Vascular problems in CFS / ME


References to vasomotor instability / vasculitis in ME (CFS) in the obtained Authorities

A most cursory glance at the medical Authorities reveals the following:

A. From the earliest reports of ME, autonomic vasomotor instability has been noted:

e.g. A.M. Ramsay: Benign Myalgic Encephalomyelitis: Update: September 1976:539-541

e.g. A.M.Ramsay: A Baffling Syndrome with a Tragic Aftermath: / November 1981:

“A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder"

B. Reference to impaired blood flow in the micro-circulation:

e.g. L.O. Simpson et al: Myalgic Encephalomyelitis: New Zealand Medical Journal: 1984: 10th October: 698-699:

"Much of the symptornatology of ME is explicable on the expected consequences of impaired blood flow in the micro-circulation"

C. Reference to vasculopathy in ME found in the major textbook on ME edited by Dr Byron Hyde:

1. page 42 (chapter 5 / Hyde)

" We routinely observe patients with severely cold extremities and a visible line demarcating the cold from the area of normal skin temperature…….. The fact that the loss of normal blood flow may be persistent has been indicated by Gilliam (ref. 18, 1938)"

2. page 62

"Patients will ... complain of severe blanching of their extremities, nose, ears, lower arms and hands as well as lower legs and feet. Observation will often reveal a blanched clearly demarcated line separating warm from icy cold tissue. The whitened extremities may persist for hours and can be extremely painful"

3. page 70:

Hyde quotes from Wallis (ref. 25,1957): "The hemorrhages are mostly around small vessels, but some are also to be seen in the free tissue"

4. page 73:

Hyde discusses the occurrence of Raynaud's Disease in ME. “This is common in ME / CFS. These acute Raynaud's Disease changes are visible"

5. paqe 87:

Dr John Richardson (Chapter 8) Re the Central Nervous System involvement in ME: "Is it myelin, is it cellular, or is it vasonervorum, i.e.. vascular?"

6. page 89:

" A liver biopsy showed ... a vasculitis of the liver"

7. paqe 91:

"Liver Function Tests are sometimes abnormal and signify sometimes a

vasculitis of the liver"

8. page 250: Dr Jay Goldstein (Chapter 23)

"SPECT scanning... may justify vasodilator therapy with calcium channel


9. page 268:

Dr Betty Dowsett (Chapter 28) "ME is a multisystem syndrome including nervous, cardiovascular, endocrine and other involvement .... Symptoms and Signs (table 2): Vasculitic skin lesions-, autonomic dysfunction, especially circulation and thermoregulation"

10. page 376: Drs Hyde and Jain (Chapter 42)

Referring to the findings of Dr John Richardson: "frequent vasomotor abnormalities"

11. re: 1934 epidemic:

"vasomotor ... disturbances were almost constant findings ... with coldness and cyanosis. It was the impression of most observers that a generalised disturbance of vasomotor control occurred in these patients"

12. re: 1965 Galveston epidemic:

Dr Leon-Sotomayer: "vascular headaches"

note that these were classed as "long-term residuals" in 100% of ME patients.

13. re: Professor Behan's lecture to CIBA, 1988:

his team was regularly able to demonstrate micro-capillary perfusion defects in the cardiac muscle of ME patients

14. re: Nightingale Clinic cardiovascular observations on over 6,000 patients with ME:

vascular headaches"; "autonomic system dysfunction with vasomotor instability"

15. page 427: Dr R. Biddle (Chapter 48)

"... lymphocytes in the CFS congregate in the perivascular (Virchow Robin) spaces of the brain... these findings do suggest that the disease may involve the perivascular spaces of the brain"

16. page 428-9:

"Dilatation of the Virchow Robin spaces ... could also suggest intracranial arterial or periarterial pathology... in particular, one would expect to find a congregation of lymphocytes in the perivascular spares around the Central Nervous System arteries ... (the literature about the Cumberland epidemic in 1955 has revealed) "an artefact that is in an anatomical position similar to that suggested by MRI studies (see ref. Wallis, idem)

17. page 430:

re: the Los Angeles 1934 epidemic- "The blood vessels throughout the nervous system were distended with red blood cells... the most characteristic change was infiltration of the blood vessel walls"

18. page 433: Dr Ismael Mena (Chapter 49)

"most probably temporal lobe perfusion defects may fingerprint primary inflammatory changes or secondary vascular impairment in these patients………the diminished uptake of this oxime can be interpreted as due to

a) diminished rCBF,

b) inflammatory regional changes .... (present in 71% of patients studied)

19. page 597: Dr L.O.Simpson (Chapter 65)

"The presence of increased percentages of nondiscocytic erythrocytes ... will impair flow in capillaries smaller than the diameter of the cells. (and) may initiate stasis in the smallest capillaries"

20. page 598:

"if the stasis did not resolve, focal lesions of ischemic necrosis would develop"

21. page 601:

"The impaired capillary flow in tissues or organs with secretory functions may result in reduced secretory activity (which) could reach pathological levels"

22. page 604:

"More attention should be paid to means of improving microcirculatory blood flow, to alleviate symptoms"

23. page 677: Dr Jon Russell (Chapter 75)

NOTE: On page 645, Professor Hugh Fudenberg, (one of the pioneers of clinical immunology and twice nominated for the Nobel Prize) states "Those (ME) patients who presented with severe muscle pains as the predominant symptoms were initially given a diagnosis of fibromyalgia": Dr Russell is the world expert on fibromyalgia (which is a component of ME).

re: the prevalence of vasculitis: "It is apparent that some patients with ... fibromyalgia also exhibit RA / SLE / vasculitis ... with a frequency that has caught the attention of clinicians"; the general prevalence of vasculitis is stated as being 0.14

D. Other Papers

24. Enterovirus infections and systemic clinical manifestations with prolonged inflammatory syndrome: association with a persistence of specific IgM antibodies.

Cathebras, P. et al. Rev Med Interne: 1993:14:10:961

Abstract: "We report 9 Gases of enteroviral infection associated with systemic inflammatory disease, including 4 cases of vasculitis .....We then reviewed 36 cases of enteroviral infection ... among them 11 cases were found to present with sub acute or chronic inflammatory disease. We conclude that enteroviruses might be important triggers of systemic inflammatory disease".

25. Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome: comparison of MR Imaging and SPECT.

Schwartz, R. B.,Garada,B.M., Komaroff A. L. et al: American Journal of Roentgenology 1994:162:935-941

"in addition to CNS lupus, other inflammatory vascular.. conditions can appear similar to CFS (ME) clinically and radiologically……As with any chronic inflammatory condition affecting the CNS, the T2-bright foci on MR in CFS (ME) may represent perivascular cellular infiltrate and / or reactive demyelination of the surrounding white matter. Alternatively, these abnormalities may reflect the result of a vasculopathy specifically involving the small vessels of the cerebral white matter; indeed, the distribution of lesions on MR in CFS (ME) is similar to that observed in occlusive arteriolar disease of any origin. The cortical defects measured with SPECT likewise may result from decreased flow through cortical arterioles owing to vasculitis. Specifically, on the basis of our observations, the white matter abnormalities seen on MR images may represent ... chronic demyelination, which appears to be irreversible".

26. SPECT Imaging of the Brain: Comparison of Findings in Patients with Chronic Fatigue Syndrome, AIDS Dementia Complex (ADC) and Major Unipolar Depression

Richard B. Schwartz, Anthony L Komaroff et al: Am. J.  Roentgenology: 1994:162:943­-951

"This study shows that CFS (ME) shares some similarities on SPECT imaging with AIDS Dementia Complex         acute changes in radionuclide uptake in the younger population may be caused by inflammatory processes at the cellular or micro vascular level .... the findings in CFS (ME) are consistent with the hypothesis that CFS (ME) ... results from a viral infection of neurons, glia or vasculature .....viral infection can provoke neurological dysfunction by interfering with intra-cellular mechanisms or membrane transport systems .... or by cerebral hypo perfusion due to vasculitis".

Quotes (verbatim) from Dr Betty Dowsett (Past President of the United Kingdom ME Association) on 11th October 1998:

a)         "Most ME patients have vasculitis" (Note that Dr Dowsett distinguishes

            between patients with ubiquitous chronic fatigue syndrome and those with

            true, defined ME, and that she was referring ONLY to patients with

            true, defined ME).

b)         “13% of ME patients are indistinguishable from multiple sclerosis".

Please note that the above does not in any way constitute

a comprehensive literature review concerning vasculitis in ME.