PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Peripheral Nervous System”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed1976

Degeneration in central and peripheral nervous systems produced by pure n-hexane: an experimental study.

Rats intoxicated with pure n-hexane, either by repetitive subcutaneous injection or by continuous inhalation, developed clinical and/or pathological evidence of peripheral neuropathy. Animals intoxicated by inhalation (400-600 ppm) developed clinical signs after forty-five days and displayed giant axonal swellings and fibre degeneration both in the central and peripheral nervous systems. The changes were most strking in tibial nerves supplying calf muscles and in selected areas of the cerebellum, medulla and spinal cord. In contrast to the usual picture associated with dying-back disease, the distal regions of proximal nerve fibres supplying calf muscles degenerated before equivalent regions of longer fibres supplying the hindfeet. The relevance of the central nervous changes to individuals recovering from toxic neuropathies and the need for a reduction of the present Threshold Limit Value (500 ppm) for human exposure are discussed.

Alkanes↗
PubMed1993

Long-term effects of vincristine on the peripheral nervous system.

Forty patients with Non-Hodgkin's Lymphoma treated with vincristine between 1984 and 1990 (cumulative dose 12 mg in 18-24 weeks) were investigated in order to evaluate the long term effects of vincristine on the peripheral nervous system. The patients were interviewed with emphasis on neuropathic symptoms. Physical and quantitative sensory examination with determination of vibratory perception and thermal discrimination thresholds were performed, four to 77 months (median 34 months) after vincristine treatment. Twenty-seven patients reported neuropathic symptoms. In 13 of these 27 patients symptoms were still present at the time of examination. In these patients sensory signs and symptoms predominated. In the other 14 patients symptoms had been present in the past. Symptoms persisted maximally 40 months since cessation of therapy. There was no age difference between patients with and without complaints at the time of examination. Normal reflexes were found in two third of patients. Neuropathic complaints were not very troublesome on the long term. It is concluded that with the above mentioned vincristine dose schedule signs and symptoms of vincristine neuropathy are reversible for a great deal and prognosis is fairly good.

Adult↗
PubMed2004

Evolution of the larval peripheral nervous system in Drosophila species has involved a change in sensory cell lineage.

A key challenge in evolutionary biology is to identify developmental events responsible for morphological changes. To determine the cellular basis that underlies changes in the larval peripheral nervous system (PNS) of flies, we first described the PNS pattern of the abdominal segments A1-A7 in late embryos of several fly species using antibody staining. In contrast to the many variations reported previously for the adult PNS pattern, we found that the larval PNS pattern has remained very stable during evolution. Indeed, our observation that most of the analysed Drosophilinae species exhibit exactly the same pattern as Drosophila melanogaster reveals that the pattern observed in D. melanogaster embryos has remained constant for at least 40 million years. Furthermore, we observed that the PNS pattern in more distantly related flies (Calliphoridae and Phoridae) is only slightly different from the one in D. melanogaster. A single difference relative to D. melanogaster was identified in the PNS pattern of the Drosophilinae fly D. busckii, the absence of a specific external sensory organ. Our analysis of sensory organ development in D. busckii suggests that this specific loss resulted from a transformation in cell lineage, from a multidendritic-neuron-external-sensory-organ lineage to a multidendritic-neuron-solo lineage.

Animals↗
PubMed2000

Reflex effects of vertebral subluxations: the peripheral nervous system. An update.

BACKGROUND: The traditional chiropractic vertebral subluxation hypothesis proposes that vertebral misalignment cause illness, disease, or both. This hypothesis remains controversial. OBJECTIVE: To briefly review and update experimental evidence concerning reflex effects of vertebral subluxations, particularly concerning peripheral nervous system responses to vertebral subluxations. DATA SOURCE: Information was obtained from chiropractic or scientific peer-reviewed literature concerning human or animal studies of neural responses to vertebral subluxation, vertebral displacement or movement, or both. CONCLUSION: Animal models suggest that vertebral displacements and putative vertebral subluxations may modulate activity in group I to IV afferent nerves. However, it is not clear whether these afferent nerves are modulated during normal day-to-day activities of living and, if so, what segmental or whole-body reflex effects they may have.

Animals↗
PubMed2001

Associations of tibia lead, DMSA-chelatable lead, and blood lead with measures of peripheral nervous system function in former organolead manufacturing workers.

BACKGROUND: The goals of the present study were to compare and contrast associations of blood lead, DMSA-chelatable lead, current tibia lead, and back-extrapolated "peak" tibia lead with four peripheral nervous system (PNS) sensory and motor function measures in older males with past exposure to organic and inorganic lead. METHODS: Data were collected from former organolead manufacturing workers with an average of 16 years since last occupational lead exposure. Current tibia lead levels were measured by (109)Cd x-ray fluorescence. Sensory pressure thresholds (index and pinky fingers) and pinch and grip strength were measured with the Pressure-Specified Sensory Device (PSSD). RESULTS: In adjusted analyses, none of the four lead biomarkers was associated with sensory pressure threshold of the index finger or pinch or grip strength. In contrast, all four biomarkers were associated (P < or = 0.10) with pressure threshold of the pinky finger. The final linear regression models accounted for a small proportion of the variance in the sensory (1-3%) and motor measures (10-21%). CONCLUSIONS: This study found no strong association between lead biomarkers and selected PNS sensory or motor function measures among former organolead manufacturing workers with no recent occupational exposure to lead. Previously reported CNS findings in this cohort suggest that the PNS may be less sensitive to the chronic toxic effects of lead in this dose range among adults. It is also possible that the PNS has a greater capacity for repair than does the CNS, or that the PNS measures were less sensitive for detection of lead-related health outcomes than were the CNS measures.

Adult↗
PubMed1999

Neurophysiological changes in the central and peripheral nervous system of streptozotocin-diabetic rats. Course of development and effects of insulin treatment.

Diabetes mellitus can affect both the peripheral and the central nervous system. However, central deficits are documented less well than peripheral deficits. We therefore compared the course of development of neurophysiological changes in the central and peripheral nervous systems in streptozotocin-diabetic rats. Sciatic nerve conduction velocities and auditory and visual evoked potentials were measured prior to diabetes induction, and then monthly after diabetes induction for 6 months. In addition, the effect of insulin treatment was examined. Treatment was initiated after a diabetes duration of 6 months and was continued for 3 months. During treatment, evoked potentials and nerve conduction were measured monthly. In a third experiment, conduction velocities in ascending and descending pathways of the spinal cord were examined after 3 and 6 months of diabetes. Impairments of sciatic nerve conduction velocities developed fully during the first 2-3 months of diabetes. In contrast, increased latencies of auditory and visual evoked potentials developed only after 3-4 months of diabetes, and progressed gradually thereafter. Insulin treatment, initiated 6 months after induction of diabetes, improved both nerve conduction velocities and evoked potential latencies. Conduction velocities in the spinal cord tended to be reduced after 3 months of diabetes and were significantly reduced after 6 months of diabetes. The present study demonstrates that in streptozotocin-diabetic rats the course of development of peripheral and central neurophysiological changes differs. Peripheral impairments develop within weeks after diabetes induction, whereas central impairments take months to develop. Insulin can reverse both peripheral and central neurophysiological alterations.

Animals↗
PubMed1998

Ultrastructural changes in the central and peripheral nervous system in the rat with experimental allergic encephalomyelitis.

The aim of the study was the evaluation of ultrastructural changes in rats central and peripheral nervous system after the introduction of experimental allergic encephalomyelitis (EAE) and after the treatment with spinal cord protein hydrolysate. Reduced structural disturbances in myelin were found after oral treatment with hydrolysate. In addition, the indications of remyelinization processes have been observed.

Animals↗
PubMedDate not supplied

The mouse mutation claw paw: forelimb deformity and delayed myelination throughout the peripheral nervous system.

We describe a murine autosomal recessive mutation claw paw (gene symbol clp), which in homozygous clp/clp mice produces striking abnormalities of limb posture within the first one or two postnatal days. Affected animals have delayed and abnormal myelination in the peripheral nervous system but not in the central nervous system, and also have persistently blocked myelination of small caliber axons that are myelinated in normal mice. Both abnormalities suggest that an important effect of the clp mutation is to impair the putative signaling mechanism by which an axon instructs a Schwann cell whether or not to myelinate it. The early onset of behavioral abnormalities in clp/clp mutant mice, as well as certain other features of the disorder, suggest that some effects of the clp gene are not accounted for by the pathological findings. The clp gene has been mapped to chromosome 7 near the Gpi-1 locus.

Animals↗
PubMed1986

Peripheral nervous system demyelination with herpes simplex virus.

Inoculation of the cornea or footpad with herpes simplex virus Type I (HSV) has been shown to produce subsequent encephalitis or myelitis respectively. Although Schwann cells become infected, there is no destruction or demyelination in the peripheral nervous system (PNS). Demyelination only occurs in the central nervous system. Previous studies have shown that the Schwann cells infected with HSV do not produce enveloped viral particles. The studies presented here demonstrate that microinjection of HSV into the sciatic nerve of mice causes focal mononuclear cell infiltration and demyelination seven days after injection. The Schwann cells in this model produced enveloped virus. These studies demonstrate that when HSV is introduced into the extracellular space of the PNS, demyelination occurs.

Animals↗
PubMed1988

Neurite extension of chicken peripheral nervous system neurons on fibronectin: relative importance of specific adhesion sites in the central cell-binding domain and the alternatively spliced type III connecting segment.

Fibronectin contains at least two domains that support cell adhesion. One is the central cell-binding domain that is recognized by a variety of cell types, including fibroblasts. The second, originally identified by its ability to support melanoma cell adhesion, is located in the alternatively spliced type III connecting segment (IIICS). Using specific adhesive ligands and inhibitory probes, we have examined the role of each of these domains in fibronectin-mediated neurite extension of neurons from chick embryo dorsal root and sympathetic ganglia. In studies using explanted ganglia, both fl3, a 75-kD tryptic fragment of human plasma fibronectin containing the central cell-binding domain, and CS1-IgG, a synthetic peptide-IgG conjugate containing the principal cell adhesion site from the IIICS, supported neurite outgrowth after adsorption onto the substrate. The maximal activities of fl3 and CSl-IgG were 45-55% and 25-30% that of intact fibronectin, respectively. Co-coating of the substrate with f13 and CS1-IgG produced an additive stimulation of neurite outgrowth, the extent of which approached that obtained with fibronectin. Similar results were obtained with purified neuronal cell preparations isolated by tryptic dissociation of dorsal root ganglia. In complementary studies, blockage of the adhesive function of either the central cell-binding domain (with mAb 333, an antiadhesive monoclonal antibody) or the IIICS (with CS1 peptide), resulted in approximately 60 or 30% reduction in fibronectin-mediated neurite outgrowth, respectively. When tested in combination, the inhibitory activities of mAb 333 and CSl were additive. From these results, we conclude that neurons from the peripheral nervous system can extend neurites on both the central cell-binding domain and the IIICS region of fibronectin, and that these cells are therefore the first normal, embryonic cell type shown to adhere to the IIICS. These results suggest that spatiotemporal fluctuations in the alternative mRNA splicing of the IIICS region of fibronectin may be important in regulation of cell adhesive events during development of the peripheral nervous system.

Animals↗
PubMed1982

Studies with antisera against peripheral nervous system myelin and myelin basic proteins. II. Immunohistochemical studies in cultures of rat dorsal root ganglion neurons and Schwann cells.

Antiserum against rat peripheral nervous system (PNS) myelin contained immunoglobulins which bound preferentially to the extracellular surfaces of myelin-related Schwann cells in intact cultures of dorsal root ganglion (DRG) neurons and Schwann cells, while antiserum against basic protein (BP) from central nervous system myelin or the PNS basic protein P2 did not. We demonstrate the presence of PNS myelin proteins P1 (identical to BP) and P2 by immunoperoxidase techniques in DRG cultures that had been treated to disrupt cellular membranes. These observations suggest that P1 and P2 are not exposed on the extracellular surfaces of myelin-related Schwann cells in culture. The results also support the hypothesis concerning the possible mechanisms by which anti-PNS myelin serum demyelinates DRG cultures, while anti-BP serum and anti-P2 serum do not.

Animals↗
PubMed2006

X-Linked inhibitor of apoptosis protein gene-based neuroprotection for the peripheral nervous system.

OBJECTIVE: The recently discovered X-linked inhibitor of apoptosis protein (XIAP) is among the most potent inhibitors of programmed cell death. In the current experiment, we examine the potential of adenoviral XIAP gene delivery to protect neurons of the peripheral nervous system using in vitro models of amyotrophic lateral sclerosis (ALS) and diabetic neuropathy. METHODS: XIAP complementary deoxyribonucleic acid was fused in frame with the green fluorescent protein sequence and cloned into a first generation adenoviral vector. The impact of XIAP gene expression on glutamate-induced apoptosis was measured in the neuronal SH-SY5Y cell line with immunohistochemistry for active caspase-3 and with cell density assays. Next, the effect of XIAP expressing neurons on the survival of uninfected neighboring neurons was measured. Finally, the impact of XIAP gene expression on glutamate-induced apoptosis was assessed in embryonic motor neuron and dorsal root ganglion cultures. RESULTS: XIAP gene expression reduced the percentage of active caspase-3 positive SH-SY5Y neurons and preserved cell density after glutamate exposure. In heterogeneously infected cultures, cells infected with XIAP were protected, but uninfected neighboring cells were not. In primary E15 models, inhibition of proapoptotic effects was demonstrated after glutamate insult in motor neurons and glucose insult in dorsal root ganglion cells. CONCLUSION: XIAP gene delivery through the neurosurgical delivery of viral vectors may provide a means for neuroprotection in ALS and diabetic neuropathy.

Amyotrophic Lateral Sclerosis↗
PubMed1998

Control of noradrenergic differentiation and Phox2a expression by MASH1 in the central and peripheral nervous system.

Mash1, a mammalian homologue of the Drosophila proneural genes of the achaete-scute complex, is transiently expressed throughout the developing peripheral autonomic nervous system and in subsets of cells in the neural tube. In the mouse, targeted mutation of Mash1 has revealed a role in the development of parts of the autonomic nervous system and of olfactory neurons, but no discernible phenotype in the brain has been reported. Here, we show that the adrenergic and noradrenergic centres of the brain are missing in Mash1 mutant embryos, whereas most other brainstem nuclei are preserved. Indeed, the present data together with the previous results show that, except in cranial sensory ganglia, Mash1 function is essential for the development of all central and peripheral neurons that express noradrenergic traits transiently or permanently. In particular, we show that, in the absence of MASH1, these neurons fail to initiate expression of the noradrenaline biosynthetic enzyme dopamine beta-hydroxylase. We had previously shown that all these neurons normally express the homeodomain transcription factor Phox2a, a positive regulator of the dopamine beta-hydroxylase gene and that a subset of them depend on it for their survival. We now report that expression of Phox2a is abolished or massively altered in the Mash1-/- mutants, both in the noradrenergic centres of the brain and in peripheral autonomic ganglia. These results suggest that MASH1 controls noradrenergic differentiation at least in part by controlling expression of Phox2a and point to fundamental homologies in the genetic circuits that determine the noradrenergic phenotype in the central and peripheral nervous system.

Animals↗
PubMedDate not supplied

Peripheral nervous system involvement in essential cryoglobulinemia and nephropathy.

The clinical and neurophysiological features of 23 patients affected by essential cryoglobulinemia (EC) have been studied. It was possible to perform sural nerve biopsy in 3 cases. Six patients were found to be affected by a peripheral neuropathy, according to the WHO criteria, while in 8 other patients clinical and neurophysiological signs of a milder peripheral nervous system (PNS) involvement were evident. The incidence of PNS involvement seems to be high (60.9%). Neurophysiological and histological studies were indicative of a mainly axonal damage.

Action Potentials↗