FDG-PET scans in patients with Kraepelinian and non-Kraepelinian schizophrenia

Abstract

We recruited 14 unmedicated patients with Kraepelinian schizophrenia (12 men and 2 women; mean age = 47 years old), 27 non-Kraepelinian patients (21 men and 6 women; mean age = 36.4 years old) and a group of 56 age- and sex-matched healthy volunteers. FDG positron emission tomography and MRI scans were coregistered for both voxel-by-voxel statistical mapping and stereotaxic regions of interest analysis. While both Kraepelinian and non-Kraepelinian patients showed equally lower uptake than healthy volunteers in the frontal lobe, the temporal lobes (Brodmann areas 20 and 21) showed significantly greater decreases in Kraepelinian than in non-Kraepelinian patients. Kraepelinian patients had lower FDG uptake in parietal regions 39 and 40, especially in the right hemisphere, while non-Kraepelinian patients had similar reductions in the left. Only non-Kraepelinian patients had lower caudate FDG uptake than healthy volunteers. While both patient groups had lower uptake than healthy volunteers in the medial dorsal nucleus of the thalamus, Kraepelinian patients alone had higher uptake in the ventral nuclei of the thalamus. Kraepelinian patients also showed higher metabolic rates in white matter. Our results are consistent with other studies indicating that Kraepelinian schizophrenia is a subgroup of schizophrenia, characterized by temporal and right parietal deficits and normal rather than reduced caudate uptake. It suggests that Kraepelinian schizophrenia may be more primarily characterized by FDG uptake decreased in both the frontal and temporal lobes, while non-Kraepelinian schizophrenia may have deficits more limited to the frontal lobe. This is consistent with some neuropsychological and prognosis reports of disordered sensory information processing in Kraepelinian schizophrenia in addition to deficits in frontal lobe executive functions shared with the non-Kraepelinian subtype.

Positron emission tomography assessment of cerebral glucose metabolic rates in autism spectrum disorder and schizophrenia

“…All ASD and schizophrenia participants were unmedicated with psychotropic substances for at least 14 days prior to scan date. Study participants in the present report were also part of our structural MRI comparison of subjects with schizophrenia and ASD (Mitelman et al 2016) and of FDG PET comparison of subjects with Kraepelinian and non-Kraepelinian schizophrenia (Bralet et al 2016), subsample of ASD subjects featured in Hazlett et al (2004) and Haznedar et al (2006). In comparison to the latter two studies, the present report employs a larger cohort of participants, analyzes different regions of interest with a newer automated region-of-interest approach.…”

Impaired brain glucose metabolism and presynaptic dopaminergic functioning in a mouse model of schizophrenia

“…In basal conditions mutant animals show abnormal glucose metabolic activity in the somatosensory/ insular cortex, auditory cortex, lateral hypothalamus, and amygdala. However, under a hyperdopaminergic state, mutant animals show a reduced metabolic activity in prefrontal cortex, a pathological condition already described from patient PET studies [18,20,28]. Interestingly, in the hyperdopaminergic condition, glucose metabolism is also abnormal in the nucleus reuniens and amygdala, two brain regions involved in the modulation of dopamine release [7,29].…”

“…Two groups of adult animals (n = 10 controls and n = 10 mutants) were used for PET scanning experiments. Both groups were studied with [ 18 One week after the second [ 18 F]-FDG acquisition, the two groups of animals were injected with 3.7 MBq/gr i.v. of [ 18 F]-F-DOPA, 30 min after the preadministration of carbidopa (10 mg/kg, i.p.…”

“…Among the most used tracer in clinical diagnostics is the fluorinated glucose analog [ 18 F]-FDG, which localizes in metabolically active tissues and accumulates in an activity-dependent manner. Many reports have shown reduced glucose metabolic rate in the frontal cortex of patients with schizophrenia, i.e., hypofrontality by [18F]-FDG PET scanning [17][18][19][20]. Presynaptic dopaminergic functioning may be also studied by a PET scanner in vivo by the administration of [ 18 F]-F-DOPA (Fluorodopa), as it is incorporated by presynaptic monoaminergic neurons, decarboxylated to [ 18 F]-fluorodopamine by the aromatic amino acid decarboxylase (AADC) and then stored in vesicles.…”

“…18 F]-F-DOPA PET scanning in control and D2 mutant animals. Red-yellow color represents a significant increase of [ 18 F]-F-DOPA incorporation in control animals and blue-white color a significant increase of [ 18 F]-F-DOPA incorporation in mutant D2 animals.…”