Tag: magnetic resonance spectroscopy

In vivo magnetic resonance spectroscopy in chronic fatigue syndrome

Abstract:

The pathogenic mechanisms of chronic fatigue syndrome (CFS) are not clearly known. Fatigue, poor short-term memory and muscle pain are the most disabling symptoms in CFS. Research data on magnetic resonance spectroscopy (MRS) of muscles and brain in CFS patients suggest a cellular metabolic abnormality in some cases.

31P MRS of skeletal muscles in a subset of patients indicate early intracellular acidosis in the exercising muscles. 1H MRS of the regional brain areas in CFS have shown increased peaks of choline derived from the cell membrane phospholipids.

Cell membrane oxidative stress may offer a common explanation for the observed MRS changes in the muscles and brain of CFS patients and this may have important therapeutic implications. As a research tool, MRS may be used as an objective outcome measure in the intervention studies. In addition, regional brain 1H MRS has the potential for wider use to substantiate a clinical diagnosis of CFS from other disorders of unexplained chronic fatigue.

 

Source: Chaudhuri A, Behan PO. In vivo magnetic resonance spectroscopy in chronic fatigue syndrome. Prostaglandins Leukot Essent Fatty Acids. 2004 Sep;71(3):181-3. http://www.ncbi.nlm.nih.gov/pubmed/15253888

 

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

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.

 

Source: Lane RJ, Barrett MC, Taylor DJ, Kemp GJ, Lodi R. Heterogeneity in chronic fatigue syndrome: evidence from magnetic resonance spectroscopy of muscle. Neuromuscul Disord. 1998 May;8(3-4):204-9. http://www.ncbi.nlm.nih.gov/pubmed/9631403

 

31P-mr spectroscopy of peripheral skeletal musculature under load: demonstration of normal energy metabolites compared with metabolic muscle diseases

Abstract:

PURPOSE: 31P-MR spectroscopy of skeletal muscle under exercise was used to obtain the range of normal variation and comparison was made for different neuromuscular diseases.

METHODS: 41 examinations of 24 volunteers and 41 investigations in 35 patients were performed on 1.5 T MR systems (Gyroscan 515 und S15/ACSII, Philips). Localised 31P-MR spectra of the calf muscle were obtained in time series with a resolution of 12 s.

RESULTS: Two types of muscle energy metabolism were identified from the pattern of spectroscopic time course in volunteers: While the first group was characterised by a remarkable decline to lower pH values during exercise, the second group showed only small pH shifts (minimum pH: 6.48 +/- 0.13 vs 6.87 +/- 0.07, p < 10(-6)) although comparable workload conditions were maintained. The pH-values correlated well with blood lactate analysis. Patients with metabolic disorders and chronic fatigue syndrome (CFS) showed decreased resting values of PCr/(PCr + Pi) and increased pH levels during exercise. PCr recovery was significantly delayed (0.31 vs 0.65 min-1, p < 0.00005) in metabolic muscle disorders but was normal in CFS patients.

CONCLUSION: Findings in volunteers indicate utilisation of different metabolic pathways which seems to be related to the fibre type composition of muscle. Reduced resting levels for PCr/(PCr + Pi), altered pH time courses, and decreased PCr recovery seem to be helpful indicators for diagnosis of metabolic muscle disorders.

Source: Block W, Träber F, Kuhl CK, Keller E, Lamerichs R, Karitzky J, Rink H, Schild HH. 31P-mr spectroscopy of peripheral skeletal musculature under load: demonstration of normal energy metabolites compared with metabolic muscle diseases. Rofo. 1998 Mar;168(3):250-7. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/9551111

Reduced oxidative muscle metabolism in chronic fatigue syndrome

Abstract:

The purpose of this study was to determine if chronic fatigue syndrome (CSF) is characterized by abnormalities in oxidative muscle metabolism. Patients with CFS according to Centers for Disease Control (CDC) criteria (n = 22) were compared to normal sedentary subjects (n = 15).

CFS patients were also tested before and 2 days after a maximal treadmill test. Muscle oxidative capacity was measured as the maximal rate of postexercise phosphocreatine (PCr) resynthesis using the ADP model (Vmax) in the calf muscles using 31P magnetic resonance spectroscopy. Vmax was significantly reduced in CFS patients (39.6 +/- 2.8 mmol/L/min, mean +/- SE) compared to controls (53.8 +/- 2.8 mmol/L/min). Two days postexercise there was no change in resting inorganic phosphate (Pi)/PCr or Vmax in the CFS patients (n = 14).

In conclusion, oxidative metabolism is reduced in CFS patients compared to sedentary controls. In addition, a single bout of strenuous exercise did not cause a further reduction in oxidative metabolism, or alter resting Pi/PCr ratios.

Comment in: Chronic fatigue syndrome and skeletal muscle mitochondrial function. [Muscle Nerve. 1997]

 

Source: McCully KK, Natelson BH, Iotti S, Sisto S, Leigh JS Jr. Reduced oxidative muscle metabolism in chronic fatigue syndrome. Muscle Nerve. 1996 May;19(5):621-5. http://www.ncbi.nlm.nih.gov/pubmed/8618560