scholarly journals Abnormalities of Dorsolateral Prefrontal Function in Women With Premenstrual Dysphoric Disorder: A Multimodal Neuroimaging Study

2013 ◽  
Vol 170 (3) ◽  
pp. 305-314 ◽  
Author(s):  
Erica B. Baller ◽  
Shau-Ming Wei ◽  
Philip D. Kohn ◽  
David R. Rubinow ◽  
Gabriela Alarcón ◽  
...  
Keyword(s):  
Premenstrual Dysphoric Disorder ◽  
Multimodal Neuroimaging ◽  
Prefrontal Function ◽  
Dorsolateral Prefrontal ◽  
Neuroimaging Study

scholarly journals In vivo glucose metabolism and glutamate levels in mGluR5 knockout mice: a multimodal neuroimaging study using [18F]FDG microPET and MRS

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yo-Han Joo ◽  
Yun-Kwan Kim ◽  
In-Gyu Choi ◽  
Hyeon-Jin Kim ◽  
Young-Don Son ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Glucose Metabolism ◽  
Cerebral Glucose Metabolism ◽  
Functional Coupling ◽  
Resonance Spectroscopy ◽  
Acute Administration ◽  
Multimodal Neuroimaging ◽  
Mk 801 ◽  
Genetic Ablation ◽  
Neuroimaging Study

Abstract Background Perturbed functional coupling between the metabotropic glutamate receptor-5 (mGluR5) and N-methyl-d-aspartate (NMDA) receptor-mediated excitatory glutamatergic neurotransmission may contribute to the pathophysiology of psychiatric disorders such as schizophrenia. We aimed to establish the functional interaction between mGluR5 and NMDA receptors in brain of mice with genetic ablation of the mGluR5. Methods We first measured the brain glutamate levels with magnetic resonance spectroscopy (MRS) in mGluR5 knockout (KO) and wild-type (WT) mice. Then, we assessed brain glucose metabolism with [18F]fluorodeoxyglucose ([18F]FDG) positron emission tomography before and after the acute administration of an NMDA antagonist, MK-801 (0.5 mg/kg), in the same mGluR5 KO and WT mice. Results Between-group comparisons showed no significant differences in [18F]FDG standardized uptake values (SUVs) in brain of mGluR5 KO and WT mice at baseline, but widespread reductions in mGluR5 KO mice compared to WT mice after MK-801 administration (p < 0.05). The baseline glutamate levels did not differ significantly between the two groups. However, there were significant negative correlations between baseline prefrontal glutamate levels and regional [18F]FDG SUVs in mGluR5 KO mice (p < 0.05), but no such correlations in WT mice. Fisher’s Z-transformation analysis revealed significant between-group differences in these correlations (p < 0.05). Conclusions This is the first multimodal neuroimaging study in mGluR5 KO mice and the first report on the association between cerebral glucose metabolism and glutamate levels in living rodents. The results indicate that mGluR5 KO mice respond to NMDA antagonism with reduced cerebral glucose metabolism, suggesting that mGluR5 transmission normally moderates the net effects of NMDA receptor antagonism on neuronal activity. The negative correlation between glutamate levels and glucose metabolism in mGluR5 KO mice at baseline may suggest an unmasking of an inhibitory component of the glutamatergic regulation of neuronal energy metabolism.

Visuospatial processing in early Alzheimer’s disease: A multimodal neuroimaging study

Cortex ◽  
2015 ◽  
Vol 64 ◽  
pp. 394-406 ◽  
Author(s):  
Heidi I.L. Jacobs ◽  
Ed H.B.M. Gronenschild ◽  
Elisabeth A.T. Evers ◽  
Inez H.G.B. Ramakers ◽  
Paul A.M. Hofman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Multimodal Neuroimaging ◽  
Visuospatial Processing ◽  
Neuroimaging Study ◽  
Early Alzheimer’S Disease

scholarly journals Understanding the neural basis of episodic amnesia in logopenic progressive aphasia: A multimodal neuroimaging study

Cortex ◽  
2020 ◽  
Vol 125 ◽  
pp. 272-287 ◽  
Author(s):  
Siddharth Ramanan ◽  
Lars Marstaller ◽  
John R. Hodges ◽  
Olivier Piguet ◽  
Muireann Irish
Keyword(s):  
Neural Basis ◽  
Multimodal Neuroimaging ◽  
Progressive Aphasia ◽  
Neuroimaging Study

A review of transcranial magnetic stimulation for treating negative symptoms of schizophrenia

2016 ◽  
Vol 33 (S1) ◽  
pp. S554-S555
Author(s):  
J. Oliveira ◽  
G. Sobreira ◽  
C.A. Moreira ◽  
M.A. Aleixo ◽  
S. Brissos
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Negative Symptoms ◽  
Current Evidence ◽  
Positive Effects ◽  
Prefrontal Function ◽  
Prefrontal Dysfunction ◽  
Pubmed Database ◽  
Dorsolateral Prefrontal ◽  
Competing Interest

IntroductionThe finding of prefrontal dysfunction in schizophrenia patients with negative symptoms (NS) has raised interest in using transcranial magnetic stimulation (TMS), which can modulate prefrontal function and dopamine release, as potential treatment for NS.ObjectiveTo briefly review current literature concerning the use of TMS as treatment for NS.AimsTo assess whether current evidence supports the use of TMS for NS.MethodsNarrative review of articles found through a PubMed database search using the keywords “transcranial magnetic stimulation”, “schizophrenia”, and “negative symptoms” between 1998 and 2015.ResultsUp to date, reviews of randomized sham-controlled studies found positive effects of TMS in NS. However, they exposed several methodological difficulties. More recent studies, reviewed in this poster, tried to overcome these, using results from multiple centers, larger samples and blinding. Various TMS techniques were studied, differing in frequency, motor threshold (MT), stimulus location, and treatment duration. Overall, TMS continues to show promising results in reducing NS; particularly rTMS 10 Hz, for at least 15 sessions on the left dorsolateral prefrontal cortex (DLPFC) at a 110% MT.ConclusionsTMS may be a useful treatment for NS for patients not responding to pharmacological treatment alone. Studies remain difficult to compare due to different measures of outcome (PANSS and SANS being the most commonly used) and techniques. Furthermore, possible modulators of response include duration of illness, cognitive symptoms amelioration, medication and their dose, and different NS may respond differently to TMS. More studies are needed to better understand the utility of TMS in NS.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Brain activation during emotion regulation in women with premenstrual dysphoric disorder

2017 ◽  
Vol 48 (11) ◽  
pp. 1795-1802 ◽  
Author(s):  
Nicole Petersen ◽  
Dara G. Ghahremani ◽  
Andrea J. Rapkin ◽  
Steven M. Berman ◽  
Letty Liang ◽  
...  
Keyword(s):  
Emotion Regulation ◽  
Menstrual Cycle ◽  
Luteal Phase ◽  
Region Of Interest ◽  
Premenstrual Dysphoric Disorder ◽  
Follicular Phase ◽  
Precentral Gyrus ◽  
Affective Symptoms ◽  
Dorsolateral Prefrontal ◽  
The Right

AbstractBackgroundDifficulties in regulating emotions are linked to the core symptoms of premenstrual dysphoric disorder (PMDD). We therefore investigated the neural substrates of emotion-regulation problems in women with PMDD.MethodsOn the basis of self-evaluations over 2 months on the Daily Record of Severity of Problems, eligible participants were assigned to two groups: PMDD and control (18 per group). Functional magnetic resonance imaging (fMRI) and a well-validated task were used to assess brain function during emotion regulation. Participants were tested twice, once during the follicular (asymptomatic) and once in the late luteal (symptomatic) phase of the menstrual cycle.ResultsWomen with PMDD gave higher ratings of negative affect in the luteal phase than in the follicular phase, and compared with healthy control participants during the luteal phase. A region-of-interest fMRI analysis indicated that during the late luteal phase, women with PMDD had hypoactivation in right dorsolateral prefrontal cortex (dlPFC) during all conditions of the emotion-regulation task, not only in the contrast that isolated emotion regulation. An exploratory whole-brain, voxel-wise analysis showed that women with PMDD had less activation in the precentral gyrus during the luteal phase than the follicular phase, and less activation in the postcentral gyrus compared with control participants.ConclusionsDuring the luteal phase of the menstrual cycle, women with PMDD experience difficulty regulating emotions. Hypoactivation in the right dlPFC may contribute to this problem, but may be related more generally to other affective symptoms of PMDD. Hypofunction in the right pre- and postcentral gyri warrants additional study.

scholarly journals Resting-state functional connectivity and psychopathology in Klinefelter syndrome (47, XXY)

2020 ◽  
Author(s):  
Ethan T. Whitman ◽  
Siyuan Liu ◽  
Erin Torres ◽  
Allysa Warling ◽  
Kathleen Wilson ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Resting State ◽  
Genetic Risk ◽  
Klinefelter Syndrome ◽  
Brain Connectivity ◽  
Brain Anatomy ◽  
Imaging Data ◽  
Resting State Functional Connectivity ◽  
Dorsolateral Prefrontal ◽  
Neuroimaging Study

Klinefelter syndrome (47, XXY; Henceforth: XXY syndrome) is a high impact but poorly understood genetic risk factor for neuropsychiatric impairment. Here, we provide the first neuroimaging study to map resting-state functional connectivity (rsFC) changes in XXY syndrome and ask how these might relate to brain anatomy and psychopathology. We collected resting state functional magnetic resonance imaging data from 75 individuals with XXY and 84 healthy XY males. We implemented a brain-wide screen to identify regions with altered global rsFC in XXY vs. XY males, and then used seed-based analysis to decompose these alterations. We further compared rsFC changes with regional changes in brain volume from voxel-based morphometry and tested for correlations between rsFC and symptom variation within XXY syndrome. We found that XXY syndrome was characterized by increased global rsFC in the left dorsolateral prefrontal cortex (DLPFC), associated with overconnectivity with diverse rsFC networks. Regional rsFC changes were partly coupled to regional volumetric changes in XXY syndrome. Within the precuneus, variation in DLPFC rsFC within XXY syndrome was correlated with the severity of psychopathology in XXY individuals. Our findings provide the first view of altered functional brain connectivity in XXY syndrome and delineate links between these alterations and those relating to both brain anatomy and psychopathology. Taken together, these insights advance biological understanding of XXY syndrome as a disorder in its own right, and as a model of genetic risk for psychopathology more broadly.

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