Central sensitization and severity of gastrointestinal symptoms in IBS, chronic pain syndromes, and inflammatory bowel disease, 2021, Midenfjord et al

Full title: Central sensitization and severity of gastrointestinal symptoms in irritable bowel syndrome, chronic pain syndromes, and inflammatory bowel disease

Abstract
Background
Central sensitization has been suggested as an explanation of the wide range of gastrointestinal and extraintestinal symptoms commonly seen in irritable bowel syndrome (IBS). In this study, the presence and level of central sensitization, and its association to gastrointestinal (GI) symptoms were explored in IBS in comparison with control groups.

Methods
We investigated patients with IBS (n = 215), chronic pain disorders (n = 36), and inflammatory bowel disease (IBD) (n = 40) and volunteers without chronic diseases (n = 112). The Central Sensitization Inventory (CSI) was translated and validated in Swedish and used together with the Highly Sensitive Person (HSP) scale to measure the presence and level of central sensitization. Furthermore, severity of GI symptoms (GSRS‐IBS and IBS‐SSS), and anxiety and depression (HAD) were determined.

Key results
The Swedish translation of CSI demonstrated excellent validity. Central sensitization, defined by validated cut‐off levels for CSI and HSP, was common in the whole cohort (40% and 28%) and in IBS (57% and 35%). Study participants with central sensitization had more severe GI symptoms, anxiety and depression, than participants without central sensitization. Strong associations were seen between CSI and GI symptom severity in the whole cohort (GSRS‐IBS: partial η2 = 0.455, p < 0.001; IBS‐SSS: partial η2 = 0.408, p < 0.001), with decreasing strength in patients with chronic pain, IBD, IBS, and volunteers.

Conclusion and Inferences
Central sensitization was common in IBS and associated with GI symptom severity, but with stronger associations in chronic pain disorders and IBD. This implies that other mechanisms may be of equal or greater importance for GI symptom severity in IBS.

Paywall, https://onlinelibrary.wiley.com/doi/10.1111/nmo.14156

 

(Note - I have not read the article itself, so may be being unfair, however ... ... ...)

I don’t understand how you can postulate a neurobiological phenomenon, but then only seek to study it using questionnaires. Where are the scans or blood tests that actually demonstrate the existence of the hypothesised phenomenon?

Further they are trying to define the relationship between that neurobiological phenomenon and biological and psychological symptoms, which in part are used as the evidence for the presence of the hypothesised phenomenon. This is as logical as studying the relationship between foot size and shoe size in wearers of high fashion brands, when your only measure of foot size is the size of shoe the person is wearing.

 

why are people talking about the hypothesis of central sensitization like it has been a proven fact as far as i have seen it is just a buzzword with zero evidence .

 

What does the CSI (cental sensitivization inventory ) look like ?
Another nuanced way with language ?

 

See The Development and Psychometric Validation of the Central Sensitization Inventory (CSI), 2013, Mayer et al

 

So a combination of leading questions similar to HADS combined with symptom presence and diagnoses.
A correlation fest for anything you want to find ?

 

The same way ME/CFS has been hypothesised as deconditioning combined with unhelpful beliefs. Say it loud enough, to enough people prepared and willing to believe it, and hey presto.