Reduced gait automaticity in female patients with chronic fatigue syndrome: Case-control study

Abstract:

Patients with chronic fatigue syndrome (CFS) report difficulties walking for a prolonged period of time. This study compares gait automaticity between women with CFS and nondisabled controls.

The “stops walking with eyes closed with secondary cognitive task” test is based on the classic “stops walking while talking” test but compares walking with eyes closed while performing a secondary cognitive task in a female CFS population (n = 34) and in female nondisabled controls (n = 38).

When initiating gate, 23.5% of patients with CFS looked toward the ground compared with only 2.6% of nondisabled controls. After 7 m, subjects were asked to close their eyes, and after another 7 m, they were asked, “How much is 100 minus 7?” Of the patients with CFS, 55.9% stopped walking compared with 5.3% of nondisabled controls. Less automated walking was observed in patients with CFS than in nondisabled controls (p < 0.001). The test-retest reliability is moderate for global stopping.

This simple test observed reduced gait automaticity in patients with CFS for the first time. Dual tasking could be helpful to address the functional limitations found in this particular study.

 

Source: Jan b Eyskens, Jo Nijs, Kristien Wouters, Greta Moorkens. Reduced gait automaticity in female patients with chronic fatigue syndrome: Case-control study. Journal of Rehabilitation Research & Development (JRRD), Volume 52 Number 7, 2015, Pages 805 — 814.
Note: You can read the full study HERE.

Epidemic myalgic encephalomyelitis

The letter below, “Epidemic myalgic encephalomyelitis,” was published in the British Medical Journal in 1978. In it, the authors maintain that ME is an organic illness that exists as a distinct clinical entity with recognizable signs and symptoms. The authors propose that the cause may be “a persistent viral infection.

 

Epidemic myalgic encephalomyelitis

Outbreaks of the paralytic disease known as epidemic myalgic encephalomyelitis have puzzled doctors all over the world in the past 30 years. One of the best known of these epidemics was that at the Royal Free Hospital in London in 1955, which affected more than 300 people. (1) Most outbreaks tend to occur in the summer, young adults are predominantly affected, and the incidence is higher in women. The evidence suggests that infection is spread by personal contact, and young hospital personnel seem particularly at risk. The features common to every epidemic include headache, unusual muscular pains (which may be severe), lymphadenopathy-often of the posterior cervical lymph nodes-and low-grade fever.(2, 3) In a minority of cases frank neurological signs can be detected by careful clinical examination: there may be nystagmus, diplopia, myoclonus, bulbar weakness, motor weakness, increased or decreased tendon reflexes, disturbances of the sphincters, and extensor plantar responses.(2-7) Fasciculations, cranial nerve lesions, and extrapyramidal signs have also been reported. Most patients complain of paraesthesiae, and sensory loss is common.”(4) One characteristic feature of the disease is exhaustion, any effort producing generalised fatigue. Often there are psychiatric abnormalities, especially emotional lability and lack of concentration.(1- 3, 4) The clinical outcome may take any of three courses: some patients recover completely, some follow a relapsing course, and some are permanently incapacitated.(3)

At a symposium held recently at the Royal Society of Medicine to discuss the disease and plan research there was clear agreement that myalgic encephalomyelitis is a distinct nosological entity. Other terms that have been used to describe the disease were rejected as unsatisfactory for various reasons: the cardinal clinical features show that the disorder is an encephalomyelitis; “Iceland disease” is not specific enough; and “neuromyasthenia” suggests a relation to myasthenia gravis whereas the muscle fatigability is different, as are the electrophysiological findings.(8) Indeed, the exhaustion and tiredness are similar to that described by patients with multiple sclerosis.(9) From the patient’s point of view the designation benign is also misleading, since the illness may be devastating. Originally the term was used because no deaths had been recorded from myalgic encephalomyelitis. Two patients who had had the disease have now been examined post mortem: one was found to have multiple sclerosis. The adjective epidemic is correct, since most cases occur in an epidemic, but the disease may be endemic, and sporadic cases may occur. (10-12)

Some authors have attempted to dismiss this disease as hysterical, (13) but the evidence now makes such a tenet unacceptable. Some purely psychiatric symptoms may well occur, particularly in patients entering the chronic phase. No doubt, too, in an epidemic some hysterical persons will simulate the symptoms of the disease. Nevertheless, the organic basis is clear-from the finding that the putative agent can be transferred to monkeys(14); the detection of an increased urinary output of creatine2 (15); the persistent finding of abnormal lymphocytes in the peripheral blood of some patients (16); the presence of lymphocytes and an increased protein concentration in the cerebrospinal fluid of occasional patients (3); and the neurological findings. At this symposium more evidence was produced to support the organic nature of the disease. Increased serum concentrations of lactic dehydrogenases and transaminases have been found in several patients examined during the acute attack. In a recent outbreak in London immunological studies showed a high incidence of serum anticomplementary activity and the presence of ill-defined aggregates on electron microscopy of acute-phase sera.(17) A perplexing finding, suggesting the possibility of a persistent virus infection, was the ability of lymphocytes from patients to proliferate and survive in vitro for up to 19 weeks. The results of electroencephalographic studies were also stated to be abnormal, confirming other reports. (10)

We still know nothing about the nature and cause of epidemic myalgic encephalomyelitis, but outbreaks are still occurring. Future epidemics should be studied by a collaborative team of neurologists, epidemiologists, virologists, and immunologists. Its findings would be important not only for the study of epidemic myalgic encephalomyelitis but also for other neurological disorders, including multiple sclerosis.

1 British Medical Journal, 1957, 2, 895.

2 White, D N, and Burtch, R B, Neurology, 1954, 4, 506.

3 Acheson, E D, American Journal of Medicine, 1959, 26, 569.

4 Gilliam, A G, Epidemiological Study of an Epidemic, Public Health Bulletin, No 240. US Public Health Service, Washington, 1938.

5 Acheson, E D, Lancet, 1955, 2, 394.

6 Pellew, R A A, Medical Journal of Australia, 1951, 1, 944.

7 Hill, R C J, South African Medical Journal, 1955, 29, 344.

8 Richardson, A T, Annals of Physical Medicine, 1956, 3, 81.

9 McAlpine, D, Compston, N D, and Lumsden, C E, Multiple Sclerosis, chap 5. Edinburgh and London, Livingstone, 1955. ”

10 Ramsay, A M, and O’Sullivan, E, Lancet, 1956, 1, 761.

11 Jelinek, J E, Lancet, 1956, 2, 494.

12 Ramsay, A M, Lancet, 1957, 2, 1196.

13 McEvedey, C P, and Beard, A W, British Medical Journal, 1970, 1, 7.

14 Pellew, R A A, and Miles, J A R, Medical Journal of Australia, 1955, 2, 480.

15 Albrecht, R M, Oliver, V L, and Poskanzer, D C, Journal of the American Medical Association, 1964, 187, 904.

16 Wallis, A L, MD Thesis, Edinburgh University, 1957.

17 Dillon, M J, et al, British Medical Journal, 1974, 1, 301.

 

Source: BRITISH MEDICAL JOURNAL 3 JUNE 1978 1436-1437

You can read and download a PDF file of the letter at:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1604957/?page=1

 

Extended B-cell phenotype in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A cross-sectional study

Abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a heterogeneous condition of unknown etiology characterized by multiple symptoms including fatigue, post-exertional malaise and cognitive impairment, lasting for at least 6 months.

Recently, two clinical trials of B-cell depletion therapy with rituximab (anti-CD20) reported convincing improvement in symptoms. A possible but undefined role for B-cells has therefore been proposed. Studies of the relative percentages of B-cell subsets in patients with ME/CFS have not revealed any reproducible differences from healthy controls (HC).

In order to explore whether more subtle alterations in B-cell subsets related to B-cell differentiation exist in ME/CFS patients we used flow cytometry to immunophenotype CD19+ B-cells. The panel utilized IgD, CD27 and CD38 (classical B-cell subsets) together with additional markers. A total of 38 patients fulfilling Canadian, Centre for Disease Control, and Fukuda ME/CFS criteria and 32 age/sex-matched HC were included.

We found no difference in percentages of classical subsets between ME/CFS patients and HC. However, we observed an increase in frequency (p<0.01) and expression (MFI; p=0.03) of CD24 on total B-cells, confined to IgD+ subsets. Within memory subsets, a higher frequency of CD21+CD38- B-cells (>20%) was associated with the presence of ME/CFS (Odds ratio: 3.47 (1.15-10.46); p=0.03) compared with HC and there was a negative correlation with disease duration.

In conclusion, we identified possible changes in B-cell phenotype in patients with ME/CFS. These may reflect altered B-cell function and if confirmed in other patient cohorts, could provide a platform for studies based on clinical course or responsiveness to rituximab-therapy.

 

Source: Fane Mensah, Amolak Bansal, Saul Berkovitz, Arti Sharma, Venkat Reddy, Maria J. Leandro and Geraldine Cambridge. Extended B-cell phenotype in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A cross-sectional study. Clin Exp Immunol. 2015 Dec 8. doi: 10.1111/cei.12749. [Epub ahead of print]