Metabolic mapping using 2D 31P-MR spectroscopy reveals frontal and thalamic metabolic abnormalities in schizophrenia

Smesny, Stefan; Rosburg, Timm; Nenadić, Igor; Fenk, Klaus Peter; Kunstmann, Sebastian; Rzanny, R.; Volz, Hans-Peter; Sauer, Heinrich

doi:10.1016/j.neuroimage.2006.12.023

Cited by 53 publications

(33 citation statements)

References 40 publications

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“…However, more recent studies have not found this to be a consistent finding (Yacubian et al 2002;Jensen et al 2006;Smesny et al 2007). No consistent patterns of abnormalities in brain creatine, choline, or myo-inositol have been observed in schizophrenia (Deicken et al 2000;Kim et al 2005;Steen et al 2005).…”

Section: Other Metabolitesmentioning

confidence: 93%

MR Spectroscopic Studies of the Brain in Psychiatric Disorders

Maddock

Buonocore

2011

Current Topics in Behavioral Neurosciences

225

196

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The measurement of brain metabolites with magnetic resonance spectroscopy (MRS) provides a unique perspective on the brain bases of neuropsychiatric disorders. As a context for interpreting MRS studies of neuropsychiatric disorders, we review the characteristic MRS signals, the metabolic dynamics,and the neurobiological significance of the major brain metabolites that can be measured using clinical MRS systems. These metabolites include N-acetylaspartate(NAA), creatine, choline-containing compounds, myo-inositol, glutamate and glutamine, lactate, and gamma-amino butyric acid (GABA). For the major adult neuropsychiatric disorders (schizophrenia, bipolar disorder, major depression, and the anxiety disorders), we highlight the most consistent MRS findings, with an emphasis on those with potential clinical or translational significance. Reduced NAA in specific brain regions in schizophrenia, bipolar disorder, post-traumatic stress disorder, and obsessive–compulsive disorder corroborate findings of reduced brain volumes in the same regions. Future MRS studies may help determine the extent to which the neuronal dysfunction suggested by these findings is reversible in these disorders. Elevated glutamate and glutamine (Glx) in patients with bipolar disorder and reduced Glx in patients with unipolar major depression support models of increased and decreased glutamatergic function, respectively, in those conditions. Reduced phosphomonoesters and intracellular pH in bipolar disorder and elevated dynamic lactate responses in panic disorder are consistent with metabolic models of pathogenesis in those disorders. Preliminary findings of an increased glutamine/glutamate ratio and decreased GABA in patients with schizophrenia are consistent with a model of NMDA hypofunction in that disorder. As MRS methods continue to improve, future studies may further advance our understanding of the natural history of psychiatric illnesses, improve our ability to test translational models of pathogenesis, clarify therapeutic mechanisms of action,and allow clinical monitoring of the effects of interventions on brain metabolicmarkers

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Section: Other Metabolitesmentioning

confidence: 93%

MR Spectroscopic Studies of the Brain in Psychiatric Disorders

Maddock

Buonocore

2011

Current Topics in Behavioral Neurosciences

225

196

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“…Two studies imaging medication-naive patients with first-episode schizophrenia and with mean ages of 24 and 26 years, respectively, found decreased levels of PMEs and increased PDEs in the prefrontal cortex, 15,16 whereas studies imaging older patients with schizophrenia (mean ages 29, 32, 37, 37 and 43 years, respectively) failed to find an increase in PDEs in cortical regions. [16][17][18][19] Increased brain levels of PDEs in the younger patients is probably one of the more direct pieces of evidence suggesting increased membrane breakdown, possibly owing to enhanced synaptic elimination in the early stages of schizophrenia. Finally, a recent metaanalysis looked at MRS studies of brain N-acetylaspartate (NAA), a metabolite thought to be an indicator of neuronal/axonal loss or neuronal metabolism.…”

Section: Patricia Boksa Phdmentioning

confidence: 99%

Abnormal synaptic pruning in schizophrenia: Urban myth or reality?

Boksa

2012

J Psychiatry Neurosci

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“…However, GroPCho returned to the control levels in Miller 2009, and studies at 30 months and 52 months, respectively. In contrast, PDE was reduced in 4 studies that included a mix of medication-naïve patients and chronic patients after a medication wash-out, in the mPFC (Volz et al, 2000), lPFC and mPFC (Smesny et al, 2007), and FL (Volz et al, 1997b;Yacubian et al, 2002). While Smesny and colleagues also found reduced PME in bilateral mPFC, Volz (in both studies) and Yacubian reported no change.…”

Section: Frontal Lobementioning

confidence: 92%

“…However, another study in FE patients with majority using medications found no differences at baseline but increased GroPEth in hippocampus at 52 months (Miller et al, 2012). Of the two studies in medication free (MF) subjects including both chronic and FE patients, one found reduction in PME in medial TL (Smesny et al, 2007), whereas there was no change in the other (Volz et al, 2000), and neither study found PDE abnormalities. The remaining studies included chronically ill patients taking medications (O'Callaghan et al, 1991;Calabrese et al, 1992;Fujimoto et al, 1992;Fukuzako et al, 1994Fukuzako et al, , 1996Jensen et al, 2002;Weber-Fahr et al, 2013) or samples that included some medication-free subjects (Deicken et al, 1995a, b;Nenadic et al, 2012).…”

Section: Temporal Lobesmentioning

confidence: 96%