Brain imaging

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Fig. 2: Different Longitudinal MRI Changes Between CFS and NC[1]

MRI, MRS, fMRI, and SPECT abnormalities have been found in chronic fatigue syndrome (CFS) patients. SPECT abnormalities appeared to correlate with clinical status.[2][3]

A hybrid MR/PET scan[4]brain study imaged neuroinflammation due to glial activation in fibromyalgia (FM).[5][6]


Magnetic resonance imaging (MRI)[edit | edit source]

White matter abnormalities of unknown etiology are commonly found on MRIs done on ME/CFS patients.[7]

Magnetic resonance spectroscopy (MRS)[edit | edit source]

Whole-brain MRS markers of neuroinflammation have been found in ME/CFS.[8]

Functional magnetic resonance imaging (fMRI)[edit | edit source]

fMRI images document neuroinflammation.[9]

Single-photon emission computed tomography (SPECT)[edit | edit source]

Dr Byron Hyde specializes in reviewing brain changes caused by ME on patients.[10]

See SPECT

Electroencephalogram (EEG)[edit | edit source]

Quantitative electroencephalogram (qEEG)[edit | edit source]

A study is underway on QEEG[11]

Radiology[edit | edit source]

Positron emission tomography (PET)[edit | edit source]

MR/PET[edit | edit source]

Whole-brain voxel-wise analyses using MR/PET scanning[5]
Combining two imaging techniques allowed researchers, for the first time, to visualize widespread inflammation, specifically mediated via glial cells, in the brains of fibromyalgia (FM) patients.[6]
In 2015, Loggia’s team[5] successfully imaged neuroinflammation — specifically the activation of glial cells — in the brains of patients with chronic pain using a new imaging approach — a combination of magnetic resonance imaging (MRI) and positron emission tomography (PET), or MR/PET scanning.[6]
MR/PET blends the structural and functional detail of tissues that an MRI gives with the sensitivity and metabolic function that PET scans provide.[6]
Specifically, PET scanning detects the radiation given off by a substance injected into a person, called a radiotracer, following its distribution throughout the body.[6]

Research[edit | edit source]

  • 2012, Basant Puri, et.al., found in a MRI study: "significant neuroanatomical changes occur in CFS, and are consistent with the complaint of impaired memory that is common in this illness; they also suggest that subtle abnormalities in visual processing, and discrepancies between intended actions and consequent movements, may occur in CFS."[12]
  • 2014, A Japanese Positron emission tomography (PET) study looked at neuroinflammation in nine patients with ME/CFS and ten controls. They measured a protein expressed by activated microglia, and found that values in the cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons were 45%–199% higher in ME/CFS patients than in healthy controls. The values in the amygdala, thalamus, and midbrain positively correlated with cognitive impairment score, the values in the cingulate cortex and thalamus positively correlated with pain score, and the value in the hippocampus positively correlated with depression score.[13][14]
The rate‐of‐change of regional WM volumes in CFS patients was significantly different from that in NCs in the left posterior part of the inferior fronto‐occipital fasciculus (IFOF) and/or arcuate fasciculus (Fig. 2). In this location, WM volume relative to global WM volume decreased with time in the CFS group while in NCs it was unchanged.[1]
  • 2016, A qEEG/LORETA study of nine controls and nine CFS patients (per DePaul Symptom Questionnaire (DSQ) and Canadian Consensus Criteria (CCC) definitions), found significantly decreased eLORETA source analysis oscillations in the occipital, parietal, posterior cingulate, and posterior temporal lobes in Alpha and Alpha-2. This research suggests that "disruptions in these regions and networks could be a neurobiological feature of the disorder, representing underlying neural dysfunction."[18]
  • 2016, A qEEG/LORETA study of one CFS patient (per DSQ and CCC definitions), found deregulation of the functional connectivity networks. This may explain the common symptom of perceived cognitive deficits such as slow thinking, difficulty in reading comprehension, reduced learning and memory abilities and an overall feeling of being in a “fog".[19]
Our case study confirmed the pattern of dysregulation in the cortex reviewed in the introduction. Furthermore, since both periods of phase shift/lock durations were found to be significantly shorter, that might contribute to an increased rate of phase reset, also seen in our data. Phase reset deregulation--phase locking periods being too brief and phase reset happening too often—appear to be consistent with the associated lower rate of information processing and reaction times found in the ME and CFS literature. These deregulated states represent the brain during nonoptimal functioning, rendering it inefficient for most types of information processing functioning, whether it is executive functioning, memory, perceptual reasoning or information processing speed. When phase lock is significantly less than normal, as in this data set, the ability of the brain to sustain commitment of resources to mediate different functions is severely compromised. Phase shift duration in this data is also hypoactive, meaning that significantly less neurons are being recruited to perform a function than normal. The results here indicate slowed verbal comprehension, executive functions, perceptual reasoning, processing speed and memory, the sum total of which is known as cognitive impairment.[19]
Figure 1: Results of LORETA current source density in a case with CFS showing widespread decreased current density for delta at 2 Hz and beta (12- 15 Hz) demonstrating a global reduction in brain functioning (blue). The higher frequencies (beta) have been shown to be a function of delta frequencies. In other words, local oscillations are under constant influence of global brain dynamics (Buzsaki, 2006).[19]
This study is the first to investigate whole-brain MRS markers of neuroinflammation in ME/CFS. We report metabolite and temperature abnormalities in ME/CFS patients in widely distributed brain areas, suggesting ME/CFS is driven by diffuse pathophysiological processes affecting the whole brain, rather than regionally limited, which is consistent with the heterogeneity of its clinical symptoms. Our findings add support to the hypothesis that ME/CFS is the result of chronic, low-level neuroinflammation. While the whole-brain results are preliminary, we note that they largely agree with past publications that use MRS in ME/CFS. These results should be replicated in future studies with larger samples to further establish the profile of pathophysiological abnormalities in the brains of ME/CFS patients. Ultimately, the development of sensitive MRI markers of ME/CFS could supplement clinical tests to help guide treatment decisions.[8]

Notable studies[edit | edit source]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. 1.01.11.2 Shan, ZY; Kwiatek, R; Burnet, R; Del Fante, P; Staines, DR; Marshall-Gradisnik, SM; Barnden, LR (Apr 28, 2016), "Progressive brain changes in patients with chronic fatigue syndrome: A longitudinal MRI study", Journal of magnetic resonance imaging: JMRI, doi:10.1002/jmri.25283, PMID 27123773 
  2. Schwartz, R B; Garada, B M; Komaroff, A L; Tice, H M; Gleit, M; Jolesz, F A; Holman, B L (Apr 1994). "Detection of intracranial abnormalities in patients with chronic fatigue syndrome: comparison of MR imaging and SPECT". American Journal of Roentgenology. 162 (4): 935–941. doi:10.2214/ajr.162.4.8141020. ISSN 0361-803X. 
  3. Schwartz, R B; Komaroff, A L; Garada, B M; Gleit, M; Doolittle, T H; Bates, D W; Vasile, R G; Holman, B L (Apr 1994). "SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression". American Journal of Roentgenology. 162 (4): 943–951. doi:10.2214/ajr.162.4.8141022. ISSN 0361-803X. 
  4. Ros, Pablo R. (May 29, 2012). "MR/PET: The Ultimate Imaging Hybrid". Imaging Technology News. Retrieved Oct 30, 2018. 
  5. 5.05.15.2 Loggia, Marco L.; Chonde, Daniel B.; Akeju, Oluwaseun; Arabasz, Grae; Catana, Ciprian; Edwards, Robert R.; Hill, Elena; Hsu, Shirley; Izquierdo-Garcia, David (Jan 8, 2015). "Evidence for brain glial activation in chronic pain patients". Brain. 138 (3): 604–615. doi:10.1093/brain/awu377. ISSN 1460-2156. 
  6. 6.06.16.26.36.46.5 Inacio, Patricia (Oct 11, 2018). "In Fibromyalgia Patients, Brain Inflammation Imaged for First Time in Study". Fibromyalgia News Today. Retrieved Oct 30, 2018. 
  7. "ME and CFS Medical Abnormalities – Brain Issues". 
  8. 8.08.18.2 "Evidence of widespread metabolite abnormalities in Myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy". link.springer.com. 2019. doi:10.1007/s11682-018-0029-4. Retrieved Jan 17, 2019. 
  9. Zeineh, Michael M; Kang, James; Atlas, Scott W; et al. (Oct 29, 2014), "Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome", Radiology, 274 (2): 517–526, doi:10.1148/radiol.14141079 
  10. "How to Read & Understand This Oasis Brain HMPAO SPECTMap". 
  11. "Volunteers Needed for ME Research Study". 
  12. Puri, BK; Jakeman, PM; Agour, M; Gunatilake, KDR; Fernando, KAC; Gurusinghe, AI; Treasaden, IH; Waldman, AD; Gishen, P (2012), "Regional grey and white matter volumetric changes in myalgic encephalomyelitis (chronic fatigue syndrome): a voxel-based morphometry 3 T MRI study", British Journal of Radiology, 85 (1015): e270-3, doi:10.1259/bjr/93889091 
  13. Nakatomi, Yasuhito; Mizuno, Kei; Ishii, Akira; et al. (Mar 24, 2014), "Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: An ¹¹C-(R)-PK11195 PET Study", Journal of Nuclear Medicine, 2014 Jun;55(6): 945-50, doi:10.2967/jnumed.113.131045, PMID 24665088 
  14. 14.014.1 Tuller, David (Nov 24, 2014), "Brains of People With Chronic Fatigue Syndrome Offer Clues About Disorder", NY Times 
  15. Zeineh, Michael M; Kang, James; Atlas, Scott W; et al. (Oct 29, 2014), "Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome", Radiology, 274 (2): 517–526, doi:10.1148/radiol.14141079 
  16. Goldman, Bruce (Oct 28, 2014), "Study finds brain abnormalities in chronic fatigue patients", Stanford Medicine News Center 
  17. Jaime S (May 5, 2016), "Progressive Brain Changes in Patients with Chronic Fatigue Syndrome: Are our Brains Starved of Oxygen?", #MEAction 
  18. Zinn, Marcie; Zinn, Mark; Jason, Leonard (2016), "Intrinsic Functional Hypoconnectivity in Core Neurocognitive Networks Suggests Central Nervous System Pathology in Patients with Myalgic Encephalomyelitis: A Pilot Study", Applied Psychophysiology and Biofeedback, 41 (3): 283-300, doi:10.1007/s10484-016-9331-3, PMID 26869373 
  19. 19.019.119.2 dr.marcie.zinn@gmail.com, Zinn ML, DePaul University, Center for Community Research, Chicago, IL, Tel/ Fax: (773) 325-4923; E-mail:; Zinn, Mark A.; Jason, Leonard (2016). "qEEG / LORETA in Assessment of Neurocognitive Impairment in a Patient with Chronic Fatigue Syndrome: A Case Report". www.sciforschenonline.org. SciForschen. doi:10.16966/2469-6714.110. ISSN 2469-6714. Retrieved Aug 28, 2018. 
  20. Nimmo, Sasha (Jul 12, 2016). "Six year study of abnormal brain changes in chronic fatigue syndrome patients". ME Australia. Retrieved Aug 23, 2018. 
  21. Crew, Bec (Jul 6, 2016). "A Bug in FMRI Software Could Invalidate 15 Years of Brain Research". ScienceAlert. Retrieved Aug 23, 2018. 
  22. Glasser, Matthew F.; Coalson, Timothy S.; Robinson, Emma C.; Hacker, Carl D.; Harwell, John; Yacoub, Essa; Ugurbil, Kamil; Andersson, Jesper; Beckmann, Christian F. (Jul 20, 2016). "A multi-modal parcellation of human cerebral cortex". Nature. 536 (7615): 171–178. doi:10.1038/nature18933. ISSN 0028-0836. 
  23. Sample, Ian (Jul 20, 2016). "Updated map of the human brain hailed as a scientific tour de force". the Guardian. Retrieved Aug 23, 2018. 
  24. CNN, Susan Scutti, (Jul 20, 2016). "Updated brain map identifies 97 new areas". CNN. Retrieved Aug 23, 2018. 
  25. M, Beth (Feb 7, 2016). "Case Study: "Brain Fog" in CFS can be seen in qEEG/Loreta - #MEAction". #MEAction. Retrieved Aug 28, 2018. 
  26. Pena, Amy (Mar 21, 2018). "Fibromyalgia Study Identifies Main Types of Patients' Cognitive Dysfunction". Fibromyalgia News Today. Retrieved Aug 28, 2018. 
  27. Johnson, Cort (Sep 24, 2018). "Brain on Fire: Widespread Neuroinflammation Found in Chronic Fatigue Syndrome (ME/CFS) - Health Rising". Health Rising. Retrieved Sep 25, 2018. 
  28. "ME/CFS Involves Brain Inflammation: Results from a Ramsay Pilot Study". YouTube. SolveCFS. Dec 14, 2018. 
  29. "Publication from Dr. Jarred Younger's SMCI Ramsay pilot study supports neuroinflammation as a factor in ME/CFS". go.solvecfs.org. Retrieved Jan 17, 2019. 

Myalgic encephalomyelitis or chronic fatigue syndrome

Myalgic encephalomyelitis or M.E. has different diagnostic criteria to chronic fatigue syndrome; neurological symptoms are required but fatigue is an optional symptom.<ref name="ICP2011primer">{{Citation


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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history