May 10th 2025: Demystifying PEM MedUni Vienna

[rapidboson]

From 10-13h (Vienna time) on May 10th there's a conference on PEM at the medical university of Vienna.
It is also available as livestream, you'll have to register.

Agenda
10:00-10:10 Welcome and introduction to the symposium

10:10-10:50 Post-exertional malaise: a cardinal symptom for patient stratification in infection-associated chronic illness. David Putrino, Mount Sinai, USA

10:50-11:30 The pathophysiology of post-exertional malaise. Christian Puta, Friedrich-Schiller-Universität Jena, Germany

11:30-12:00 The impact of post-exertional malaise on rehabilitation setup and efficiency.
Ralf Harun Zwick, LBI Rehabilitation, Therme Wien Med, Austria

12:00-12:30 Post-exertional malaise in children: Overlaps and differences in symptoms, diagnosis and treatment. Beate Biesenbach, Rehabilitation kokon, Rohrbach-Berg, Austria

12:30-12:50 Physiotherapy and post-exertional malaise: practical insights. Verena Hackl, Medical University of Vienna, Austria

12:50-13:00 Wrap up

13:00-13:30 Networking with food and beverages

 

[Trish]

I hope someone can provide notes on what was said. Too sort notice for me.
I'd like to know what they think rehab and physio can do and what they think they know about pathophysiology of PEM.

 

[rapidboson]

I'm not sure anything new or groundbreaking has been shared.
Amongst different clinical or scientific groups, they found an increased active and resting lactate level.

Beta 2 receptor involvement (and thus potentially autoantibodies) in exercise-induced lymphocyte migration was mentioned by Prof Puta.
For the most part, it seems like his talk followed the review paper they brought out last year.

Upon physical activity, affected patients exhibit a reduced systemic oxygen extraction and oxidative phosphorylation capacity. Accumulating evidence suggests that these are mediated by dysfunctions in mitochondrial capacities and microcirculation that are maintained by latent immune activation, conjointly impairing peripheral bioenergetics. Aggravating deficits in tissue perfusion and oxygen utilization during activities cause exertional intolerance that are frequently accompanied by tachycardia, dyspnea, early cessation of activity and elicit downstream metabolic effects. The accumulation of molecules such as lactate, reactive oxygen species or prostaglandins might trigger local and systemic immune activation. Subsequent intensification of bioenergetic inflexibilities, muscular ionic disturbances and modulation of central nervous system functions can lead to an exacerbation of existing pathologies and symptoms.

Some new data from their "Bio-sig PEM" study (looks interesting!) was shared - increased lactate levels being one preliminary finding.

 

[rapidboson]

I don't know if the talks were recorded and will be shared.