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To evaluate possible pathophysiologic links between cerebral changes in diabetic patients detected by proton magnetic resonance spectroscopy and clinical as well as laboratory parameters. The brains of 30 patients with diabetes mellitus and 30 healthy volunteers were examined using a STEAM sequence (TR 1500 ms, TE 20 ms). We measured in occipital gray matter and parietal white matter in a 1.5-Tesla magnet. Laboratory parameters were acquired before and after the examination. In diabetic patients a significant elevation of the myo-inositol/creatine ratio in gray and white matter was present (p = 0.006). Choline/creatine ratio in gray matter was elevated compared to normal controls (p = 0.002). No correlation with laboratory parameters was detected. Myo-inositol was even more elevated in patients with polyneuropathy (p = 0.024). No correlation with age or sex was detected. The changes found in diabetes are similar to those found in patients with Alzheimer's disease, dialysis, and after renal transplant, suggesting a similar etiology. Elevated myo-inositol may not only indicate osmolar changes in glial cells but also glial cell alteration due to amyloid or amylin deposition with formation of neurofibrillary tangles, especially as these changes are found in all of these diseases and no correlation to osmolar deterioration exists.

Hepatic encephalopathy is a common problem in cirrhosis. The pathogenesis of this complication of advanced liver disease still remains unclear. Magnetic resonance spectroscopy was used to assess prospectively cerebral metabolism in 51 patients with histologically proven cirrhosis (Child-Pugh classes A, B, and C, 18, 18, and 15, respectively) and 36 healthy volunteers. According to the results of psychometric tests, overt hepatic encephalopathy, subclinical encephalopathy, and no encephalopathy were found in 14, 21, and 16 patients, respectively. Myoinositol/creatine ratios in gray (.36 +/- .17) and white (.35 +/- .22) matter voxel were reduced significantly (P < .0001) in cirrhotic patients compared with healthy volunteers (gray matter, .51 +/- .11; white matter, .64 +/- .16). In addition, patients showed a significant reduction (P = .024) in white matter choline/creatine ratio (.77 +/- .27) compared with controls (.92 +/- .25), and glutamine/glutamate level was elevated in cirrhotic patients compared with controls (gray matter, P < .0001; white matter, P = .036). Changes in cerebral myoinositol and glutamine/glutamate levels correlated significantly with the severity of hepatic encephalopathy (P < .0001). However, these metabolic alterations were also detected in patients without hepatic encephalopathy (normal psychometric test results). N-acetyl aspartate/creatine ratios did not differ between patients and controls. Magnetic resonance imaging detected bright basal ganglia in 37 patients, which correlated significantly with portal-systemic shunting and elevation of glutamine/glutamate, but not with the degree of hepatic encephalopathy. In conclusion, magnetic resonance imaging and spectroscopy showed that alterations of cerebral metabolism are common in patients with cirrhosis, even without evidence of clinical or subclinical hepatic encephalopathy.

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