[Critically ill polyneuropathy].

B Neundörfer

doi:10.1055/s-2007-996350

Home/Archive/PubMed

PubMed · 9445837

[Critically ill polyneuropathy].

B Neundörfer

View original source ↗Export metadata ↓

Abstract

"Critically ill" polyneuropathy occurs in patients with artificial respiration. It is more frequent in men than in women. The most frequent underlying diseases, in the course of which CIP was found, were pneumonias, traumas and major surgery. In most cases sepsis and/or multiple organ dysfunction syndrome can be observed. Symmetrical motor polyneuropathy is the typical clinical pattern. In many cases the thoracic muscles are also involved. In some cases facial pareses and ophthalmoplegia may occur. Sensory disturbances are rather rare. The EMG often shows a myopathic pattern in addition to the neuropathic pattern. Morphologically, CIP is an axonal degeneration. The rate of lethality is high. In surviving patients there is a 50% chance of full remission.

Explore related subjects

Axons Critical Illness Electromyography Female Humans Male Multiple Organ Failure Muscle, Skeletal Neurologic Examination Polyneuropathies Prognosis Respiration, Artificial Retrograde Degeneration Risk Factors Sepsis English Abstract Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

B Neundörfer. 1997. [Critically ill polyneuropathy].. https://doi.org/10.1055/s-2007-996350

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels.

Diffuse axonal injury (DAI) is one of the most common and important pathologies resulting from the mechanical deformation of the brain during trauma. It has been hypothesized that calcium influx into axons plays a major role in the pathophysiology of DAI. However, there is little direct evidence to support this hypothesis, and mechanisms of potential calcium entry have not been explored. In the present study, we used an in vitro model of axonal stretch injury to evaluate the extent and modulation of calcium entry after trauma. Using a calcium-sensitive dye, we observed a dramatic increase in intra-axonal calcium levels immediately after injury. Axonal injury in a calcium-free extracellular solution resulted in no change in calcium concentration, suggesting an extracellular source for the increased post-traumatic calcium levels. We also found that the post-traumatic change in intra-axonal calcium was completely abolished by the application of the sodium channel blocker tetrodotoxin or by replacement of sodium with N-methyl-d-glucamine. In addition, application of the voltage-gated calcium channel (VGCC) blocker omega-conotoxin MVIIC attenuated the post-traumatic increase in calcium. Furthermore, blockade of the Na(+)-Ca(2+) exchanger with bepridil modestly reduced the calcium influx after injury. In contrast to previously proposed mechanisms of calcium entry after axonal trauma, we found no evidence of calcium entry through mechanically produced pores (mechanoporation). Rather, our results suggest that traumatic deformation of axons induces abnormal sodium influx through mechanically sensitive Na(+) channels, which subsequently triggers an increase in intra-axonal calcium via the opening of VGCCs and reversal of the Na(+)-Ca(2+) exchanger.

Axons↗

PubMed2001

A novel method for correlating internal and external structure of individual myelinated nerve fibres.

A new method is described that enables longitudinal and cross sections of an individual nerve fibre to be cut at multiple specified sites along the fibre by the use of a unique marker system. In this way the internal structure of the fibre can be correlated with the external appearance. Individual myelinated nerve fibres are teased apart in epoxy resin and mounted onto a carbon-coated slide, and after orientation and marking of specific sites of interest are snap frozen to liberate the orientated and marked fibres for embedding on the surface of an epoxy resin block for subsequent longitudinal or transverse sectioning. This method is particularly useful for the correlative study of the myelin-axon relationships.

Axons↗

PubMed2001

Expression of calbindin D28K in the dopaminergic mesotelencephalic system in embryonic and fetal human brain.

A subset of tyrosine-hydroxylase (TH) neurons of the substantia nigra (A9) containing calbindin D28K (CaBP) appeared to be less vulnerable to cell death induced by Parkinson's disease than the subset containing dopamine (DA) alone. Because grafting procedures of fetal human neurons are increasingly used in the therapy of Parkinson's disease, it is important to study the development of DA neurons coexpressing CaBP. In humans, the genesis of TH immunoreactivity of A9, of the ventral tegmental area (A10), and of the retrorubral area (A8) occurred during a 2-week period from the 4. 5th gestational week (g.w.) in the ventricular zone of the floor plate and the contiguous basal plate of the mesencephalon and diencephalon, i.e., the prosomeres p1-p3. Double-immunolabeled TH-CaBP neurons were detected from 5.5 g.w. on, in the first wave of DA neuron's migration, and were observed in their final residence in the dorsal A9 by 10.5 g.w. Calretinin immunoreactivity was expressed in TH-immunoreactive (IR) neurons from 10.5 g.w. on. Ascending TH-CaBP-IR axons were observed toward the telencephalon from 6-7 g.w. , reaching the anlage of the nucleus accumbens and amygdaloid complex at 10.5 g.w., but were not detected in the ganglionic eminence at this latter stage. Dopaminergic patches were detected at 13 g.w. in the anlage of the putamen, but no TH-CaBP-IR fibers were observed in the matrix at this stage. In conclusion, even if CaBP immunoreactivity was detected in TH-IR cell bodies during the embryonic period, the TH-CaBP-IR axonal terminal was observed earlier in some limbic-related areas than in the matrix compartment of the basal ganglia in humans.

Axons↗