Hippocampal volume in florid and recovered DID, DDNOS, and healthy controls: Three MRI studies

2002 ◽  
Author(s):  
Ellert R. S. Nijenhuis ◽  
Thomas Ehling ◽  
Allard Krikke
2019 ◽  
Vol 32 (5) ◽  
pp. 282-284
Author(s):  
Raffaella Calati ◽  
Maura Boldrini ◽  
Ismaïl Bensassi ◽  
Jerome J. Maller ◽  
Chantal Meslin ◽  
...  

2018 ◽  
Vol 79 (3-4) ◽  
pp. 192-199 ◽  
Author(s):  
Kyunghun Kang ◽  
Uicheul Yoon ◽  
Jinwoo Hong ◽  
Shin Young Jeong ◽  
Pan-Woo Ko ◽  
...  

Background: The first aim of our study was to determine whether cortical 18F-florbetaben retention was different between healthy controls and idiopathic normal-pressure hydrocephalus (INPH) patients. Our second aim was to investigate whether there were any relationships between 18F-florbetaben retention and either hippocampal volume or clinical symptoms in INPH patients. Methods: Seventeen patients diagnosed with INPH and 8 healthy controls underwent studies with magnetic resonance imaging and 18F-florbetaben positron emission tomography imaging. Results: Automated region-of-interest analysis showed significant increases in 18F-florbetaben uptake in several brain regions in INPH patients compared to control subjects, with especially remarkable increases in the frontal (bilateral), parietal (bilateral), and occipital (bilateral) cortices. In the INPH group, right hippocampal volume was found to be negatively correlated with right frontal 18F-florbetaben retention. Korean-Mini Mental State Examination scores negatively correlated with right occipital 18F-florbetaben retention. Higher 18F-florbetaben retention correlated significantly with a higher Clinical Dementia Rating Scale score in the right occipital cortex. Conclusions: Our results indicate that INPH might be a disease exhibiting a characteristic pattern of cortical 18F-florbetaben retention. 18F-florbetaben retention in the frontal cortex may be related to hippocampal neuronal degeneration. Our findings may also help us understand the potential pathophysiology of cognitive impairments associated with INPH.


2017 ◽  
Vol 1 (1) ◽  
pp. 01-02
Author(s):  
Micki Dexte

The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls.


2013 ◽  
Vol 25 (4) ◽  
pp. 206-214 ◽  
Author(s):  
Jamila Ahdidan ◽  
Leslie Foldager ◽  
Raben Rosenberg ◽  
Anders Rodell ◽  
Poul Videbech ◽  
...  

ObjectiveThe main aim of the present study was to replicate a previous finding in major depressive disorder (MDD) of association between reduced hippocampal volume and the long variant of the di- and triallelic serotonin transporter polymorphism inSLC6A4on chromosome 17q11.2. Secondarily, we also hypothesised that 5-HTTLPR may be a risk factor for MDD.MethodsQuantitative magnetic resonance imaging (MRI) of the hippocampus was studied in 23 inpatients suffering from MDD and in 33 healthy controls. Normalised volumetric MRI data of hippocampus were assessed with adjustment for total brain volume and tensor-based morphometry was used to elucidate structural brain differences. A triallelic genetic marker resulting from twoSLC6A4promoter region polymorphisms, 5-HTTLPR and rs25531, was analysed for association with MDD and quantitative traits.ResultsHealthy controls had a smaller relative hippocampal volume (relative to brain size) but a larger total brain volume compared with patients with MDD. For patients compared with healthy controls, atrophy was found in the right temporal lobe and pons medulla. Allele and genotype frequencies were strikingly different from the previous study that we aimed to replicate, and no significant associations with the serotonin transporter polymorphism were found.ConclusionsThe present quantitative and morphometric MRI study was not able to replicate the previous finding of association between reduced hippocampal volume in depressed patients and the serotonin transporter polymorphism.


2015 ◽  
pp. 47 ◽  
Author(s):  
Christina McCrae ◽  
Andrew O'Shea ◽  
Jeff Boissoneault ◽  
Karlyn Vatthauer ◽  
Michael Robinson ◽  
...  

2011 ◽  
Vol 26 (S2) ◽  
pp. 1426-1426
Author(s):  
V. Kumari ◽  
S. Raghuvanshi ◽  
A. Sumich ◽  
I. Barkataki ◽  
P. Taylor ◽  
...  

IntroductionDysfunctional impulsivity reflects ‘recklessness without deliberation and evaluation of consequences’ and has negative consequences whereas functional impulsivity reflects ‘rapid responding to situational demands in order to maximise one's circumstances’ and often has positive consequences (1).ObjectiveTo examine the functional brain basis of dysfunctional impulsivity in healthy people and in people with schizophrenia.MethodsThirteen healthy controls and 21 schizophrenia patients (10/21 with serious repetitive violence) underwent fMRI during a Go/ NoGo task. Dysfunctional impulsivity was indexed using the Impulsiveness subscale and functional impulsivity using the Venturesomeness subscale of the Impulsiveness-Venturesomeness-Empathy questionnaire (2).ResultsViolent patients had elevated Impulsiveness scores relative to non-violent patients and controls. Impulsiveness did not correlate significantly with task performance in healthy controls or patients. Impulsiveness, but not Venturesomeness, scores correlated during the NoGO condition with lower activity in the anterior cingulate (AC) in controls, and lower inferior temporal and hippocampal activity in patients.ConclusionsThese findings accord with previously reported associations between reduced hippocampal volume and dysfunctional impulsivity in schizophrenia (3) and, combined with our earlier observations of reduced AC activation during a working memory task in violent antisocial individuals (4), suggest that the influence of dysfunctional impulsivity in antisocial and criminal behaviour is mediated via deficient (inhibitory) functions of the AC and hippocampus.


2020 ◽  
Vol 82 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Josh A. Firth ◽  
Lee Smith ◽  
Jerome Sarris ◽  
Davy Vancampfort ◽  
Felipe Schuch ◽  
...  

2018 ◽  
Vol 102 ◽  
pp. 159-167 ◽  
Author(s):  
Ismaïl Bensassi ◽  
Jorge Lopez-Castroman ◽  
Jerome J. Maller ◽  
Chantal Meslin ◽  
Marilyn Wyart ◽  
...  

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