ABSTRACT
Wernicke's encephalopathy (WE) is a disease classically associated with nutrition deficiency. It is characterized by typical symptoms like confusion, ataxia and ophthalmoparesis, and developes due to thiamine deficieny in alcoholic patients. Recently, it has been shown that WE could ocur in patients with gastric carcinoma without a history of alcohol use. In this paper, we have made some suggestions about early diagnosis, treatment and prevention of WE by discussing the development of WE in a patient with unresectable gastric carcinoma, who had been inpatient for a long time and given radiotherapy and chemotherapy.
ABSTRACT
OBJECTIVE: The aim of this study was to use MR spectroscopy to determine whether the brain metabolism of children with psychomotor delay of unknown cause differs from that of children without psychomotor delay. SUBJECTS AND METHODS: Twenty children (10 girls, 10 boys; mean age, 8.65 years; range, 4-15 years) with psychomotor delay and 19 children without psychomotor delay who served as controls (nine girls, 10 boys; mean age, 8.79 years; range, 6-13 years) were evaluated with multivoxel MR spectroscopy of the brain. The Stanford-Binet test and Wechsler Intelligence Scale for Children-Revised were used to evaluate developmental quotient. Psychomotor delay was assessed as severe (developmental quotient, < 50), moderate (developmental quotient, 50-75) and mild (developmental quotient, > 75). The controls had a developmental quotient greater than 95. Spectra were acquired from eight specific voxels at the bilateral parasagittal frontal and parietal gray matter and the bilateral frontal and parietal white matter at the level of the centrum semiovale. The ratios of N-acetylaspartate (NAA) to choline (Cho), NAA to creatine (Cr), and choline to creatine were determined. RESULTS: Thirteen children had minor and seven children had moderate psychomotor delay. In the psychomotor delay group, the right frontal white matter NAA/Cho, NAA/Cr, and Cho/Cr ratios were 1.45 +/- 0.18, 1.95 +/- 0.33, and 1.36 +/- 0.27; in the control group the ratios were 1.46 +/- 0.23, 2.04 +/- 0.33, and 1.41 +/- 0.19. The ratios for the left frontal lobe white matter were 1.34 +/- 0.21, 2.01 +/- 0.33, and 1.55 +/- 0.26 in the psychomotor delay group and 1.42 +/- 0.15, 2.17 +/- 0.34, and 1.53 +/- 0.25 in the control group. The ratios for the right parietal lobe white matter were 1.80 +/- 0.38, 2.04 +/- 0.43, and 1.18 +/- 0.35 in the psychomotor delay group and 1.89 +/- 0.31, 2.16 +/- 0.30, and 1.17 +/- 0.23 in the control group. The left parietal lobe white matter ratios were 1.66 +/- 0.36, 2.08 +/- 0.35, and 1.35 +/- 0.29 in the psychomotor delay group and 1.81 +/- 0.29, 2.17 +/- 0.35, and 1.22 +/- 0.26 in the control group. CONCLUSION: Metabolite distribution varied with brain region in children with and those without psychomotor delay. No significant difference was found between the brain metabolite ratios of children with psychomotor delay of unknown cause and those of age-matched children without psychomotor delay.
