Asbjørn Mohr Drewes

Abnormal neuronal response to rectal and anal stimuli in patients with idiopathic fecal incontinence

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Abnormal neuronal response to rectal and anal stimuli in patients with idiopathic fecal incontinence. / Haas, S; Brock, C; Krogh, K; Gram, M; Lundby, L; Drewes, A M; Laurberg, S.

I: Neurogastroenterology and Motility, Bind 27, Nr. 7, 07.2015, s. 954-62.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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@article{cad606c24abf442a89a2b40ad5ce135f,
title = "Abnormal neuronal response to rectal and anal stimuli in patients with idiopathic fecal incontinence",
abstract = "BACKGROUND: The pathophysiology behind idiopathic fecal incontinence (IFI) is poorly understood. We hypothesized abnormal sensory pathways along the brain-gut axis as a key player in this disease, reflected in cortical evoked potentials (CEP) from mechanical stimuli of the rectum and the anal canal.METHODS: CEPs were recorded during repeated rapid balloon distensions of the rectum and anal canal in 19 women with IFI (mean age: 60 ± 14, mean Wexner score: 14.7 ± 2.9) and in 19 healthy women (mean age: 56 ± 11, mean Wexner score: 1.1 ± 1.3). Latencies, amplitudes and topography of CEPs elicited by rectal distension were compared between the groups. CEPs from both rectal and anal distensions were examined using spectral band analysis of single sweeps determining the relative amplitude of five spectral bands as a proxy of neuronal processing.KEY RESULTS: Compared to controls IFI patients had prolonged latency of CEPs from rectal distension by up to 27% (p < 0.001) while amplitudes and topography were similar (all p > 0.7 and all p > 0.23). Spectral analysis of CEPs from rectal distensions showed no difference (all p > 0.1) between groups. However, analysis of CEPs following distension of the anal canal resulted in abnormally low activity in beta (8-12 Hz; p < 0.001) band and high activity in the gamma (32-70 Hz; p = 0.04) band in patients.CONCLUSIONS & INFERENCES: IFI seems to be associated with impaired ano-rectal sensory functions in both the afferent fibers to the brain and the cortical processing of anal sensory pathways. This may play a central role for the pathogenesis of IFI.",
author = "S Haas and C Brock and K Krogh and M Gram and L Lundby and Drewes, {A M} and S Laurberg",
note = "{\textcopyright} 2015 John Wiley & Sons Ltd.",
year = "2015",
month = jul,
doi = "10.1111/nmo.12567",
language = "English",
volume = "27",
pages = "954--62",
journal = "Neurogastroenterology and Motility",
issn = "1350-1925",
publisher = "Wiley-Blackwell Publishing Ltd.",
number = "7",

}

RIS

TY - JOUR

T1 - Abnormal neuronal response to rectal and anal stimuli in patients with idiopathic fecal incontinence

AU - Haas, S

AU - Brock, C

AU - Krogh, K

AU - Gram, M

AU - Lundby, L

AU - Drewes, A M

AU - Laurberg, S

N1 - © 2015 John Wiley & Sons Ltd.

PY - 2015/7

Y1 - 2015/7

N2 - BACKGROUND: The pathophysiology behind idiopathic fecal incontinence (IFI) is poorly understood. We hypothesized abnormal sensory pathways along the brain-gut axis as a key player in this disease, reflected in cortical evoked potentials (CEP) from mechanical stimuli of the rectum and the anal canal.METHODS: CEPs were recorded during repeated rapid balloon distensions of the rectum and anal canal in 19 women with IFI (mean age: 60 ± 14, mean Wexner score: 14.7 ± 2.9) and in 19 healthy women (mean age: 56 ± 11, mean Wexner score: 1.1 ± 1.3). Latencies, amplitudes and topography of CEPs elicited by rectal distension were compared between the groups. CEPs from both rectal and anal distensions were examined using spectral band analysis of single sweeps determining the relative amplitude of five spectral bands as a proxy of neuronal processing.KEY RESULTS: Compared to controls IFI patients had prolonged latency of CEPs from rectal distension by up to 27% (p < 0.001) while amplitudes and topography were similar (all p > 0.7 and all p > 0.23). Spectral analysis of CEPs from rectal distensions showed no difference (all p > 0.1) between groups. However, analysis of CEPs following distension of the anal canal resulted in abnormally low activity in beta (8-12 Hz; p < 0.001) band and high activity in the gamma (32-70 Hz; p = 0.04) band in patients.CONCLUSIONS & INFERENCES: IFI seems to be associated with impaired ano-rectal sensory functions in both the afferent fibers to the brain and the cortical processing of anal sensory pathways. This may play a central role for the pathogenesis of IFI.

AB - BACKGROUND: The pathophysiology behind idiopathic fecal incontinence (IFI) is poorly understood. We hypothesized abnormal sensory pathways along the brain-gut axis as a key player in this disease, reflected in cortical evoked potentials (CEP) from mechanical stimuli of the rectum and the anal canal.METHODS: CEPs were recorded during repeated rapid balloon distensions of the rectum and anal canal in 19 women with IFI (mean age: 60 ± 14, mean Wexner score: 14.7 ± 2.9) and in 19 healthy women (mean age: 56 ± 11, mean Wexner score: 1.1 ± 1.3). Latencies, amplitudes and topography of CEPs elicited by rectal distension were compared between the groups. CEPs from both rectal and anal distensions were examined using spectral band analysis of single sweeps determining the relative amplitude of five spectral bands as a proxy of neuronal processing.KEY RESULTS: Compared to controls IFI patients had prolonged latency of CEPs from rectal distension by up to 27% (p < 0.001) while amplitudes and topography were similar (all p > 0.7 and all p > 0.23). Spectral analysis of CEPs from rectal distensions showed no difference (all p > 0.1) between groups. However, analysis of CEPs following distension of the anal canal resulted in abnormally low activity in beta (8-12 Hz; p < 0.001) band and high activity in the gamma (32-70 Hz; p = 0.04) band in patients.CONCLUSIONS & INFERENCES: IFI seems to be associated with impaired ano-rectal sensory functions in both the afferent fibers to the brain and the cortical processing of anal sensory pathways. This may play a central role for the pathogenesis of IFI.

U2 - 10.1111/nmo.12567

DO - 10.1111/nmo.12567

M3 - Journal article

C2 - 25903483

VL - 27

SP - 954

EP - 962

JO - Neurogastroenterology and Motility

JF - Neurogastroenterology and Motility

SN - 1350-1925

IS - 7

ER -