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List of muscle biopsy studies

Discussion in 'Latest ME/CFS Research' started by Snow Leopard, Jul 24, 2012.

  1. Snow Leopard

    Snow Leopard Senior Member

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    With discussion about Julia Newton's (ongoing) muscle biopsy study, I though I'd start a list of all the muscle biopsy studies that have been conducted so far. I personally feel this is a neglected area and one that is necessary, for the fatigue in ME/CFS is likely to be due to poor cellular recovery after fatiguing activity and as such, I feel that more studies need to be done on a cellular level.


    The list so far:


    Acta Neuropathol. 1991;83(1):61-5.
    http://www.ncbi.nlm.nih.gov/pubmed/1792865

    Mitochondrial abnormalities in the postviral fatigue syndrome.

    Behan WM, More IA, Behan PO.

    Source

    Department of Pathology, University of Glasgow, Scotland.

    Abstract

    We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.


    Aust N Z J Med. 1985 Jun;15(3):305-8.
    http://www.ncbi.nlm.nih.gov/pubmed/3864422

    Chronic relapsing myalgia (? Post viral): clinical, histological, and biochemical studies.

    Byrne E, Trounce I, Dennett X.

    Abstract

    Two patients with persistent myalgia characterised by onset after an ill-defined systemic illness, marked fluctuations in the severity of the symptoms, and normal neuromuscular examination with the exception of variable muscle tenderness on deep palpation, may have a forme fruste of myalgic encephalomyelitis. Differentiation from psychogenic muscle pain is important in management. Muscle histology revealed non-specific Type II fibre atrophy. Mitochondrial respiration was assayed polarographically in intact organelles in vitro and revealed a mild depression of State 3 respiration rates with Site I and Site II substrates.


    Neurosci Lett. 1996 Apr 19;208(2):117-20.
    http://www.ncbi.nlm.nih.gov/pubmed/8859904

    Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.

    Vecchiet L, Montanari G, Pizzigallo E, Iezzi S, de Bigontina P, Dragani L, Vecchiet J, Giamberardino MA.

    Source

    Institute of Medical Pathophysiology, 'G. D'Annunzio' University of Chieti, Italy.

    Abstract

    Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects. Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscles (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150-3000 times the normal values. By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripberal mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.


    Free Radic Biol Med. 2000 Dec 15;29(12):1252-9.
    http://www.ncbi.nlm.nih.gov/pubmed/11118815

    Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome.

    Fulle S, Mecocci P, Fanó G, Vecchiet I, Vecchini A, Racciotti D, Cherubini A, Pizzigallo E, Vecchiet L, Senin U, Beal MF.

    Source

    Lab. Interuniversitario di Miologia, Dip. Biologia Cellulare e Molecolare, Universitá di Perugiá, Perugia, Italy.

    Abstract

    Chronic fatigue syndrome (CFS) is a poorly understood disease characterized by mental and physical fatigue, most often observed in young white females. Muscle pain at rest, exacerbated by exercise, is a common symptom. Although a specific defect in muscle metabolism has not been clearly defined, yet several studies report altered oxidative metabolism. In this study, we detected oxidative damage to DNA and lipids in muscle specimens of CFS patients as compared to age-matched controls, as well as increased activity of the antioxidant enzymes catalase, glutathione peroxidase, and transferase, and increases in total glutathione plasma levels. From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia. These data support an organic origin of CFS, in which muscle suffers oxidative damage.


    Hum Mol Genet. 1995 Apr;4(4):751-4.
    http://www.ncbi.nlm.nih.gov/pubmed/7633428

    Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome.

    Zhang C, Baumer A, Mackay IR, Linnane AW, Nagley P.

    Source
    Department of Biochemistry, Monash University, Clayton, Victoria, Australia.


    J R Soc Med. 1988 June; 81(6): 326–329.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1291623/

    Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.

    L C Archard, N E Bowles, P O Behan, E J Bell, and D Doyle

    Abstract

    Enterovirus-specific probes have been prepared by reverse transcription of conserved sequences in purified Coxsackie B2 virus genomic RNA and molecular cloning techniques. These probes were used in quantitative slot blot hybridizations to test for the presence of enterovirus-specific RNA in skeletal muscle biopsy specimens from 96 patients who had suffered from the postviral fatigue syndrome myalgic encephalomyelitis for up to 20 years. Biopsy specimens from 20 patients were positive for the presence of virus-specific RNA with hybridization signals more than three standard deviations greater than the mean of the normal muscle controls. Biopsies from the remaining 76 patients were indistinguishable from the controls. These data show that enterovirus RNA is present in skeletal muscle of some patients with postviral fatigue syndrome up to 20 years after onset of disease and suggest that a persistent virus infection has an aetiological role.


    J Neurol Neurosurg Psychiatry. 1998 Mar;64(3):362-7.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2169994/

    Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome.

    Lane RJ, Barrett MC, Woodrow D, Moss J, Fletcher R, Archard LC.

    Source

    Division of Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, London, UK.

    Abstract

    OBJECTIVES:

    To examine the proportions of type 1 and type 2 muscle fibres and the degree of muscle fibre atrophy and hypertrophy in patients with chronic fatigue syndrome in relation to lactate responses to exercise, and to determine to what extent any abnormalities found might be due to inactivity.

    METHODS:

    Quadriceps needle muscle biopsies were obtained from 105 patients with chronic fatigue syndrome and the proportions of type 1 and 2 fibres and fibre atrophy and hypertrophy factors were determined from histochemical preparations, using a semiautomated image analysis system. Forty one randomly selected biopsies were also examined by electron microscopy. Lactate responses to exercise were measured in the subanaerobic threshold exercise test (SATET).

    RESULTS:

    Inactivity would be expected to result in a shift to type 2 fibre predominance and fibre atrophy, but type 1 predominance (23%) was more common than type 2 predominance (3%), and fibre atrophy was found in only 10.4% of cases. Patients with increased lactate responses to exercise did have significantly fewer type 1 muscle fibres (p<0.043 males, p<0.0003 females), but there was no evidence that this group was less active than the patients with normal lactate responses. No significant ultrastructural abnormalities were found.

    CONCLUSION:

    Muscle histometry in patients with chronic fatigue syndrome generally did not show the changes expected as a result of inactivity. However, patients with abnormal lactate responses to exercise had a significantly lower proportion of mitochondria rich type 1 muscle fibres.


    Neuromuscul Disord. 1998 May;8(3-4):204-9.
    http://www.ncbi.nlm.nih.gov/pubmed/9631403

    Heterogeneity in chronic fatigue syndrome: evidence from magnetic resonance spectroscopy of muscle.

    Lane RJ, Barrett MC, Taylor DJ, Kemp GJ, Lodi R.
    Source

    Division of Clinical Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, London, UK.

    Abstract

    It has been shown previously that some patients with chronic fatigue syndrome show an abnormal increase in plasma lactate following a short period of moderate exercise, in the sub-anaerobic threshold exercise test (SATET). This cannot be explained satisfactorily by the effects of 'inactivity' or 'deconditioning', and patients with abnormal lactate responses to exercise (SATET +ve) have been found to have significantly fewer Type 1 muscle fibres in quadriceps biopsies than SATET -ve patients. We performed phosphorus magnetic resonance spectroscopy on forearm muscles of 10 SATET +ve patients, 9 SATET -ve patients and 13 sedentary volunteers. There were no differences in resting spectra between these groups but at the end of exercise, intracellular pH in the SATET +ve patients was significantly lower than in both the SATET -ve cases and controls (P < 0.03), and the SATET +ve patients also showed a significantly lower ATP synthesis rate during recovery (P < 0.01), indicating impaired mitochondrial oxidative phosphorylation. These observations support other evidence which indicates that chronic fatigue syndrome is a heterogeneous disorder, and confirms the view that some chronic fatigue syndrome patients have a peripheral component to their fatigue.


    Int J Immunopathol Pharmacol. 2009 Apr-Jun;22(2):427-36.
    http://www.ncbi.nlm.nih.gov/pubmed/19505395

    Functional characterization of muscle fibres from patients with chronic fatigue syndrome: case-control study.

    Pietrangelo T, Toniolo L, Paoli A, Fulle S, Puglielli C, Fanò G, Reggiani C.
    Source

    Dept. Basic and Applied Medical Sciences (BAMS), Center for Excellence on Ageing (CeSI), University - G. dAnnunzio- Chieti-Pescara, Chieti, Italy.

    Abstract

    Chronic fatigue syndrome (CFS) is a disabling condition characterized by unexplained chronic fatigue that impairs normal activities. Although immunological and psychological aspects are present, symptoms related to skeletal muscles, such as muscle soreness, fatigability and increased lactate accumulation, are prominent in CFS patients. In this case-control study, the phenotype of the same biopsy samples was analyzed by determining i) fibre-type proportion using myosin isoforms as fibre type molecular marker and gel electrophoresis as a tool to separate and quantify myosin isoforms, and ii) contractile properties of manually dissected, chemically made permeable and calcium-activated single muscle fibres. The results showed that fibre-type proportion was significantly altered in CSF samples, which showed a shift from the slow- to the fast-twitch phenotype. Cross sectional area, force, maximum shortening velocity and calcium sensitivity were not significantly changed in single muscle fibres from CSF samples. Thus, the contractile properties of muscle fibres were preserved but their proportion was changed, with an increase in the more fatigue-prone, energetically expensive fast fibre type. Taken together, these results support the view that muscle tissue is directly involved in the pathogenesis of CSF and it might contribute to the early onset of fatigue typical of the skeletal muscles of CFS patients.


    Mitochondrion. 2011 Sep;11(5):735-8. Epub 2011 Jun 2.
    http://www.ncbi.nlm.nih.gov/pubmed/21664495

    Mitochondrial enzymes discriminate between mitochondrial disorders and chronic fatigue syndrome.

    Smits B, van den Heuvel L, Knoop H, Küsters B, Janssen A, Borm G, Bleijenberg G, Rodenburg R, van Engelen B.

    Source

    Neuromuscular Center Nijmegen, Department of Neurology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

    Abstract

    We studied the extent of mitochondrial involvement in chronic fatigue syndrome (CFS) and investigated whether measurement of mitochondrial respiratory chain complex (RCC) activities discriminates between CFS and mitochondrial disorders. Mitochondrial content was decreased in CFS compared to healthy controls, whereas RCC activities corrected for mitochondrial content were not. Conversely, mitochondrial content did not discriminate between CFS and two groups of mitochondrial disorders, whereas ATP production rate and complex I, III and IV activity did, all with higher activities in CFS. We conclude that the ATP production rate and RCC activities can reliably discriminate between mitochondrial disorders and CFS.


    Infectious Diseases in Clinical Practice
    http://journals.lww.com/infectdis/A..._Involvement_in_Patients_with_Chronic.10.aspx

    Cardiac Involvement in Patients with Chronic Fatigue Syndrome as Documented with Holter and Biopsy Data in Birmingham, Michigan, 1991-1993

    Lerner, Martin A.; Goldstein, James; Chang, Chung-ho; Zervos, Marcus; Fitzgerald, James T.; Dworkin, Howard J.; Lawrie-Hoppen, Claudine; Korotkin, Steven M.; Brodsky, Marc; O'Neill, William

    Abstract

    We report the prevalence of abnormal oscillating T-waves at Holter monitoring in a consecutive case series of 67 chronic fatigue syndrome (CFS) patients from an infectious diseases center in Birmingham, Michigan, in the years 1991-1993, and compare these abnormal T-waves to similar tests in 78 non-CFS patients matched for age, place, time, and the absence of known other confounding medical diseases. Patients in both groups had normal resting 12-lead electrocardiograms (ECGs), rest/stress myocardial perfusion studies (thallium 201 or TC-99 sestamibi studies and two-dimensional echocardiograms (except for the incidental findings of mitral valve prolapse without significant regurgitation or, an incidental nonsignificant aortic stenosis). The prevalence of labile T-wave abnormalities by Holter monitoring was greater in CFS patients than in non-CFS patients (P <.01). Repetitive T-wave flattening was a sensitive indicator of the presence of CFS. The absence of these abnormal T-waves made the diagnosis of CFS unlikely (statistical sensitivity, 0.96). The combination (e.g., the presence of both oscillating T-wave flattenings plus T-wave inversions) was an accurate indicator of the possible presence of CFS. Right ventricular endomyocardial biopsies in CFS patients showed a single patient with a lymphocytic myocarditis. Light and electron microscopic cardiomyopathic changes were present in the others.


    J Neurol Neurosurg Psychiatry. 2003 Oct;74(10):1382-6.
    http://www.ncbi.nlm.nih.gov/pubmed/14570830

    Enterovirus related metabolic myopathy: a postviral fatigue syndrome.

    Lane RJ, Soteriou BA, Zhang H, Archard LC.

    Source

    Division of Clinical Neurosciences and Psychological Medicine, Imperial College, London SW7, UK.

    Abstract
    OBJECTIVE:

    To detect and characterise enterovirus RNA in skeletal muscle from patients with chronic fatigue syndrome (CFS) and to compare efficiency of muscle energy metabolism in enterovirus positive and negative CFS patients.
    METHODS:

    Quadriceps muscle biopsy samples from 48 patients with CFS were processed to detect enterovirus RNA by two stage, reverse transcription, nested polymerase chain reaction (RT-NPCR), using enterovirus group specific primer sets. Direct nucleotide sequencing of PCR products was used to characterise the enterovirus. Controls were 29 subjects with normal muscles. On the day of biopsy, each CFS patient undertook a subanaerobic threshold exercise test (SATET). Venous plasma lactate was measured immediately before and after exercise, and 30 minutes after testing. An abnormal lactate response to exercise (SATET+) was defined as an exercise test in which plasma lactate exceeded the upper 99% confidence limits for normal sedentary controls at two or more time points.
    RESULTS:

    Muscle biopsy samples from 20.8% of the CFS patients were positive for enterovirus sequences by RT-NPCR, while all the 29 control samples were negative; 58.3% of the CFS patients had a SATET+ response. Nine of the 10 enterovirus positive cases were among the 28 SATET+ patients (32.1%), compared with only one (5%) of the 20 SATET- patients. PCR products were most closely related to coxsackie B virus.
    CONCLUSIONS:

    There is an association between abnormal lactate response to exercise, reflecting impaired muscle energy metabolism, and the presence of enterovirus sequences in muscle in a proportion of CFS patients.


    J Med. 1993;24(2-3):145-60.
    http://www.ncbi.nlm.nih.gov/pubmed/8409778

    Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy.

    Bowles NE, Bayston TA, Zhang HY, Doyle D, Lane RJ, Cunningham L, Archard LC.

    Source

    Department of Biochemistry, Charing Cross and Westminster Medical School, London, England.

    Abstract

    Molecular hybridization using an enterovirus group specific probe detected virus RNA in muscle biopsy samples from 25 of 96 cases of inflammatory muscle disease and similarly from 41 of 158 cases of postviral fatigue syndrome (PFS). Enterovirus RNA was detected in only two of 152 samples of control muscle. The inflammatory myopathy group comprised patients with polymyositis (PM), juvenile dermatomyositis (JDM) or adult dermatomyositis (DM), and all showed the presence of an inflammatory infiltrate and fiber necrosis on histological examination of a muscle biopsy sample. In contrast, muscle samples from the PFS group were histologically normal except for non-specific changes such as occasional single fiber atrophy. By analogy with enteroviral myocarditis, which can progress to a post-inflammatory disease with persistence of virus in myocardium and disposes to the rapid development of dilated cardiomyopathy, we propose that PFS syndrome may be a sequela of a previous inflammatory viral myopathy.


    J Gen Virol. 1990 Jun;71 ( Pt 6):1399-402.
    http://www.ncbi.nlm.nih.gov/pubmed/2161907

    Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.

    Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC.

    Source

    Department of Biochemistry, Charing Cross and Westminster Medical School, London, U.K.

    Abstract

    A subgenomic restriction fragment from cDNA prepared from Coxsackie B2 virus (CVB2) RNA was subcloned into a riboprobe vector allowing the production of enteroviral group-specific RNA probes complementary to either the positive (genomic) or negative (template) strand of enteroviral RNA. These riboprobes were used to follow productive infection of cultured cells by CVB2; as expected, positive strand RNA was synthesized in approximately 100-fold excess over negative strand. RNA was extracted from muscle biopsy samples from patients with chronic fatigue syndrome and probed for the presence of enteroviral RNA. In cases where enteroviral RNA was detected the amounts of positive and negative strands of enteroviral RNA were approximately equal, in contrast to the situation in lytic infection of cultured cells. This suggests that enterovirus persistence in muscle is due to a defect in control of viral RNA synthesis.


    Br Med Bull. 1991 Oct;47(4):852-71.
    http://www.ncbi.nlm.nih.gov/pubmed/1665379

    Persistent virus infection of muscle in postviral fatigue syndrome.

    Cunningham L, Bowles NE, Archard LC.

    Source

    Department of Biochemistry, Charing Cross and Westminster Medical School, London, UK.

    Abstract

    Nucleic acid was extracted from muscle biopsy samples from a series of highly selected patients suffering from chronic muscle fatiguability following a viral infection (Postviral Fatigue Syndrome: PVFS). Samples were examined for the presence of enteroviral RNA sequences or Epstein-Barr (EBV) virus DNA sequences by molecular hybridisation as these two agents have been implicated by retrospective serology in the aetiology of PVFS. We found enteroviral RNA in 24% of biopsy samples and EBV DNA in a further 9% of biopsy samples: no biopsy was positive for both enteroviral RNA and EBV DNA. In addition, in the case of enteroviruses we found that the persisting virus is defective in control of RNA replication as both strands of enteroviral RNA are present in similar amounts: this is unlike the asymmetric synthesis of genomic RNA seen in a productive, cytolytic enterovirus infection. The implications of these data in relation to mechanisms of viral persistence and muscle dysfunction are discussed.


    Br Med Bull. 1991 Oct;47(4):872-85.
    http://www.ncbi.nlm.nih.gov/pubmed/1665380

    Amplification and identification of enteroviral sequences in the postviral fatigue syndrome.

    Gow JW, Behan WM.

    Source

    University Department of Neurology, Southern General Hospital, Glasgow, UK.

    Abstract

    Evidence from several sources has long suggested that enteroviruses might play a role in the postviral fatigue syndrome (PVFS). We used the most sensitive molecular virological method available at present, the polymerase chain reaction (PCR) amplification technique, to look for enteroviral copies in peripheral blood leucocytes and muscle from a well-defined group of patients. We demonstrated that our PCR method amplified a sequence common to a wide range of enteroviral serotypes. A highly significant number of the muscle biopsies (53%: P = less than 0.001) from the patients were positive for enteroviral sequences. With regard to the leucocyte samples, 16% in both patient and control were positive. The PCR results on the peripheral blood leucocytes were in keeping with serological findings, in showing that the level of exposure to enteroviruses seemed to be the same in patients and controls: it was therefore of the greatest interest that patients were 6.7 times more likely to have enteroviral genome in their muscle. We conclude that persistent enteroviral infection plays a role in the pathogenesis of PVFS, also providing preliminary evidence that severe mitochondrial injury is one of the mechanisms involved.


    BMJ. 1991 March 23; 302(6778): 692–696.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1669122/


    Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.

    J W Gow, W M Behan, G B Clements, C Woodall, M Riding, and P O Behan

    Abstract

    OBJECTIVE--To determine the presence of enteroviral sequences in muscle of patients with the postviral fatigue syndrome. DESIGN--Detection of sequences with the polymerase chain reaction in a well defined group of patients with the syndrome and controls over the same period. SETTING--Institute of Neurological Sciences, Glasgow. SUBJECTS--60 consecutive patients admitted to the institute with the postviral fatigue syndrome who had undergone extensive investigation to exclude other conditions. 41 controls from the same catchment area without evidence of fatigue, all undergoing routine surgery. MAIN OUTCOME MEASURES--Routine investigations, serological screen for antibodies to a range of viruses, and presence of enteroviral RNA sequences in muscle biopsy specimens. RESULTS--15 (25%) patients and 10 (24.4%) controls had important serological findings. 12 patients had neutralising antibody titres of greater than or equal to 256 to coxsackieviruses B1-5 (six positive for enteroviral RNA sequences, six negative); three were positive for Epstein-Barr virus specific IgM (two positive, one negative). Six controls had similar neutralising antibody titres to coxsackieviruses (all negative); one was positive for Epstein-Barr virus specific IgM (negative); and three had titres of complement fixing antibody greater than or equal to 256 to cytomegalovirus (all negative). Overall, significantly more patients than controls had enteroviral RNA sequences in muscle (32/60, 53% v 6/41, 15%; odds ratio 6.7, 95% confidence interval 2.4 to 18.2). This was not correlated with duration of disease, patient and age, or to raised titres of antibodies to coxsackieviruses B1-5. CONCLUSIONS--Persistent enteroviral infection of muscle may occur in some patients with postviral fatigue syndrome and may have an aetiological role.


    Clin Infect Dis. 1994 Jan;18 Suppl 1:S126-9.
    http://www.ncbi.nlm.nih.gov/pubmed/8148439

    Studies on enterovirus in patients with chronic fatigue syndrome.

    Gow JW, Behan WM, Simpson K, McGarry F, Keir S, Behan PO.

    Source

    Department of Neurology, University of Glasgow, Scotland, United Kingdom.

    Abstract

    A large study on 121 patients with the chronic fatigue syndrome (CFS) that examined muscle biopsy samples for enterovirus by means of polymerase chain reaction analysis was carried out. The results were compared with those obtained from 101 muscle biopsy specimens from patients with a variety of other neuromuscular disorders (OND), including neurogenic atrophies, dystrophies, and mitochondrial, metabolic, and endocrine myopathies. Thirty-two (26.4%) of the biopsy specimens from the group of patients with CFS were positive, compared with 20 (19.8%) from the group of patients with OND, a difference that was not significant. This finding is in contrast to those of our previous smaller study in which significantly more patients with CFS than control subjects (53% [32 of 60] vs. 15% [6 of 41]) had enterovirus RNA sequences in their muscle. It was concluded that it is unlikely that persistent enterovirus infection plays a pathogenetic role in CFS, although an effect in initiating the disease process cannot be excluded.

    Ann Intern Med. 1994 Jun 1;120(11):972-3.
    http://www.ncbi.nlm.nih.gov/pubmed/8172448

    Enterovirus in the chronic fatigue syndrome.

    McGarry F, Gow J, Behan PO.

    [Case report which describes the detection EV RNA by PCR in the hypothalamus, brainstem, heart, and muscle of an individual with CFS who committed suicide; control tissues were negative.]

    J Med Virol. 2003 Dec;71(4):540-7.
    http://www.ncbi.nlm.nih.gov/pubmed/14556267

    Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects.

    Douche-Aourik F, Berlier W, Féasson L, Bourlet T, Harrath R, Omar S, Grattard F, Denis C, Pozzetto B.

    Source

    Laboratory of Bacteriology-Virology (GIMAP), Faculté de Médecine Jacques Lisfranc, Saint-Etienne, France.

    Abstract

    Enterovirus RNA has been found previously in specimens of muscle biopsy from patients with idiopathic dilated cardiomyopathy, chronic inflammatory muscle diseases, and fibromyalgia or chronic fatigue syndrome (fibromyalgia/chronic fatigue syndrome). These results suggest that skeletal muscle may host enteroviral persistent infection. To test this hypothesis, we investigated by reverse transcription-polymerase chain reaction (RT-PCR) assay the presence of enterovirus in skeletal muscle of patients with chronic inflammatory muscle diseases or fibromyalgia/chronic fatigue syndrome, and also of healthy subjects. Three of 15 (20%) patients with chronic inflammatory muscle diseases, 4 of 30 (13%) patients with fibromyalgia/chronic fatigue syndrome, and none of 29 healthy subjects was found positive. The presence of VP-1 enteroviral capsid protein was assessed by an immunostaining technique using the 5-D8/1 monoclonal antibody; no biopsy muscle from any patient or healthy subject was found positive. The presence of viral RNA in some muscle biopsies from patients exhibiting muscle disease, together with the absence of VP-1 protein, is in favor of a persistent infection involving defective viral replication.
    Snowdrop, Simon, Enid and 2 others like this.
  2. Gamboa

    Gamboa Senior Member

    Messages:
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    136
    Canada
    Very interesting.Too bad these studies are so old.

    My doctor , Dr. Byron Hyde , is interested in getting a muscle biopsy done on me but it is not an easy test to get ordered. I am supposed to be looking into it myself since I used to work at the Ottawa Hospital in the Pathology Lab and might have some connections. The problem, as usual, is convincing the doctors that ME/CFS is real and has real, measurable pathologies. I'm concerned that I will convince someone to do a muscle biopsy on me, they will find nothing wrong, and everyone will continue to believe that ME/CFS is all in the mind. I hate visiting my old work place and colleagues since they all say how great I look and I can tell most are thinking there is nothing wrong with me.

    By the way, I have had a two day exercise test using the Pacific Fatigue Lab Protocol ( the Stephens Protocol?) and had measurable abnormalities in my aerobic metabolic pathway. I went into anaerobic metabolism early which causes a buildup of lactic acid in the muscles and fatigue. I also had abnormal metabolites showing up in a urine test done by Nutrichem Labs, illustrating a problem with aerobic metabolism. This is why Dr. Hyde is interested in getting the muscle biopsy done.
  3. Snow Leopard

    Snow Leopard Senior Member

    Messages:
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    Likes:
    1,426
    Australia
    Yes, there is a disappointing lack of studies in the last 10 years.

    Though this list is by no means exhaustive and I have added a few more to the list today..
  4. mon âme

    mon âme

    Messages:
    1
    Likes:
    0
    Gamboa,

    This muscle biopsy is for diagnostic purposes or does Dr. Hyde have a treatment plan? Personally, I don't see the point of going through all this if there is not treatment for it.
  5. Gamboa

    Gamboa Senior Member

    Messages:
    182
    Likes:
    136
    Canada
    It would be for diagnostic purposes. I will go through anything (well almost anything) to get proof that something is physically wrong with me. Along with actual proof comes respect. The more documented abnormalities the better. It could also be useful for insurance purposes at a later date. At the moment I am getting disability payments but you never know when that might change.

    I am also very inquisitive and need to know exactly why I don't feel well.
    Sea likes this.
  6. RYO

    RYO

    Messages:
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    Likes:
    4
    North Carolina
    Coxsackie virus has been known to cause viral cardiomyopathy. Here is an article that reviews use of interferon b. http://circ.ahajournals.org/content/107/22/2793
    You can also google Innate and adaptive immune responses against picornaviruses and their counteractions: An Overview (Andreas Dotzauer)
  7. Enid

    Enid Senior Member

    Messages:
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    UK
    Gee whiskers - having had everything passing as Polio, MS, Parkinsons enormously painful nerve testing - do you think we can get there. And oh yes we will. But they must join research. One aspect only - got more pathology - lets find the b.... cause setting into motion. At this stage we know Immume dysregulation - there's the real cause. - and why.

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