Overactive bladder as a dysfunction of the autonomic nervous system - A narrative review.
Autonomic nervous system
Dynamic pupillometry
Heart rate variability
Overactive bladder
Sympathetic skin response
Journal
European journal of obstetrics, gynecology, and reproductive biology
ISSN: 1872-7654
Titre abrégé: Eur J Obstet Gynecol Reprod Biol
Pays: Ireland
ID NLM: 0375672
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
05
07
2021
revised:
13
10
2021
accepted:
25
01
2022
pubmed:
19
2
2022
medline:
23
3
2022
entrez:
18
2
2022
Statut:
ppublish
Résumé
Overactive bladder (OAB) is a common condition with increasing prevalence. However, its aetiology is not fully understood. The main symptoms are sudden urge to urinate, with or without incontinence; increased daytime frequency; and nocturia. OAB-like symptoms can be caused by a number of diseases, including urinary tract infections, neurologic and metabolic diseases, and neoplasms. The final diagnosis is made after excluding all the abovementioned factors. Autonomic nervous system (ANS) dysfunction has also been identified as a possible cause of so-called 'idiopathic OAB'. In order to check this hypothesis, many studies have measured ANS activity in patients with OAB by means of dynamic pupillometry, heart rate variability and sympathetic skin response. These non-invasive, fast and reliable tests assess ANS function - both sympathetic and parasympathetic - indirectly. ANS activity depends on many factors, such as age, gender, baseline level and a number of environmental stimuli. An imbalance between the sympathetic nervous system and the parasympathetic nervous system can lead to homeostatic disruption and the subsequent development of many diseases, including OAB. This narrative review summarizes the most important studies concerning the putative influence of the ANS on OAB symptoms.
Identifiants
pubmed: 35180512
pii: S0301-2115(22)00031-8
doi: 10.1016/j.ejogrb.2022.01.022
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
102-107Informations de copyright
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