Regional brain metabolism as the predictor of performance on the Trail Making Test in schizophrenia. A 18FDG PET covariation study
Language English Country Sweden Media print
Document type Controlled Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't
PubMed
17159818
PII: NEL270506A05
Knihovny.cz E-resources
- MeSH
- Basal Metabolism MeSH
- Frontal Lobe metabolism physiology MeSH
- Adult MeSH
- Fluorodeoxyglucose F18 metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Brain Mapping MeSH
- Adolescent MeSH
- Brain metabolism MeSH
- Positron-Emission Tomography methods MeSH
- Psychomotor Performance * MeSH
- Schizophrenia metabolism MeSH
- Trail Making Test * MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Controlled Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Fluorodeoxyglucose F18 MeSH
OBJECTIVES: With the aim to indicate the functional anatomical substrate of cognitive dysfunction in schizophrenia we evaluated the relationship between resting brain metabolism and performance on the Trail Making Test (TMT). As the prerequisite analysis we compared the performance in Part A and B of the TMT between schizophrenic patients and controls. Resting brain metabolism was investigated by (18)FDG positron emission tomography (PET) as the probe for the relative regional synaptic strength and density. METHODS: (18)FDG PET data were analyzed by SPM99 with TMT A and B as the covariate (p< or =0.001). RESULTS: Schizophrenic patients (N=42) had worse performance in both TMT A and B compared to controls (N=42). In schizophrenic subjects (18)FDG PET did not predict the performance on Part A (psychomotor speed) but predicted that for Part B (set-shifting and flexibility) of the TMT. The (18)FDG uptake in the superior, middle and inferior frontal gyruses bilaterally was associated with better performance in the TMT B. The negative covariation between 18FDG uptake and time spent in the TMT B was detected in the temporal and parietal cortices, pre- and postcentral gyruses, precuneus limbic regions (anterior cingulate, uncus) and the pons. CONCLUSIONS: Our data indicate that hypometabolism in the frontal lobes and hypermetabolism in the temporo-parieto-limbic regions is the neurobiological basis for deficient TMT B performance in schizophrenia.