Magnetic resonance spectroscopy in evaluating cerebral metabolite imbalance in chronic obstructive pulmonary disease

Olfat M El-Shinnawy, Eman M Khedr, Mohamed M Metwally, Alaa EL-din Thabiet Hassan, Ahmad M Shaddad, Radwa Kamel Soliman

Egyptian Journal of Bronchology 2018 12(1):14-19

Rationale Magnetic resonance spectroscopy (MRS) is a powerful research tool and has been proved to provide additional clinically relevant information for several diseases such as brain tumors, metabolic disorders, and systemic diseases. Aim The aims of this study were to evaluate cerebral metabolic imbalance in chronic obstructive pulmonary disease (COPD) and to correlate the abnormalities with spirometric and gasometric parameters. Patients and methods In a case–control study, eight COPD patients and eight age-matched and sex-matched healthy control individuals were compared. 1H-MRS was performed using 1.5-T MRI/MRS scanner. Using 1H-MRS single-voxel technique, N-acetyl aspartate/choline (NAA/Cho), choline/creatine (Cho/Cr), and N-acetyl aspartate/creatine (NAA/Cr) ratios were estimated and compared in both groups. Results There were significant differences regarding the distribution of neurotransmitters in the temporal lobe only between COPD and control groups; there were significant positive correlations between the NAA/Cho ratio at the thalamus with both partial pressure of arterial carbon dioxide and base excess or base deficit. However, there was a significant positive correlation between the Cho/Cr ratio at the thalamus and forced vital capacity (l), and a significant positive correlation between the NAA/Cr ratio at the thalamus and BMI, and a negative correlation between the NAA/Cr ratio at the thalamus and partial pressure of arterial oxygen. There was a significant negative correlation between the NAA/Cr ratio at the temporal lobe and partial pressure of arterial carbon dioxide. Conclusion MRS provided an insight to study the neurochemical changes that occur in COPD patients. Chronic hypoxemia and hypercapnia seem to play a key role in the pathophysiology of neurochemical changes in COPD.

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