Authored by Colleen Steckel
In November 2020 it was decided by the ME International Board to ask for donations that would cover the cost of purchase and shipment of pulse oximeters to members.
All of the board members who have myalgic encephalomyelitis have used pulse oximeters and other devices to measure heart rate and recognized the importance of having this vital information.
In preparation for sending out pulse oximeters the volunteers created an explanation sheet about the usefulness of pulse oximeters. See HERE: https://www.me-international.org/uploads/1/2/7/6/127602984/pulse_oximeter_info_sheet_201231.pdf
In December enough donations came in to purchase the first 50 BodyMed pulse oximeters at a discount through Milliken Medical of Ohio. A Thrivent Financial “Action Team” grant of $250 as part of their #LiveGenerously program was secured which helped cover the purchase. Individual donations came in to cover the remaining cost for the purchase as well as supplies and mailing costs.
Requests quickly came in from around the world. On January 8, 2021 the first shipment of pulse oximeters was sent out to members in the US, Canada, Norway, Australia and the UK. The entire project is managed by volunteers. Requests will be filled on a first come first serve basis. We are in the process of sending out the first 50.
Funds are needed to continue fulfilling requests. Please donate so we can continue this project. To see more information and to donate go to: https://www.me-international.org/pulse_oximeters.html A thank you to Lisa Edelsward (Canada) for the beautiful poem graphic on this donation page.
WHY DO BRAIN SCANS? -
UNDERSTANDING ME & SPECT BRAIN SCANS
SPECT scans measure how blood flows into the brain at a point in time. Blood flow is impacted by many factors including diet, lifestyle, medications, age, and genetics. This is different than an MRI which looks for any abnormalities in the structure of the brain. Another option for testing is a functional MRI (fMRI) which looks at the brain in action (used mostly in research) and not available to anyone who has metal implants. Another thing to consider is an fMRI does not emit radiation, as magnetic forces are used to collect information. In a SPECT scan, the patient is exposed to a small amount of radiation.
More information about SPECT scans can be found in Dr Hyde’s writings from the Nightingale Research Foundation. The Nightingale Research Foundation Definition of Myalgic Encephalomyelitis (M.E.) (2016) booklet with information presented at the IACFS/ME Conference Fort Lauderdale, Florida and Cornell University (2016) has detailed SPECT information starting on page 11.
A Sept 2019 thesis paper titled Quantitative Electroencephalographic Assessment of ME/CFS: Support for a Novel Diagnostic Protocol by Andrew E Pellegrini discusses the findings of Dr. Hyde and showed qEEG testing could also be used to find abnormalities in ME patients.
MY EXPERIENCE GETTING A SPECT SCAN
In June 2020, my husband took me for two consecutive SPECT scans; a “thinking” scan on day one and a “resting brain” scan on day 2.
Working with CereHealth® personnel at CereScan®, who answered my multitude of questions, helped me feel confident this was a worthwhile endeavor to get the answers about the changes in cognition I had seen as a result of acquiring myalgic encephalomyelitis in 1989.
PREPARING FOR THE SCANS
A lengthy history/symptom questionnaire was done via my home computer. Options for filling out the questionnaire include online, pen and paper, or verbal (where CereHealth staff walks the patient through each question). Filling out the form can be done in multiple sittings.
A cognitive assessment was taken using my home computer. This had to be done all in one sitting and consisted of several different kinds of memory and cognition exercises.
NOTE: There is a loud bell sound at the beginning which shocked me as I wasn’t expecting it and I had my volume set too high. An improvement to their test would be to do a volume level test to make sure it’s at a reasonable volume and a notification so the sound is expected. The results from that showed very low scores in psychomotor speed, reaction time, simple attention and motor speed. Also, below average composite memory and verbal memory were noted. Those findings coincide with my daily experience.
Shortly before leaving for the scans, I did an intake interview over the phone. This covered making sure I knew what to expect and a chance to get any last-minute questions I had answered.
The day before the test, I stopped some medications that would interfere with the scans and was given routine instructions to avoid caffeine, alcohol, nicotine and marijuana.
NOTE: All of my work with CereHealth in Colorado was done via phone/email.
GETTING THE SCANS
CereHealth is based in Colorado but has coordinated with other outpatient radiology facilities to perform the test to their specifications. As everyone’s travel experience will be different, I won’t go into those details other than to say that traveling to Florida during the COVID-19 outbreak was a daunting experience, but the lab where I had the test done was making good efforts to keep everyone safe.
Day 1 – Scan at 8 am. Travel time to the office was about 40 minutes so we gave ourselves an hour to get there. Several warnings were given in the paperwork that the radiopharmaceutical injection used is time sensitive and being late to the appointment could result in not being able to perform the test and me being charged for the radiopharmaceutical.
The infusion is technetium Tc99m exametazime. I am highly reactive to most things and was concerned despite reassurances that others have had no issues. I felt no reaction at all to this injection. As is common for me, I tasted the saline used to prep the infusion line but, other than that, noticed no effects at all.
DAY 1 – CONCENTRATION – Process Details
As can be seen from the picture, I was allowed to wear my face mask for the procedure. This is nothing like an MRI. There is no thumping. The sounds I heard were closer to the sounds one would hear getting a dental x-ray; movement of the machine and then silence with occasional mechanical clicks.
As I understood the importance of not moving during the scans, I spoke with them about my involuntary muscle twitching and was pleased to learn they had a head strap as well as a Velcro body wrap that would help me to stay still. The head strap was comfortable across my forehead and the body wrap covered my upper body area using Velcro so it could be tightened to comfort. It was not uncomfortable and I felt more secure knowing that if I had a muscle spasm it was unlikely to affect the scans. A light blanket helped keep me from getting chilled during the procedure.
Here is the list of all of the partnering clinic locations CereHealth uses at this time:
According to CereHealth’s clinician: “CereScan’s affiliated clinics are located in areas where the GE radiopharmaceutical is accessible. We are limited by this accessibility and may not be able to partner with clinics in certain states/regions. Our sixteen clinics follow CereScan’s specific imaging protocols and their nuclear medicine technologists/staff are trained by CereScan’s Chief Nuclear Medicine Technologist.”
The SPECT scans are read using CereMetrix®, which is an FDA-cleared radiology tool for SPECT analysis. Results are expected within about 2 weeks. These were emailed to me through a HIPAA secure email service. They were also sent to my doctor.
My results: “The nature, location, and pattern of these abnormalities is primarily consistent with the scientific literature pertaining to traumatic brain injury (TBI).”
An option at CereHealth after getting the lab results is to do a consultation which may not be covered by insurance.
The consultation included the overall understanding of how the scans were read. It was noted that the interpreting physician who read the scans has many years of experience and was not given my history or diagnosis prior to the reading; thus, doing a blind reading. He did review my medical history after the reading to provide context to the information found. This radiologist has a lot of experience and has testified as an expert witness.
As part of the video chat consultation, the clinician walked me through the scans using the software used to read the scans while I followed along on my computer screen. She was able to move images of the brain around and show inner regions and discuss the areas that showed abnormal blood flow. The interpreting physician read the scans using 2 points of deviation from normal. During the consultation, the clinician was able to alter the program to see my scans at 1.65 deviation of normal which expanded the areas of abnormality. (2 points of deviation are normal for reading brain scans.)
The findings helped to explain some of the following symptoms I deal with regularly: disorientation to time/place, headaches, muscle pain, confusion, difficulty with concentration, distractibility, disorganization, visual processing, depth perception, difficulty learning new things, losing things, problems with language/word finding, as well as long and short term memory problems.
NOTE: This consultation does not include a written report, so it is important to take good notes to look back on if needed.
CereHealth can provide a set of images (which are also included on your imaging report), and a CD of the raw data at your request. They can send the SPECT information to your neurologist, and their clinician can provide support if they have questions.
WHY 2 SCANS?
The resting scan is the normal method and that is the scan used to compare to a population database. The “thinking” scan has no population data to compare to so is only compared to the patient’s resting scan.
The following is a quote from the CereHealth clinician: “A normal, healthy response to the concentration task means that blood flow increases to the brain when it works harder. (Think about it this way: when you are running, your heart pumps faster and more blood flows through the heart. Same with the brain, but instead of running, you are thinking).
In cases where TBIs or other neurological conditions are present, we will actually see the opposite response, where blood flow decreases in the brain during concentration. Basically, the harder you ask your brain to work, the more it shuts down. This is a paradox (it is doing the inverse of what it should be doing) and the brain is deactivating (i.e. working less). This deactivation can come from a TBI, toxic injury, and is a common finding in a person with ADD/ADHD.”
My scans showed this abnormality as can be seen in this comparison between my brain at baseline and during concentration.
Comparing my results to the IC Primer
Part of the consultation explained the difference between Segami software (what is shown in the IC Primer) and the CereMetrix software. CereHealth previously used Segami software so they have experience to discuss comparison. Some limitations to Segami include an inability to share the scan technology for others to review the scans as well as Segami did not have the details in the subcortical area of the brain that Ceremetrix provides. (Info on Segami from 2018 so that may have changed since then.)
The top picture on the right, from page 4 of the IC Primer, shows a white area. That area is a lack of information which my scans included. My scans did not show the same pattern of blood flow issues as shown in the Primer, but it did show some areas that overlapped.
“SPECT imaging can identify what is called a “toxic/hypoxic encephalopathy”. This type of neurological condition can result from a single exposure and/or chronic exposure to an environmental toxin such as carbon monoxide, mold, heavy metals, Lyme disease, HHV-6 (and other viruses) and even substance abuse (alcohol, cocaine, heroin, etc.). This process can also occur after a hypoxic event, where the brain was deprived of oxygen (such as a near-drowning experience, problems with anesthesia, anaphylaxis, etc.).
A toxic/hypoxic encephalopathy in SPECT imaging is described as a “patchy, diffuse, scattered pattern” of reduced blood flow. In this type of injury, almost all brain areas can be affected, including the subcortical structures. In a traumatic brain injury pattern, we see what are called “focal, dominant, or more specific” areas of reduced blood flow. In many cases, the mechanism of injury relates to where the radiologist sees damage in the brain. For example, a football player who makes helmet-to-helmet contact and has a concussion/TBI may show a focal area of reduced blood flow in his forehead region (frontal lobe), and other parts of the brain may appear unaffected.” The source for this information is the clinician at CereHealth
Here is the information for insurance:
CereHealth indicated that one resting scan should be sufficient to see any abnormalities that might help diagnose ME. I found the comparison between the two provided information that may prove valuable. The current cash rates for this procedure are:
WAS IT WORTH IT FOR ME?
Prior to this test, I had only one other brain scan which was an MRI to rule out Multiple Sclerosis. There were no findings noted by the neurologist on the MRI. Because ME can be mistaken for MS, it is important early in the diagnosis process to have MS ruled out.
Confirming an ME diagnosis is a long process. Getting these SPECT scan results, even though it was 30 years since onset, gave me and my medical team a better understanding of what was happening and verified my limitations were based on biological issues and had nothing to do with my attitude.
I am grateful that my scans could also benefit future research. Early in the process I was excited to learn that CereHealth has conducted multiple studies and participated in projects with various Contract Research Organizations. CereHealth’s software has the ability to gather a wealth of deidentified patient data to run correlational analyses and quantify SPECT imaging data. Their team has the connections to quickly mobilize an active or retrospective study to further examine complex neurological conditions. They encourage patients to authorize the release of their health information into their deidentified database so these studies may be performed to contribute to the medical field and benefit other patients in the future. I gave permission to have my scans available for future study.
CONFIRMING AN ME DIAGNOSIS IS A LONG ROAD
One of the benefits of the IC Primer is it provides a flashlight in the dark forest we all wander through trying to find answers. Using the IC Primer has provided me insight into the symptoms and disease process to feel confident I have been properly diagnosed. It has also given me management and treatment tools to improve my quality of life.
There is nothing easy about living with ME, but making sure our medical team is using the most accurate and up to date information and proper testing can significantly improve quality of life for those dealing with ME.
Colleen Steckel – Sudden onset Myalgic Encephalomyelitis August 1989
Disclaimer: I was given no discount or financial gain from CereHealth. This is my personal experience and not to be considered medical advice.
UPDATED 5/30/20 - Added links to the scripts of both videos (below).
ME International has recently released its first video, entitled "Myalgic Encephalomyelitis - Understanding Diagnosis" on our YouTube Channel.
Click HERE for the LONG version - Transcript
Click HERE for the SHORT version - Transcript
Many different disease descriptions have been created since the recognition and labeling of ME by Dr. Ramsay in the 1950s. Several criteria later broadened the patient population to include many patients who did not fit the original description.
In 2011 a group of experts with over 500 years of combined experience created a consensus criteria known as the International Consensus Criteria (#MEICC). ME-International supports the adoption of the #MEICC and the International Consensus Primer for ME (#MEICPrimer), which is a comprehensive primer for doctors.
We strongly believe that adoption of the #MEICC will ensure research is focused on the distinct ME patient population without including patients who fall into the wider category known as ME/CFS-SEID or CFS-Fukuda.
These videos discuss the history of ME, the lived experience, including recognition of the most severe patients, a full description of how to diagnose using the International Consensus Criteria as well as the challenges of getting a diagnosis. Proper diagnosis is vital for patients to get proper treatment.
ME-International believes that worldwide adoption of the #MEICC to diagnose and treat, is the fastest way to improve the quality of life of people with ME.
Information not to be considered medical advice.
ME ICC: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2796.2011.02428.x
IC Primer: https://d3n8a8pro7vhmx.cloudfront.net/meadvocacy/pages/2292/attachments/original/1554817421/Myalgic_Encephalomyelitis_International_Consensus_Primer_2012.pdf?1554817421
Please sign the #PwME4ICC petition at Change.org at https://www.change.org/p/the-us-department-of-health-and-human-services-cdc-adopt-the-distinct-disease-myalgic-encephalomyelitis-me-as-defined-by-icc-now
Authored by John Duncan UPDATED 4/29/20
Perhaps one of the most characteristic signs of Myalgic Encephalomyelitis (ME) is the intolerance to any type of exertion whether it is of a passive type brought on by surroundings (hearing a voice, seeing lights), or an effortful type (lifting a cup, holding a conversation). Given this bizarre sign, it is only natural that for many of us and many doctors, the mitochondrion has been a perennial suspect.
Unfortunately, by the end of the 1990s many early findings regarding the mitochondria, such as increased enteroviral RNA in patient's muscle mitochondria , deletions of mitochondrial DNA  and abnormal mitochondrial morphology  were not followed up or not replicated by other studies.
However, virtually all of the research in the 1990s and 2000s is fraught with inappropriately using heterogeneous groups of patients due to bad definitions, small sample sizes and widely varying diagnostic experience by study investigators. When two studies are at odds it is often unclear which to accept and which to reject. In the case of the mitochondria, it is very tempting to believe some of the reports of abnormalities were not given a fair chance due to follow-up studies selecting different groups of patients as a consequence of the Fukuda or Oxford Criteria.
The Need for Good Selection Criteria in Practice
The problem of selecting a single disease picture and not many, can be solved by using a rigorous criteria of selection such as the International Consensus Criteria (ICC). It can likely be decreased by using criteria of selection which require the cardinal signs and symptoms of Myalgic Encephalomyelitis; such as the Canadian Consensus Criteria (CCC). Lastly, if the patient group is very severe and has been tested for alternative diagnoses, the study is more likely to be applicable to ME patients at large. This is assumed because many disorders like Sleep Apnea, Chronic Headaches, Nonspecific chronic pain which fall into a broad criteria (e.g. CDC's Fukuda definition) are not likely to have the severe drop of function seen in the worst-off ME patients.
Hopefully the use of stringent criteria for ME, larger study sizes, and the ability to group patients by temporal stages, will prevent current studies from repeating the mishmash of past decades.
Recently, in trying to develop an assay for ME, the Ron Davis group at Stanford found an altered electrical signal (impedance) in patients' cells when subjected to osmotic stress . This suggests in a harsh environment patients' cells don't have the energy to maintain their voltage gradients–unlike normal cells which do. Besides its usefulness as a diagnostic, Davis's finding also implicates deficient cellular energy, and therefore the mitochondria, in ME patients.
Other Studies Directly Implicate the Mitochondria
Julia Newton's group at Newcastle University found reduced mitochondria function  in both severely and moderately affected patients. Interestingly, they found "disease severity does not correlate with mitochondrial function and even those with a moderate form of the disease show evidence of mitochondrial dysfunction." This means the mitochondria function is more like a switch flipped for all patients than a gradient of effect or finding only in a subset. However, severely affected patients did have greater respiratory acidification due to impairments in glycolysis not seen in moderate ones. A straightforward interpretation would be impairment to mitochondrial function is a prerequisite for disease but that downstream effects of disease can impair vital cellular processes like glycolysis.
Another new study by Bhupesh Prusty of the University of Wurzburg, and UCSD’s Robert Naviaux has found that mitochondria from ME patients show dramatic fragmentation in comparison to controls .
In an experiment with culture cells with latent HHV-6 (containing Human Herpesvirus 6 DNA–but not actual virus particles) chemical reactivation of HHV-6 resulted in the production of several viral RNAs but not major viral proteins. Significantly, Prusty and Naviaux found HHV-6 reactivation induced mitochondrial fragmentation, oxidative changes, and decreased antiviral resistance. When fluid from the cell culture of the HHV-6 reactivated cells was transferred to a new group of cells (not exposed to HHV-6), mitochondrial fragmentation and oxidative changes also occurred in these cells but with increased antiviral resistance! 
The last experiment involved transferring not HHV-6 infected cell culture fluid but rather blood serum from ME patients to new cells. This serum transfer induced an identical state of mitochondrial fragmentation, oxidative change, and antiviral resistance! These experiments show that one or more molecule types induced by HHV-6 reactivation are secreted to the outer fluid and can function to induce mitochondrial fragmentation, oxidative changes, and antiviral properties in distant cells. Not only that, but the serum of ME patients acts in exactly this manner (suggesting we have a molecular factor(s) in our blood similar, or the same as, that secreted by the HHV-6 reactivated cells–and which is causing harmful changes to our mitochondria).
A common thread to mitochondrial findings by both Davis and Prusty is the presence of a serum factor, or factors, which could be transferred to the cells of healthy people and inflict the ME cells’ phenotype on well cells. How far this commonality extends (for instance whether serum factor(s) found in Davis's impedance study is the same as the factor(s) found in Prusty's study of mitochondrial fragmentation) is currently unknown.
There are two main implications:
Some of the most precocious intra-cellular findings stem from the finding of an abnormal, cleaved, 37 kiloDalton RNase L and dramatic reduction in actin in patients’ cells by the late Robert Suhadolnik . In “Chronic Fatigue Syndrome: a biological approach” , by Kenny De Meirleir and colleagues, these findings are expanded into a panoply of intra-cellular dysregulation including defective activation of RNase L by 2-5-A dimers produced by 2-5’A oligoadenylate synthetase, cleavage of Rnase L by m-calpain, and abnormalities in the cell state reminiscent of incompletely induced apoptosis (an essential cell disposal process culminating in cell death). Given the role of mitochondria in both cellular energy and apoptosis, it is hoped that the mitochondrial fragmentation research and antiviral induction research can explain the significance of these findings in a panoramic manner.
One indicator of scientific progress is the ability to place important observations in a single theoretical framework. The findings of induction of mitochondrial fragmentation and a cellular viral resistance state by patient serum could explain one such finding: the impairment of pyruvate dehydrogenase found by Fluge and Mella of Haukeland University, Norway. Prusty’s findings indicated that the mitochondrial fragmentation (caused by both patient serum and HHV-6 infected cell supernatant) potently impaired this very complex!
However starved our own mitochondria may be, this is a very exciting time for mitochondria research in ME and we must ensure these researchers are not starved of funding!
1.) Bowles NE, Bayston TA, Zhang HY, Doyle D, Lane RJ, Cunningham L, Archard LC. Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy. J Med. 1993;24(2-3):145-60. PubMed PMID: 8409778.
2.) Vecchiet L, Montanari G, Pizzigallo E, Iezzi S, de Bigontina P, Dragani L, Vecchiet J, Giamberardino MA. Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome. Neurosci Lett. 1996 Apr 19;208(2):117-20. PubMed PMID: 8859904.
3.) Chunfang Zhang, Alessandra Baumer, Ian R. Mackay, Anthony W. Linnane, Phillip Nagley, Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome, Human Molecular Genetics, Volume 4, Issue 4, April 1995, Pages 751–754
4.) Behan WM, More IA, Behan PO. Mitochondrial abnormalities in the postviral fatigue syndrome. Acta Neuropathol. 1991;83(1):61-5. PubMed PMID: 1792865.
5.) Esfandyarpour R, Kashi A, Nemat-Gorgani M, Wilhelmy J, Davis RW. A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Proc Natl Acad Sci U S A. 2019 May 21;116(21):10250-10257. doi: 10.1073/pnas.1901274116. Epub 2019 Apr 29. PubMed PMID: 31036648; PubMed Central PMCID: PMC6535016.
6.) Tomas C, Elson JL, Strassheim V, Newton JL, Walker M. The effect of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) severity on cellular bioenergetic function. PLoS One. 2020 Apr 10;15(4):e0231136. doi: 10.1371/journal.pone.0231136. eCollection 2020. PubMed PMID: 32275686; PubMed Central PMCID: PMC7147788.
8.) Schreiner P, Harrer T, Scheibenbogen C, Lamer S, Schlosser A, Naviaux RK and Prusty BK. Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. ImmunoHorizons April 1, 2020, 4 (4) 201-215; DOI
9.) Suhadolnik, RJ. Dysregulated 2-5 Synthetase/Rnase L/Pkr Pathways in Cfs. NIH Grantome. 1997.
10.) DeMeirleir, K. & Englebienne, P. Chronic fatigue syndrome: a biological approach. (CRC Press, 2002).
Image Source (used with permission): https://twitter.com/BhupeshPrusty/status/1233508017368436737/photo/1
Guest blog by: Joan McParland, Founder & Voluntary Coordinator