Prevalence of Central Sensitization in Postural Tachycardia Syndrome, 2026, Gabrielle T. Mathew, BS

Mij

Senior Member (Voting Rights)
Key Points
Question What is the prevalence of central sensitization syndrome in postural tachycardia syndrome (POTS)?

Findings This case-control study of 305 patients found a high prevalence (86.5%) of central sensitization syndrome in individuals with POTS.

Meaning These findings suggest that co-occurring central sensitization syndrome may exacerbate the disease burden in POTS; enhancing knowledge of this comorbidity could lead to more precise and comprehensive diagnostics and treatment strategies.

Abstract
Importance A previous study showed a high prevalence of central sensitization syndrome (CSS) in patients with autonomic symptoms. The prevalence of CSS in postural tachycardia syndrome (POTS), a form of dysautonomia, is unknown.

Objectives To analyze the prevalence of CSS in POTS.

Design, Setting, and Participants This case-control study included patients with a POTS diagnosis confirmed by autonomic testing at Brigham and Women’s Faulkner Hospital between 2022 and 2025. Data were analyzed from April to August 2025.

Exposure POTS with and without CSS.

Main Outcomes and Measures Central Sensitization Inventory (to assess central sensitization syndrome [CSS]), COMPASS-31 (autonomic symptoms), Neuropathy Total Symptom Score-6 (NTSS-6, sensory symptoms), PROMIS (global health), and autonomic testing (Valsalva maneuver, deep breathing, sudomotor function, and head-up tilt) with skin biopsies. Primary outcome was the central sensitization inventory score with secondary outcomes individual test performances.

Results This study included 305 patients with POTS, of whom 264 (86.6%) met criteria for CSS (mean [SD] age, 33.21 [10.75] years; 30 males [11.4%]; 234 females [88.6%]). Patients with CSS compared with those without CSS had longer duration of symptoms, were more frequently female, exhibited higher rates of anxiety (195 [73.9%] vs 20 [48.8%]; P = .002), depression (168 [63.6% vs 14 [34.1%]; P = .001), fibromyalgia (46 [17.4%] vs 0 [0%]; P = .008), irritable bowel syndrome (IBS, 90 [34.1%] vs 7 [17.1%]; P = .046), headaches (176 [66.7%] vs 12 [29.3 %]; P < .001), treatment with antihistamine medication (136 [51.5%] vs 13 [31.7%]; P = .03), psychiatric medication (163 [61.7%] vs 17 [41.5 %]; P = .02), pain medication (127 [48.1%] vs 8 [19.5%]; P = .001), and gastrointestinal medication (82 [31.1%] vs 5 [12.2 %]; P = .02), and had higher COMPASS-31 scores (51.93 [13.23] vs 31.18 [10.49]; P < .001), NTSS-6 scores (11.32 [4.86] vs 4.44 [3.32]; P < .001), NRS scores (3.26 [2.73] vs 0.54 [1.21]; P < .001), and worse PROMIS scores (20.36 [5.45] vs 27.96 [4.73]; P < .001). Autonomic tests showed lower orthostatic end-tidal carbon dioxide (27.59 [6.39] mm HG vs 29.46 [4.68] mm HG; P = .002) and a greater orthostatic decline in cerebral blood flow velocity (17.08 [8.72] cm/sec vs 13.68 [5.04] cm/sec; P < .001) in the CSS group. Both groups had similar prevalence of autonomic failure (223 [84.5%] vs. 33 [80.5%]; P = .67, mostly mild intensity), and abnormal skin biopsy (43% in both groups).

Conclusions and Relevance These findings suggest that CSS was common in patients with POTS and may represent a higher-order sequela of cerebrovascular, respiratory, and autonomic dysregulation. This heightened central processing may amplify symptom perception through altered interoceptive signaling. Central sensitization and autonomic impairment may coexist, and management should focus on both conditions.
LINK
 
Central Sensitization Inventory (to assess central sensitization syndrome [CSS])
That alone means this research may aswell go in the bin.

It’s absurd that commonly used questionnaires like the Central Sensitisation Inventory, includes questions such as “do you have Fibromyalgia/CFS” as points towards Central Sensitisation, as if it was already proven that these things were caused by central sensitisation.

Central Sensitisation Inventory
A score of 40 or more on this questionnaire:
View attachment 10677

For goodness sake - if I'm interpreting that statement correctly, the Neblett et al study found that 45% of participants who presumably had some well documented physical reason for their pain were labelled as having central sensitisation syndrome using this CSI Inventory. Does that not give anyone pause for thought before using the CSI?

The authors of the study that is the subject of this thread said this about the CSI:

We should probably have a thread for this nonsense questionaire.
 
These findings highlight that CSS is not merely a comorbid condition but potentially a downstream consequence of the complex cerebrovascular, respiratory, and autonomic perturbations intrinsic to POTS. Specifically, these results show strong links between CSS and symptom severity. The increased symptom burden seen in patients with POTS and CSS can be attributed to heightened central nervous system sensitivity to autonomic and sensory stimuli due to disrupted interoceptive processing pathways.

Enhanced interoception increases awareness of internal body sensation, such as heartbeat, vasomotor, and other autonomic activities. CSS has been linked to neuroinflammation in the brain and spinal cord characterized by microglial activation and the release of proinflammatory mediators. Imaging studies showed functional alterations in neural circuits that also regulate autonomic function, such as the anterior cingulate cortex, insula, and brainstem.

As key regions in interoceptive processing, the anterior cingulate and insula, may cause faulty processing of autonomic signals with a net effect of amplifying the symptoms burden. According to this concept neuroinflammation associated with central sensitization and altered proprioception may help explain the disproportionate symptom burden observed in the CSS group despite relatively mild abnormalities on standard autonomic testing. The validity of this concept can be tested by targeting neuroinflammation and/or interoception.

OK, possible and the anterior cingulate cortex is coming up in LC neuroimaging studies. But... and I'm sure I'd qualify on the CSS questionnaire with eg noise and light hypersensitivity, however I would strongly maintain that I am now much less aware of things like heart rate. At times I can be slowly moving around the house at 130 bpm, unaware until my watch subsequently informs me. Are my interoceptive processing pathways disrupted? Maybe. But are they compensating in the opposite direction due to a newly and peripherally imposed set point of pathophysiology?
 
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