potentials (SEPs) were also recorded. Direct infusion of pentylenetetrazol (PTZ) into the brain induced epileptic discharges on the EEGs and active dilation of cerebral arterioles, which was accompanied by an increase in systemic blood pressure (BP). The present model, in which we can change cerebral blood flow (CBF) and/or cerebral metabolism without directly affecting the systemic circulation, will provide a new approach to brain research.

Animals↗
PubMed1999

Neuronal age influences the response to neurite outgrowth inhibitory activity in the central and peripheral nervous systems.

Axonal regeneration is abortive in the central nervous system (CNS) of adult mammals, but readily occurs in the injured peripheral nervous system (PNS). Recent experiments indicate an important role for both intrinsic neuronal features and extrinsic substrate properties in determining the propensity for axonal regrowth. In particular, certain components of adult mammalian CNS myelin have been shown to exert a strong inhibitory influence on neurite outgrowth. To determine whether the potent neurite outgrowth inhibitory activity found in CNS myelin may also be present in PNS myelin and to study the influence of neuronal age on neurite outgrowth, we used a cryoculture assay in which dissociated rat dorsal root ganglion (DRG) neurons of different ages were challenged to extend neurites on fractionated myelin and cryostat sections from the PNS (sciatic nerve and myelin-free degenerated sciatic nerve) and CNS (optic nerve) of adult rats. The CNS environment of the optic nerve did not support E17 to P8 DRG neurite adhesion or outgrowth. E17 DRG neurons, unlike their older counterparts, however, were able to attach and extend neurites onto normal sciatic nerve and onto purified PNS myelin. In contrast, a vigorous neurite outgrowth response from all the ages tested was observed on the myelin-free degenerated sciatic nerve. These results indicate that PNS myelin is a potent inhibitor of neurite outgrowth and that DRG neuronal age plays an important role in determining the propensity for neurite outgrowth and regenerative response on inhibitory PNS and CNS substrata.

Animals↗
PubMed1993

Localization of GM1 and GD1b antigens in the human peripheral nervous system.

Serum antibodies against ganglioside GM1 and/or GD1b are frequently detected in autoimmune neuropathies such as multifocal motor neuropathy, IgM paraproteinemic neuropathy and Guillain-Barré syndrome. Some of them bind to GM1 or GD1b monospecifically but others cross-react with both of the antigens. In order to investigate the respective localizations of GM1 and GD1b antigens in the human peripheral nervous system, an immunohistochemical study was performed using two mouse monoclonal antibodies, each monospecific to GM1 and GD1b. GGR12, monospecific to GD1b, bound to neurons in dorsal root ganglia and sympathetic ganglia, and some parts of the peripheral myelin, mainly the paranodal areas. However GMB16, monospecific to GM1, did not bind to either neurons or myelin. GD1b antigen present on neurons and paranodal myelin in the peripheral nervous system can be a target antigen of serum antibodies in autoimmune neuropathies. Further effort should be made to reveal the localization of GM1 antigen in the human peripheral nervous system.

Antibodies, Monoclonal↗
PubMed1998

Steroid 5alpha-reductase type 1 immunolocalized in the rat peripheral nervous system and paraganglia.

Steroid 5alpha-reductase is an enzyme that converts a number of steroids with a C-4, 5 double bond and C-3 ketone to 5alpha-reduced metabolites. This enzyme has been suggested to play a role in brain development and myelination in the rat nervous system. In the present study, we examined the cellular and subcellular localization of the enzyme immunocytochemically in the rat peripheral nervous system and paraganglia using a polyclonal antibody against rat 5alpha-reductase type 1. Light and electron microscopical studies localized 5alpha-reductase in the Schwann cells of myelinated and unmyelinated nerve fibres, the satellite cells of the ganglia, the enteric glial cells and the supporting/sustentacular cells of the paraganglia. In the myelinated nerve fibres, immunoreactivity was observed in the outer loops, the nodes of Ranvier and the Schmidt-Lanterman incisures. Subcellularly, the immunoreactivity was localized in the cytoplasm of various glial cells. No immunoreactivity was observed in the myelin membrane, the axon or the neuronal perikaryon. These findings suggest that 5alpha-reductase is widely distributed in glial cells, and that, in addition to myelination, 5alpha-reduced steroids play a role in some glial functions in the peripheral nervous system.

Animals↗
PubMed2002

Gastric effects of galanin and its interaction with leptin on brainstem neuronal activity.

Galanin is a 29-amino acid peptide that is widely distributed throughout the central nervous system, peripheral nervous system, and gastrointestinal and genitourinary tracts. Leptin is a hormone secreted from adipose tissue and the gut and other tissues. In this study, using an in vitro neonatal rat preparation, we investigated the gastric effects of galanin and its interaction with leptin on nucleus tractus solitarius (NTS) neurons receiving gastric vagal inputs. We showed that peripheral gastric galanin (300 nM) produced a mean inhibition response of 53.2 +/- 2.1% compared with the control level of 100% (P < 0.01) in 27 of 58 neurons tested. A concentration-dependent effect of galanin on NTS neuronal activity was observed. The galanin receptor antagonist [galanin-(1-12)-Pro3-(Ala-Leu)2-Ala amide], or M40, significantly reversed the galanin-induced inhibition effect (P < 0.01). In contrast, we showed that the peripheral gastric effect of leptin (10 nM) produced a mean activation response of 167.4 +/- 8.2% compared with the control level. The NTS neurons that we recorded could respond to both galanin and leptin or respond to only one of them. Subsequently, we evaluated gastric interactions between galanin and leptin on NTS unitary activity when galanin (100 nM) and leptin (10 nM) were applied together in the gastric compartment. We observed that the effect of leptin when applied alone (168.8 +/- 7.7%) was reduced to 146.2 +/- 4.7% after coapplication of both compounds (P < 0.05 compared with leptin alone; P < 0.01 compared with galanin alone, 55.1 +/- 3.2%). Our data suggest that galanin modulates the leptin signals, which regulate the ingestive process in neonates.

Animals↗
PubMed1986

Neurotrophic activity in the central and peripheral nervous systems of the cat. Effects of injury.

Neurotrophic activity for ciliary ganglion neurons in culture was found in both central and peripheral nervous system of the cat. The activity found in extracts of spinal cord supported the survival of 100% of the test neurons during 24 h and was characterized by a slope of -56 +/- 13 in the linear portion of the dose-response curve. Sciatic nerve extract supported the survival of only 60% of the test neurons; it dose-response curve had a slope of -20 +/- 4. Extracts of meninges, spinal rootlets, dorsal root ganglia and muscle supported 100% of the test neurons; two slopes were observed in their dose-response curves, which coincided with those of spinal cord and sciatic nerve dose-response curves. The two different slopes may correspond to two different active molecules, tentatively denominated I and II, having distinct distributions in the assayed tissues. In the spinal cord, both direct injury and deafferentation led to increases in neurotropic activity. In the peripheral nervous system, transections leading to death of dorsal root ganglion neurons or to degeneration of their axons were accompanied by decreases in activity II. Activity I in dorsal roots and dorsal root ganglia was unaffected by injury and may be associated with non-neuronal cells or extracellular matrix components.

Animals↗
PubMed1991

Central and peripheral nervous system demyelination after infection with Mycoplasma pneumonia: evidence of an autoimmune process.

We have reported a unique case of multiple central and peripheral nervous system abnormalities after a serologically documented infection due to Mycoplasma pneumoniae. The evidence suggests that this organism is capable of causing demyelination, probably through an autoimmune process. This case may help to provide further insight into the pathogenetic mechanisms involved in other demyelinating diseases in which the triggering exogenous agent is unknown. Certainly this case demonstrated that both central and peripheral nervous system demyelination can occur and that patients with M pneumoniae infections should be observed closely for possible development of neurologic symptoms.

Adult↗
PubMed1999

Disease associated prion protein may deposit in the peripheral nervous system in human transmissible spongiform encephalopathies.

There is increasing evidence indicating involvement of the peripheral nervous system (PNS) in the pathogenesis of transmissible spongiform encephalopathies (TSEs). Immunocytochemically detectable deposits of TSE-specific abnormal prion protein (PrP(sc)) are considered as a surrogate marker for infectivity. We used anti-PrP immunocytochemistry to trace PrP(sc) deposition in spinal and enteric ganglia, and peripheral nerve in Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker disease (GSS), and fatal familial insomnia. Discrete PrP(sc) deposits were detectable only in a few posterior root nerve fibers in an adaxonal location in one of nine CJD and the one GSS patients examined. Follicular dendritic cells of the gut and enteric nervous system were not labeled. Thus, PrP(sc) may spread to the PNS in different forms of human prion disease. In contrast to our observations in experimental scrapie (Groschup et al., Acta Neuropathol, this issue), the deposits were scant. Possible explanations for this discrepancy comprise strain difference, or centripetal (experimental scrapie) versus centrifugal (sporadic and genetic human prion diseases) spread of PrP(sc), resulting in different patterns and amounts of PrP(sc) accumulation in the PNS.

Adult↗
PubMed1985

Comparison of the effects of detomidine and xylazine on some alpha 2-adrenoceptor-mediated responses in the central and peripheral nervous systems.

The effects of detomidine, a novel veterinary sedative analgesic, on some alpha 2-adrenoceptor-mediated responses in the central and peripheral nervous systems were studied. In pithed rats, detomidine was a very potent agonist at both pre- and postsynaptic alpha 2-adrenoceptors. Doses of 1.9 micrograms/kg and 6.5 micrograms/kg inhibited electrically induced tachycardia by 50% and increased mean blood pressure by 50 mmHg, respectively. In comparison, xylazine, though similar in specificity, was 40 times less potent than detomidine in this preparation. In unanaesthetized rats, detomidine both caused sedation and induced complex changes in body temperature. Low doses caused decreases in rectal temperature but these were reversed as the dose was increased. The decrease in rectal temperature could be blocked by yohimbine. Prazosin somewhat inhibited but did not eliminate the hyperthermia seen with the very high doses of detomidine. Xylazine caused much more severe falls in rectal temperature which could not be completely antagonized by alpha 2-adrenoceptor blockade. Both detomidine and xylazine caused dose-dependent mydriasis in anaesthetized rats, detomidine being about 10 times more potent than xylazine. The mydriatic effects of detomidine could be prevented by alpha 2- but not by alpha 1-adrenoceptor blockade. It is concluded that detomidine is a potent and rather specific alpha 2-adrenoceptor agonist in the central and peripheral nervous systems. In comparison with xylazine, detomidine has higher potency and greater specificity, especially at central alpha 2-adrenoceptors.

Animals↗
PubMed2001

Formation and effects of neuroactive steroids in the central and peripheral nervous system.

This chapter summarizes several observations that emphasize the importance of neuroactive steroids in the physiology of the central and peripheral nervous systems. A new, and probably important, concept is emerging: Neuroactive steroids not only modify neuronal physiology but also intervene in the control of glial cell functions. The data presented here underscore that (1) the mechanism of action of the various steroidal molecules may involve both classical (progesterone and androgens) and nonclassical steroid receptors [gamma-aminobutyric acid type A (GABAA) receptor], (2) in many instances, the actions of hormonal steroids are not due to their native molecular forms but to their 5 alpha- and 3 alpha,5 alpha-reduced metabolites, (3) several neuroactive steroids exert dramatic actions on the proteins proper of the peripheral myelin (e.g., glycoprotein Po and peripheral myelin protein 22), and (4) the effects of steroids and of their metabolites might have clinical significance in cases in which the rebuilding of the peripheral myelin is needed (e.g., aging, peripheral injury).

Androgens↗
PubMed1992

Expression of the T-lymphocyte activation gene, F5, by mature neurons.

F5 was first identified as an mRNA expressed by activated but not resting T-lymphocytes. Subsequent studies suggested that it also is selectively expressed by mature neurons. Although the F5 protein coding sequence is highly conserved, the function of the F5-encoded protein is unknown. The present studies were undertaken to define the anatomic distribution, cellular specificity, and developmental pattern of F5 mRNA expression in the mouse nervous system, addressing specifically the question of whether the expression pattern of F5 corresponds to that of known ligand-receptor or signal-transduction systems. The use of a nonradioactive in situ hybridization method and paraffin-embedded sections provided excellent morphological preservation and a high degree of cellular resolution. F5 mRNA was detected in the central nervous system, peripheral nervous system, and retina in cells having the location and morphological features of neurons. Combined in situ hybridization histochemistry for F5 mRNA and immunofluorescence staining for cell-specific markers confirmed that neurons expressed F5 mRNA but astrocytes did not. The neuronal expression of F5 mRNA had two interesting features. First, the level of expression appeared to correlate directly with the size of the neuronal perikarya, the length of the axonal projection, or the extent of dendritic arborization. Second, F5 mRNA appeared late in post-natal development. These observations are of interest because of preliminary data suggesting that F5 may function as a substrate for protein kinase C, which demonstrates a similar expression pattern in the nervous system.

Animals↗
PubMed2000

Mitochondrial myopathy diagnosis.

Oxidative phosphorylation (OXPHOS) accounts for approximately 95% of the adenosine triphosphate (ATP) produced by the cell. The central nervous system, peripheral nervous system, cardiac muscle, skeletal muscle, and smooth muscle are highly susceptible to dysfunction of this complex enzyme system. Although most OXPHOS diseases are multisystem disorders, the neuromuscular manifestations are often prominent and play an important role in patient diagnosis. To assist the neurologist in evaluating these complex patients, this article focuses on selected samples of OXPHOS diseases with identifiable neuromuscular abnormalities and presents an evaluation algorithm to facilitate patient diagnosis.

Algorithms↗