What research do you want to see? (study ideas)

Longitudinal changes in data from wearables, from triggering illness onset - step count, sleep hours, resting heart rate

The linked study was just for Covid-19, not post-Covid19 ME/CFS, but shows what could be done

Andy

Thread 'Assessment of Prolonged Physiological and Behavioral Changes Associated With COVID-19 Infection, 2021, Radin et al'

Introduction

Long-term COVID symptoms marked by autonomic dysfunction1 and cardiac damage2 following COVID-19 infection have been noted for up to 6 months after symptom onset,3 but to date have not been quantified, to our knowledge. Previous studies have found that wearable data can improve real-time detection of viral illness4 or discrimination of individuals with COVID-19 vs other viral infections.5 Wearable devices provide a way to continuously track an individual’s physiological and behavioral metrics beginning when healthy (ie, before infection), during...
  • Andy
  • covid-19 heart rate long covid monitoring resting heart rate study idea tachycardia wearables
  • Replies: 4
  • Forum: Long Covid research
  • Like
 
Hutan said:
That is, any hypothesis for ME/CFS needs to explain why a person seemingly can have Covid-19 one time and not get ME/CFS, but can be exposed another time and get ME/CFS.

As far as I know, there hasn't been much study of people who got ME/CFS after their second or later Covid-19 infection. Perhaps looking for the factors that might tip someone towards ME/CFS in those people might be useful.
Click to expand...
Suggestion of a study to characterise the people and environments when a second or later Covid-19 exposure triggers post-Covid-19 ME/CFS. Is there any factor that seems to be present or absent when ME/CFS happens?

Even just collecting a well-diagnosed cohort to really confirm that this phenomenon is real would be useful.
 
Reduced prepulse inhibition associated with fibromyalgia in two studies. It might be good to test this in ME/CFS.

Alterations in excitatory and inhibitory brainstem interneuronal circuits in fibromyalgia: Evidence of brainstem dysfunction, 2014, Kofler et al
Objective:
Patients with fibromyalgia syndrome (FMS) perceive stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role.

Methods:
Blink reflex, blink reflex excitability recovery, and prepulse inhibition of the blink reflex - representing brainstem excitability - were assessed in 10 female patients with FMS and 26 female healthy controls.

Results:
Unconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls. Blink reflex excitability recovery was enhanced in patients versus controls at all intervals tested. Prepulses significantly suppressed R2 area and increased R2 latency in patients and controls. However, R2 area suppression was significantly less in patients than in controls (patients: to 80.0 ± 28.9%, controls: to 47.8 ± 21.7%). The general pattern of corresponding changes in R2c was similar.

Conclusions:
Blink reflex is normal, whereas blink reflex excitability recovery is enhanced and blink reflex prepulse inhibition is reduced in patients with FMS, suggesting functional changes at the brainstem level in FMS.

Significance:
Reduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.
Web | DOI | Clinical Neurophysiology | Paywall

Prepulse inhibition of the blink reflex in functional neurological disorder and fibromyalgia, 2025, Edwards et al
Prepulse inhibition reflects subcortical sensory integration, where a low-intensity peripheral stimulus (prepulse) reduces the amplitude of a reflex response to a subsequent high-intensity stimulus. As a measure of pre-attentive sensory gating, prepulse inhibition has been found to be altered in small cohorts of patients with functional disorders, including functional motor disorder and fibromyalgia, suggesting a shared deficit in sensory information processing. However, prior studies have not demonstrated consistent associations between prepulse inhibition abnormalities and clinical measures.

We hypothesized that widespread pain and somatic symptoms in somatic symptom disorders may result from a general deficit in the interpretation of bodily signals, potentially linked to abnormalities in sensory filtering as measured by prepulse inhibition.

In this study, we examined 140 participants across four age- and sex-matched groups: 35 patients clinically categorized with functional motor disorder without fibromyalgia, 35 with both functional motor disorder and fibromyalgia, 35 with fibromyalgia only, and 35 healthy controls. A weak electrical stimulus to the index finger served as the prepulse, delivered 100 ms before supraorbital nerve stimulation to elicit the R2 component of the blink reflex. Prepulse inhibition was calculated as the percent reduction in R2 amplitude.

Across all groups, lower prepulse was significantly associated with higher scores on the Fibromyalgia Severity Scale, consisting of Widespread Pain Index and Symptom Severity Scale. In patients with functional motor disorder, no association was found between prepulse inhibition size and objectively rated motor symptom severity.

These findings suggest that impaired early sensory processing at subcortical level is related to “fibromyalgianess” in people with functional motor disorder and fibromyalgia. Abnormal prepulse inhibition may serve as an objective transdiagnostic marker of fibromyalgia symptomatology or fibromyalgianess, including widespread pain and other non-motor symptoms in functional disorders, highlighting a potential role of sensory gating deficits in the pathophysiology of fibromyalgia-spectrum manifestations.
Web | DOI | S4ME | PDF | Brain | Open Access
 
I agree, the biomarker hunt is stalled. We need more work on the persistence of the virus after the initial infection. What happens to the leftovers? Forget the cure for a minute and just map out the damage path. That's the only way forward.
 
FicaR94 said:
I agree, the biomarker hunt is stalled. We need more work on the persistence of the virus after the initial infection. What happens to the leftovers? Forget the cure for a minute and just map out the damage path. That's the only way forward.
Click to expand...

Disagree. The viral persistence folks should just leave the field and free up funds for more useful research.
 
Last edited:
FicaR94 said:
I agree, the biomarker hunt is stalled. We need more work on the persistence of the virus after the initial infection. What happens to the leftovers? Forget the cure for a minute and just map out the damage path. That's the only way forward.
Click to expand...

I don’t know enough to say whether or not sufficient research has been done for us to now reject the viral persistence theory or not, however I do agree that I struggle to understand the fishing approach that involves trying out different drugs when we don’t yet understand the underlying causes of the condition.

I won’t object to any drug that turns out to help, but to me it seems more logical to try to understand the underlying condition before deciding on treatments.
 
Viral persistence doesn’t even make sense. ME/CFS is no more heterogenous than other diseases, something that is the opposite of what you’d expect if it was caused by the continuous presence of any random virus.
 
I would like to See Post mortem research and more on the advanced stages rather than ticking the “severe m.e” box by including us in studies that are primarily designed for the whole community vs exploring what can go wrong as things snowball and persist for a long time.
 
Cinders66 said:
I would like to See Post mortem research and more on the advanced stages rather than ticking the “severe m.e” box by including us in studies that are primarily designed for the whole community vs exploring what can go wrong as things snowball and persist for a long time.
Click to expand...
Does anyone know of any autopsy studies currently recruiting in the UK?
 
V.R.T. said:
Does anyone know of any autopsy studies currently recruiting in the UK?
Click to expand...
In the UK, From what I saw on Facebook, although, led by patients doing the work, The ME association went back to the topic of post-mortem research & having an arrangement with Manchester to set them up as required, after shelving it due to costs, they haven't actually done any for various reasons, which considering it was on the agenda as far back as 2010 or before, is a … :(. The MRC have been funding an hiv brain bank for years. For ME, There seems much more interest in not advancing certain areas than advancing them.
 
Last edited:
You must log in or register to reply here.
Back
Top Bottom