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Tests for ME
Ten Diagnostic Tests for Myalgic Encephalomyelitis (ME)
This is a summary of information from the Quarterly Journal of the Australia (Victoria) "Emerge" newsletter (Winter 2008) compiled by Dr Nicole Phillips. It may be worth giving to the doctor or GP or if you are undergoing a medical examination at, or for work, as front line medical staff are receiving confusing research information on the causes and tests for ME.
Cardio-pulmonary exercise test with measurement of VO2 max, anaerobic threshold and maximal heart rate and respiration
This test is referred to in Disability and CFS by Dr Daniel Peterson. The test is well established and sedentary and ill norms are published. See medical paper "Diminished Cardiopulmonary Capacity During Post-Exertional Malaise (Abstract J Mark Van Ness PhD, C Snell and S Stevens). On the absence of a second exercise test, the lack of significant difference would suggest no functional impairment in ME patients.
But a second test the following day
should be done, to indicate functional impairment in ME, and atypical recovery response.
SPECT; PET and MRI brain scans
Some researchers have observed differences in blood flow to the brain, in ME, but studies remain unconfirmed. Brain imaging can demonstrate abnormalities such as reduced blood flow in areas involved in autonomic nervous system, sleep, concentration and pain including the frontal cortices, anterior cinglate and cerebellum. Exercise exacerbates restricted blood flow to the brain and can affect it for up to 72 hours. There are altered patterns of brain activation, altered serontonergic neurotransmission and reduced acetyle-caritine uptake. The Wernicke area for understanding and coherent speech may show evidence of reduced activity after exercise. Bright spots on scans could be evidence of arteriolar vasculopathy which could signify micro-vascular inflammation. Some researchers have demonstrated that all ME patients have reduced renal blood flow. Researcher Dr Gurdun Lange (USA) states that, major cognitive deficiency is found in information processing and that studies are becoming consistent on reduced blood flow to brain. There are spinal fluid abnormalities and MRI scans show altered patterns of brain activation in ME.
MRI brain scan indicates mitochondrial dysfunction and can indicate high lactic acid spikes near and around the hippocampus. MRI scanning is good to rule out gross abnormalities, such as brain tumours and obvious areas of brain damage while SPECT can help verify hypoperfusion in the brain.
Dr Jonathan Kerr 2007 IACFC/ME London Conference stated that genes expression studies indicate three main abnormalities in ME. Immune system, mitochondrial function and G-protein signaling. Seven genes are upregulated in MCS, associated with apoptosis, pesticides, mitochondrial function, demyelination and viral binding sites.
Muscle atrophy - research indicates mild to severe muscle atrophy on type II fibres. This suggests mitochondrial disorder precipitated by virus infection.
These are the two branches of the immune system. Some ME patients have over activation of the TH2 branch and under activation of the TH1 branch. This could cause an increased rate of allergy and sensitivity on the one hand and difficulty fighting off pathogens on the other.
Natural Killer (NK) Cell and T Cell Function Test
NK and T-cells are two other components of the immune system. Sets of patients have been shown to have reduced NK cells number and poor T-cell functioning. This would interfere with immune ability to find infected cells and kill them.
Abnormalities of the 2-5A pathway (RNase-L ratio)
Impaired Cellular Immune Response in ME
Two abnormalities in the responses cells have to infection in the interferon pathway have been documented. An antiviral enzyme in this pathway called the "RNase L" have been shown to be fragmented in many patients. Also an increased activity of another enzyme called protein-kinase PR (PKR) that is involved in killing cells infected with pathogens. This suggest immune system could have trouble finding pathogens and killing cells infected.
Viral antibodies include Coxsackie B bacteria, including HHV - 6, mycoplasma. See Wisconin Viral Research group
. Some patients clearly have persistent virus in the brain.. Symptoms observed in ME are compatibile with viral aetiology. Many infectious agents have been cited inluding Epstein Barr virus (glandular fever), parvovirus, enteroviruses, Q fever, mycoplasma and HHV. It would seem that infection is the most likely prime case of ME:
Test 8 Heart Function
There are two possible tests:
a) Impedance Cardiology (available at teaching hospitals)
b) 24 House Holter Monitoring: repetively oscillating T wave inversion and/or T wave flats during 24 hour monitoring
NB If a doctor insists on a
regular exercise stress test
e.g. to check ability to work, these two studies below should be referenced which show that a stress test MUST BE FOLLOWED THE NEXT DAY with another one to show post-exertional debility.
Legal and Scientific Consideration of the Exercise Stress Test J of CFS
Vol 14, No 2, 2007 pp61-75 M Ciccolella, R Staci, MA Stevens, CR Snell, M van Ness.
Available in pdf at
Tilt Table Tests
NB 97% of ME patients demonstrated vasovagal syncope (neurally mediated hypotension) on tilt able testing. Care should be taken with this test and it could cause serious effects in some ME patients.
In ME, Chronic Orthostatic Intolerance (COI) the ability to sustain upright activity (sitting, standing, walking) is very common. Long periods of standing still is particularly taxing in MCS. Lying flat rest the heart and is recuperative in ME.
(low oxygen levels)
Dr Paul Cheney found evidence of diastolic dysfunction in MCS with evidence of another cardiac abnormality (PFO) which results in hypoxia (low oxygen levels related to metabolic needs).
He stated that the cardiac index of ME patients can be so severe that it falls between the value of a patient with a heart attack and those in shock.
Neurocognitive testing and sleep studies
Neurocognitive performance is decreased in ME - information processing speed, working memory and information learning.
Sleep studies suggest the presence of:
impaired sleep efficiency
fragmented skeep architecture
decrease of type 3 and 4 sleep
abnormal REM sleep patterns
changes in daytime alertness
CT scans show reduced adrenal gland size, and there may be changes to thyroid levels (but thyroxin treatment is not recommended in ME)
Reduced HPA function
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