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

 
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.
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
 
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