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Glucose metabolism serves as the central source of energy for the human brain. Little is known about the effects of blood glucose level (BGL) on higher-order cognitive functions within a physiological range (e.g., after overnight fasting). In this randomized, placebo-controlled, double blind study, we assessed the impact of overnight fasting (14 h) on brain activation during a working memory task. We sought to mimic BGLs that occur naturally in healthy humans after overnight fasting. After standardized periods of food restriction, 40 (20 male) healthy participants were randomly assigned to receive either glucagon to balance the BGL or placebo (NaCl). A parametric fMRI paradigm, including 2-back and 0-back tasks, was used. Subclinically low BGL following overnight fasting was found to be linked to reduced involvement of the bilateral dorsal midline thalamus and the bilateral basal ganglia, suggesting high sensitivity of those regions to minimal changes in BGLs. Our results indicate that overnight fasting leads to physiologically low levels of glucose, impacting brain activation during working memory tasks even when there are no differences in cognitive performance.

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The human brain depends mainly on glucose supply from circulating blood as an energy substrate for its metabolism. Most of the energy produced by glucose catabolism in the brain is used to support intrinsic communication purposes in the absence of goal-directed activity. This intrinsic brain function can be detected with fMRI as synchronized fluctuations of the BOLD signal forming functional networks. Here, we report results from a double-blind, placebo controlled, cross-over study addressing changes in intrinsic brain activity in the context of very low, yet physiological, blood glucose levels after overnight fasting. Comparison of four major resting state networks in a fasting state and a state of elevated blood glucose levels after glucagon infusion revealed altered patterns of functional connectivity only in a small region of the posterior default mode network, while the rest of the networks appeared unaffected. Furthermore, low blood glucose was associated with changes in the right frontoparietal network after cognitive effort. Our results suggest that fasting has only limited impact on intrinsic brain activity, while a detrimental impact on a network related to attention is only observable following cognitive effort, which is in line with ego depletion and its reliance on glucose.

A surprisingly positive attitude toward ECT was found in our study among all 3 groups of German psychiatrists, which might further help improve patients' access to this treatment.

Previous literature has shown that hypoglycemia influences the intensity of the BOLD signal. A similar but smaller effect may also be elicited by low normal blood glucose levels in healthy individuals. This may not only confound the BOLD signal measured in fMRI, but also more generally interact with cognitive processing, and thus indirectly influence fMRI results. Here we show in a placebo-controlled, crossover, double-blind study on 40 healthy subjects, that overnight fasting and low normal levels of glucose contrasted to an activated, elevated glucose condition have an impact on brain activation during basal visual stimulation. Additionally, functional connectivity of the visual cortex shows a strengthened association with higher-order attention-related brain areas in an elevated blood glucose condition compared to the fasting condition. In a fasting state visual brain areas show stronger coupling to the inferior temporal gyrus. Results demonstrate that prolonged overnight fasting leads to a diminished BOLD signal in higher-order occipital processing areas when compared to an elevated blood glucose condition. Additionally, functional connectivity patterns underscore the modulatory influence of fasting on visual brain networks. Patterns of brain activation and functional connectivity associated with a broad range of attentional processes are affected by maturation and aging and associated with psychiatric disease and intoxication. Thus, we conclude that prolonged fasting may decrease fMRI design sensitivity in any task involving attentional processes when fasting status or blood glucose is not controlled.

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Einleitung Das Tourette-Syndrom ist eine neuropsychiatrische Erkrankung, die sich im Kindes-und Jugendalter manifestiert und deren charakteristisches Merkmal das Auftreten von motorischen und vokalen Tics ist. Nahezu 150 Jahre nach der Erstbeschreibung durch Jean Itard und Gilles de la Tourette erscheinen viele Fragen hinsichtlich der Ätiologie und der neurobiologischen Grundlagen dieses Syndromes noch weitgehend ungeklärt. Ferner stellen der Erkrankungsbeginn im Kindesoder Jugendalter, die für die Betroffenen vielfach ausgrenzende und unberechenbar erscheinende Symptomatik sowie das häufige Auftreten psychiatrischer Komorbiditäten eine besondere therapeutische Herausforderung dar. Der folgende Artikel soll einen Überblick über die klinische Symptomatik, den Erkrankungsverlauf, die Modelle zur Ätiopathogenese, die neurobiologischen Grundlagen sowie das therapeutische Vorgehen geben.Epidemiologie Tic-Störungen stellen ein häufiges Phänomen im Kindes-und Jugendalter dar, wenngleich die Angaben zur Prävalenz in verschiedenen Studien zum Teil deutlich differieren. Die Gründe hierfür sind Unterschiede in den zugrunde gelegten diagnostischen Kriterien (einfache Tic-Störungen vs. Tourette-Syndrom) sowie den epidemiologischen Methoden (populations-vs. klinikbasierter Ansatz), der fluktuierende Erkrankungsverlauf sowie das zum Teil nur transiente Vorliegen von Tics. Frühere Schätzungen gingen von einer Prävalenz von 0,05 % aus [1]. Eine aktuelle, populationsbasierte Arbeit beziffert die Prävalenz des Tourette-Syndroms bei 13-Jährigen auf 0,3 -0,7 % und die Prävalenz chronischer Tic-Störungen auf 0,5 -1,1 % [2]. Diese Daten decken sich mit den Ergebnissen anderer Arbeiten zum Tourette-Syndrom, in denen Prävalenzraten von 0,6 -1 % beschrieben werden [3, 4]. Das Tourette-Syndrom tritt bei Jungen etwa 3 -bis 4-mal häufiger auf als bei Mädchen [7].Das Tourette-Syndrom -mehr als "nur" Tics Sebastian Vocke, Irene Neuner Erste Symptome zeigen sich im Kindesalter und stürzen die Betroffenen oft in die soziale Ausgrenzung. Dabei ist das Tourette-Syndrom eine neuropsychiatrische Erkrankung, die mit Psychoedukation, Psycho-und Pharmakotherapie behandelt werden kann. PSYCH up2date 6 2012 DOI http://dx.Tics sind kurz andauernde, rasch einschießende, unwillkürliche, nicht zweckgebundene, stereotype und wiederkehrende muskuläre Aktionen (motorische Tics) oder Lautäußerungen (vokale oder phonetische Tics).