PFR is a physical therapy that should be considered as the initial treatment in patients with fecal incontinence. An improvement can be expected in up to 67 percent of patients. Initial good results can predict overall outcome.

Anal sphincter tears are common in patients presenting with rectal prolapse and faecal incontinence. The faecal incontinence associated with prolapse appears to be multifactorial in aetiology. Anal sphincter defects are likely to contribute to persistent faecal incontinence or recurrence following rectal prolapse. Endoanal ultrasound derived knowledge of anal sphincter injury may guide surgical management in problematic cases.

Endoanal ultrasound was used in the investigation of 26 patients with faecal incontinence. In each case images of the anal sphincter were taken at rest and during contraction or squeezing (dynamic). Better definition of the normal anal sphincter or anal sphincter defects was obtained in 16 (62%) of the patients with imaging during contraction. In eight of the 13 patients with a sphincter defect there was better definition of the defect and increased separation of the ends of the sphincter during contraction. Imaging during contraction improves diagnostic accuracy and is a useful adjunct with endoanal ultrasound.

No abstract

Understanding how the enteric nervous system controls gastrointestinal function requires an account of the different classes of nerve cells present in the gut wall. Accurately quantifying immunohistochemically identified neurones, would make it possible to characterize changes underlying disorders such as slow transit constipation. Until now, quantification of classes of neurones has relied on antisera to Neuron Specific Enolase (NSE) or Protein Gene Product 9.5 (PGP9.5), however, both stain nerve fibres, making accurate counting of cell bodies unreliable. Anti‐Human Neuronal Protein Antibodies (Hu) were originally isolated from patients with paraneoplastic encephalomyelitis and paraneoplastic neuropathies and have been tested here as a marker for all neurons in the human myenteric plexus. Specimens of colon were obtained from the uninvolved margins of specimens from 10 patients undergoing elective surgery for carcinoma and were either fixed fresh, or maintained in organ culture for 3 days. Nerve cell bodies were identified using double labelling techniques to compare Hu (mouse monoclonal anti Hu, Chemicon, CA) and NSE antisera for quantification. In both fresh and cultured tissue, neuronal somata were readily identified using the Hu antibody but few axons or varicosities were labelled. In double‐stained preparations, Hu labelling consistently revealed more nerve cell bodies than NSE. In addition, counting was more reliable due to the lack of staining of nerve fibres which obscured some cell bodies in NSE or PGP9.5‐stained preparations. We used preparations triple labeled with antisera raised against nitric oxide synthase (NOS), choline acetyltransferase (ChAT) and Hu, to determine the size of these major populations. Approximately 47 + 1% (mean + SD, n= 4) of all myenteric nerve cell bodies were immunoreactive for NOS and 52 + 2% were immunoreactive for ChAT. In each preparation, approximately 8 + 2% of NOS cells also contained ChAT. In 5 + 1% of neurons, neither NOS nor ChAT was detectable. Anti‐Hu antiserum makes possible reliable labeling of all enteric neurons in the human colon, allowing accurate quantification of different populations of enteric neurones in normal and diseased tissue.