PubMed HealthSearch

PubMed · 8273392

Electrorectography in chronic proctitis.

Abstract

Rectal electrical activity, measured by electrorectography (ERG), was studied in 18 patients with chronic proctitis (11 ulcerative and 7 bilharzial proctitis). Mean age was 36.6 +/- 9.4 (SD) years. Eight healthy volunteers were included as controls. Monopolar recordings were made from silver-silver chloride electrodes situated 1 cm from the tip of the catheter, which was applied to the rectal mucosa. Signals from the electrode were displayed on a U-V recorder. Rectal neck and rectal pressures were recorded simultaneously. Pacesetter potentials (PP) were also recorded from all subjects. The healthy volunteers had a mean frequency of 2.6 +/- 0.6 cycles per minute (cpm), an amplitude of 2.4 +/- 0.5 mV, and a velocity of 4.3 +/- 0.5 cm/sec. The potentials had the same frequency and regular rhythm when the test was repeated and were followed randomly by bursts of action potentials (AP). The rectal pressure increased simultaneously with the AP. In the proctitis patients the PP frequency was higher than normal (mean 8.2 +/- 1.6 cpm in patients with bilharziasis and 8.9 +/- 2.1 cpm in those with ulcerative proctitis) (p < 0.001), whereas the amplitude and velocity were lower than normal (p < 0.05 and p < 0.01, respectively). APs had higher frequency and amplitude and were accompanied by higher rectal pressure than in the normal volunteers. The increased PP, or tachyrectia, may be due to rectal wall or rectosigmoid pacemaker irritation caused by proctitis, whereas the diminished amplitude and velocity may be caused by a diseased rectal wall. The increased AP frequency and amplitude seem to cause increased rectal contractile activity with a resulting tenesmus.(ABSTRACT TRUNCATED AT 250 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Shafik. Electrorectography in chronic proctitis.. https://doi.org/10.1007/bf01659142

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

KEEP EXPLORING

Related citations

Primary cortical representation of sounds by the coordination of action-potential timing.

Cortical population coding could in principle rely on either the mean rate of neuronal action potentials, or the relative timing of action potentials, or both. When a single sensory stimulus drives many neurons to fire at elevated rates, the spikes of these neurons become tightly synchronized, which could be involved in 'binding' together individual firing-rate feature representations into a unified object percept. Here we demonstrate that the relative timing of cortical action potentials can signal stimulus features themselves, a function even more basic than feature grouping. Populations of neurons in the primary auditory cortex can coordinate the relative timing of their action potentials such that spikes occur closer together in time during continuous stimuli. In this way cortical neurons can signal stimuli even when their firing rates do not change. Population coding based on relative spike timing can systemically signal stimulus features, it is topographically mapped, and it follows the stimulus time course even where mean firing rate does not.

Action Potentials

A primary acoustic startle pathway: obligatory role of cochlear root neurons and the nucleus reticularis pontis caudalis.

Davis et al. (1982) proposed a primary acoustic startle circuit in rats consisting of the auditory nerve, posteroventral cochlear nucleus, an area near the ventrolateral lemniscus (VLL), nucleus reticularis pontis caudalis (PnC), and spinal motoneurons. Using fiber-sparing lesions, the present study reevaluated these and other structures together with the role of neurons embedded in the auditory nerve [cochlear root neurons (CRNs)], recently hypothesized to be involved in acoustic startle. Small electrolytic lesions of the VLL of ventrolateral tegmental nucleus (VLTg) failed to eliminate startle. Large electrolytic lesions including the rostral ventral nucleus of the trapezoid body (rVNTB) and ventrolateral parts of PnC or lesions of the entire PnC blocked startle. However, small NMDA-induced lesions of the rVNTB failed to block startle, making it unlikely that the rVNTB itself is part of the startle pathway. In contrast, NMDA lesions of the full extension of the ventrolateral part of the PnC blocked startle completely, suggesting that the ventrolateral part of the PnC is critically involved. Bilateral kainic acid lesions of CRNs also blocked the startle reflex completely, providing the first direct evidence for an involvement of CRNs in startle. This blockade probably was not caused by damage to the auditory nerve, because the lesioned animals showed intact compound action potentials recorded from the ventral cochlear nucleus. Hence, a primary acoustic startle pathway may involve three synapses onto (1) CRNs, (2) neurons in PnC, and (3) spinal motoneurons.

Action Potentials