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P-31 magnetic resonance spectroscopy (MRS) to detect abnormalities in energy metabolism of muscle tissue in mitochondrial encephalomyopathies and migraine?

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Citation

Jauslin, M., Dydak, U., Henning, A., Sprott, H., Boesiger, P., & Sandor, P. (2006). P-31 magnetic resonance spectroscopy (MRS) to detect abnormalities in energy metabolism of muscle tissue in mitochondrial encephalomyopathies and migraine?. Poster presented at 16th Migraine Trust International Symposium, London, UK.


Cite as: https://hdl.handle.net/21.11116/0000-0004-B61B-1
Abstract
Background: Previous studies have shown abnormalities in the recovery rate of the phosphocreatin signal normalized
with pH (TPCr/pH) after physical exercise in patients with Mitochondrial Encephalomyopathies (ME) with a well-
demonstrated defect in the energy metabolism.
Objective: To study the hypothesis of systemic energy failure in migraine by comparing the recovery rate TPCr/pH after
physical exercise in healthy volunteers (HV), ME as positive controls and in migraine patients with aura (MA) using a short exercise paradigm.
Methods: The calf muscles of 10 ME, 11 MA and 25 HV were examined with 31 P magnetic resonance spectroscopy (MRS). A
timeseries of 100 MRS measurements (6 seconds each) was recorded with a surface coil on a 1.5 T Philips Intera MR Scanner: rest (20 spectra) – exercise (20) – recovery (60). The pH values and the recovery rates TPCr/pH were calculated
from the postprocessed spectra. A sequence of increasingly rigorous quality criteria was applied to the data.
Results and Conclusion: The results of 7 ME, 5 MA and 18 HV fulfilled rigorous quality criteria and were therefore included into analysis. Independently of the level of applied quality criteria, no difference in TPCr/pH after exercise was found between ME and HV. This result is most likely due to the too short and sprintlike exercise paradigm which would not allow the oxidative metabolism to run at its full capacity and therefore is insufficient to yield the MR-detectable abnormalities in mitochondrial function of ME and MA.