Webinar - ME/CFS Involves Brain Inflammation: Results from a Ramsay Pilot Study - Jarred Younger

MeSci

Senior Member (Voting Rights)
Source: Solve ME/CFS Initiative

Date: December 13, 2018

Time: 18:00-19:00 UTC

URL: https://register.gotowebinar.com/register/1541028613190392835

ME/CFS Involves Brain Inflammation: Results from a Ramsay Pilot Study
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Presented by Jarred Younger, PhD, Ramsay Award Program - 2016 Class, Director and Associate Professor Neuroinflammation, Pain and Fatigue Laboratory at the University of Alabama, Birmingham

Description: Join Dr. Jarred Younger for a discussion of his new research findings that indicate brain inflammation plays a significant role in the pathophysiology of ME/CFS. With pilot funding from SMCI's Ramsay Award Program, Dr. Younger used a non-invasive imaging technique to measure temperature and other brain chemistry indicators in individuals with ME/CFS and control subjects. The results showed distinctly elevated brain temperature, indicative of inflammation, in patients. The involvement of brain inflammation in the development and progression of ME/CFS has long been an area of interest, but there has been a lack of direct evidence to support the connection. This seminal study further validates that neuroinflammation is occurring in ME/CFS patients and has the potential to point the way to an objective marker and effective medical treatments.

Dr. Jarred Younger obtained his PhD in Experimental Psychophysiology at the University of Tennessee in Knoxville in 2003. Dr. Younger then completed postdoctoral fellowships in pain medicine and neuroimaging at Arizona State University and Stanford University before joining the faculty at Stanford in 2009. In 2014, he transferred to the University of Alabama at Birmingham, where he currently directs the Neuroinflammation, Pain and Fatigue Laboratory.

His lab uses neuroimaging, immune monitoring, and clinical trial techniques to develop new diagnostic tests and treatments for pain and fatigue disorders.
 
I hope this will be available for viewing after. The information he shared at the OMF symposium was informative. The information about the microglia explains why some of us see reduction in symptoms using Low Dose Naltrexone. While some react badly to LDN, I have found it to be the only prescription (other than my heart medication) that reliably improves my day to day living. It does NOT reduce my PENE, but it definitely lowers my pain levels and reduces my "I'm dying right now" feeling.

It also explains why it takes a while for the LDN to be effective. It takes a while to calm the microglia down... and it takes consistency to keep them calmer.

Link to his talk at OMF:
 
Source: Solve ME/CFS Initiative

Date: December 13, 2018

Time: 18:00-19:00 UTC

URL: https://register.gotowebinar.com/register/1541028613190392835

ME/CFS Involves Brain Inflammation: Results from a Ramsay Pilot Study
----------------------------------------------------------

Presented by Jarred Younger, PhD, Ramsay Award Program - 2016 Class, Director and Associate Professor Neuroinflammation, Pain and Fatigue Laboratory at the University of Alabama, Birmingham

Description: Join Dr. Jarred Younger for a discussion of his new research findings that indicate brain inflammation plays a significant role in the pathophysiology of ME/CFS. With pilot funding from SMCI's Ramsay Award Program, Dr. Younger used a non-invasive imaging technique to measure temperature and other brain chemistry indicators in individuals with ME/CFS and control subjects. The results showed distinctly elevated brain temperature, indicative of inflammation, in patients. The involvement of brain inflammation in the development and progression of ME/CFS has long been an area of interest, but there has been a lack of direct evidence to support the connection. This seminal study further validates that neuroinflammation is occurring in ME/CFS patients and has the potential to point the way to an objective marker and effective medical treatments.

Dr. Jarred Younger obtained his PhD in Experimental Psychophysiology at the University of Tennessee in Knoxville in 2003. Dr. Younger then completed postdoctoral fellowships in pain medicine and neuroimaging at Arizona State University and Stanford University before joining the faculty at Stanford in 2009. In 2014, he transferred to the University of Alabama at Birmingham, where he currently directs the Neuroinflammation, Pain and Fatigue Laboratory.

His lab uses neuroimaging, immune monitoring, and clinical trial techniques to develop new diagnostic tests and treatments for pain and fatigue disorders.

My understanding of biology is non-existent. But could the increase in brain temperature explain why so many of us feel ''feverish'' although our temperature is in normal range when measured with something like a thermometer?
 
I suppose our body temperature could be a reaction to a higher brain temperature. So if the 'thermostat' is in the brain and it's registering 'hot', then the body works to cool everything down.

That's such a consistent result in that PR poll (a slightly low body temperature), and it's certainly consistent with my experience. I'm surprised it's not mentioned more often. I found that my temperature normalised when I was feeling better and was lower when I was quite unwell. Body temperature might be one way to work out if an intervention is having an effect.
 
There is the added complexity that for women with menstrual cycles, body temperature rises around ovulation (approx mid cycle) and stays higher for the second half of the cycle by about half a degree C.

I assume when Jarred Younger talks about elevated temperature in the brain he means it is higher than the temperature of the blood entering the brain, so it's relative to core body temperature at the time for that individual.
 
I hope this will be available for viewing after. The information he shared at the OMF symposium was informative. The information about the microglia explains why some of us see reduction in symptoms using Low Dose Naltrexone. While some react badly to LDN, I have found it to be the only prescription (other than my heart medication) that reliably improves my day to day living. It does NOT reduce my PENE, but it definitely lowers my pain levels and reduces my "I'm dying right now" feeling.

It also explains why it takes a while for the LDN to be effective. It takes a while to calm the microglia down... and it takes consistency to keep them calmer.

Link to his talk at OMF:



Thanks for sharing that, he’s a very good speaker and the research looks great. He seems to think we need pet scan research but hasnt funding. I’m wondering why when it’s such an important area and if we could crowd fund. I’m guessing for a 20 20 study it would cost at least £250,000

Today my brain feels very hot as it always does in flare up

I’m glad a UK charity is funding younger now. There’s a lack of ME brain research over here
 
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One question, I saw he said the sensitised microglia could be set off with small activity, which to me sounded like PEM. However in MS or Parkinson’s where they also have fatigue and microglia activation, they don’t get our type PEM so what’s the added factor? He did say in the big picture everything came together rather than one theory vs another...
 
One question, I saw he said the sensitised microglia could be set off with small activity, which to me sounded like PEM. However in MS or Parkinson’s where they also have fatigue and microglia activation, they don’t get our type PEM so what’s the added factor? He did say in the big picture everything came together rather than one theory vs another...
The only semi-convincing (but unevidenced) model I've seen for PEM is Myhill's. It even factors in the time delay. But I'm not sure how it fits with other models.
 
One question, I saw he said the sensitised microglia could be set off with small activity, which to me sounded like PEM. However in MS or Parkinson’s where they also have fatigue and microglia activation, they don’t get our type PEM so what’s the added factor? He did say in the big picture everything came together rather than one theory vs another...
It's a good question. Why does neuroinflammation affect different brain areas in different diseases? Still so much more to discover.
 
One question, I saw he said the sensitised microglia could be set off with small activity, which to me sounded like PEM. However in MS or Parkinson’s where they also have fatigue and microglia activation, they don’t get our type PEM so what’s the added factor? He did say in the big picture everything came together rather than one theory vs another...

It's a good question. Why does neuroinflammation affect different brain areas in different diseases? Still so much more to discover.

Maybe activity triggers both neuroinflammation and PEM in ME, and something different triggers neuroinflammation in other diseases.
 
I keep meaning to buy a thermometer to see what my body temperature actually is. I feel extremely hot most of the time and my partner says I am like a heater with the amount of heat I radiate out. I wouldn’t be surprised if the thermometer said my temperature was normal or slightly lower though.
 
It's a good question. Why does neuroinflammation affect different brain areas in different diseases? Still so much more to discover.

Thanks yes I’d forgotten he said certain brain areas associated with sickness response Were affected in us , probably different with Parkinson’s

Maybe activity triggers both neuroinflammation and PEM in ME, and something different triggers neuroinflammation in other diseases.

Yes in addition to above , our systemic issues with exertion might trigger the brain inflammation in ways which doesn’t happen in other illness with other types of it. That’s why lumping ME in with MUS, FM, IBS, CF is not helpful.

I’m guessing with autoimmune illness it depends what the immune system decides to attack , every illness has different manifestations.

Also If the sickness behaviour drivers in the brain are part of our illness, they might be primed to interpret activity as “bad” as a protective response and only allow a certain amount before they see it as a threat to the sick body ? Or primed to respond highly to peripheral fatigue in ways which doesn’t happen in MS.
 
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Just to confound things, it’s been found that normal body temperature is not actually 98.6. Normal is within a small range and not a precise three digit figure, the average is a little under 98.6.
In celcius normal body temperature is between 36.0 and 37.5 degrees. It is a wide range and it depends on many variables including where you measure from.
https://en.m.wikipedia.org/wiki/Human_body_temperature
 
Years ago I tracked my body temperature for one month. My body temperature dropped down to 95-96 F when I was in next day delayed PEM from exercising. Went back up to normal on day 3 when I was back to baseline.

I did not feel any difference in brain temperature sensation though.
 
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