Associations between brain morphology, inflammatory markers and symptoms of fatigue, depression or anxiety in active and remitted Crohn's disease.

BACKGROUND: Fatigue and psychosocial impairments are highly prevalent in IBD, especially during active disease. Disturbed brain-gut-interactions may contribute to these symptoms. This study examined associations between brain structure, faecal calprotectin and symptoms of fatigue, depression and anxiety in persons with Crohn's Disease (CD) in different disease states. METHODS: In this prospective observational study, n=109 participants (n=67 persons with CD, n=42 healthy controls) underwent cranial magnetic resonance imaging, provided stool samples for analysis of faecal calprotectin and completed questionnaires to assess symptoms of fatigue, depression and anxiety. We analysed differences in grey matter volume (GMV) between patients and controls and associations between regional GMV alterations, neuropsychiatric symptoms and faecal calprotectin. RESULTS: Symptoms of fatigue, depression and anxiety were increased in patients with CD compared to controls, with highest scores in active CD. Patients exhibited regionally reduced GMV in cortical and subcortical sensorimotor regions, occipitotemporal and medial frontal areas. Regional GMV differences showed a significant negative association with fatigue, but not with depression or anxiety. Subgroup analyses revealed symptom-GMV-associations for fatigue in remitted, but not in active CD, while fatigue was positively associated with faecal calprotectin in active, but not remitted disease. CONCLUSION: Our findings support disturbed brain-gut-interactions in CD which may be particularly relevant for fatigue during remitted disease. Reduced GMV in the precentral gyrus and other sensorimotor areas could reflect key contributions to fatigue pathophysiology in CD. A sensorimotor model of fatigue in CD could also pave the way for novel treatment approaches.

Feasibility of an Intervention Delivered via Mobile Phone and Internet to Improve the Continuity of Care in Schizophrenia: A Randomized Controlled Pilot Study.

Schizophrenia is a severe mental illness associated with a heavy symptom burden and high relapse rates. Digital interventions are increasingly suggested as means to facilitate continuity of care, relapse prevention, and long-term disease management for schizophrenia spectrum disorders. In order to investigate the feasibility of a mobile and internet-based aftercare program, a 2-arm randomized controlled pilot study was conducted. The program could be used by patients for six months after inpatient treatment and included psychoeducation, an individual crisis plan, optional counseling via internet chat or phone and a supportive monitoring module. Due to the slow pace of enrollment, recruitment was stopped before the planned sample size was achieved. Reasons for the high exclusion rate during recruitment were analyzed as well as attitudes, satisfaction, and utilization of the program by study participants. The data of 25 randomized patients suggest overall positive attitudes towards the program, high user satisfaction and good adherence to the monitoring module. Overall, the results indicate that the digital program might be suitable to provide support following discharge from intensive care. In addition, the study provides insights into specific barriers to recruitment which may inform future research in the field of digital interventions for severe mental illness.

Exploring cortical predictors of clinical response to electroconvulsive therapy in major depression.

Electroconvulsive therapy (ECT) is a rapid and highly effective treatment option for treatment-resistant major depressive disorder (TRD). The neural mechanisms underlying such beneficial effects are poorly understood. Exploring associations between changes of brain structure and clinical response is crucial for understanding ECT mechanisms of action and relevant for the validation of potential biomarkers that can facilitate the prediction of ECT efficacy. The aim of this explorative study was to identify cortical predictors of clinical response in TRD patients treated with ECT. We longitudinally investigated 12 TRD patients before and after ECT. Twelve matched healthy controls were studied cross sectionally. Demographical, clinical, and structural magnetic resonance imaging data at 3 T and multiple cortical markers derived from surface-based morphometry (SBM) analyses were considered. Multiple regression models were computed to identify predictors of clinical response to ECT, as reflected by Hamilton Depression Rating Scale (HAMD) score changes. Symptom severity differences pre-post-ECT were predicted by models including demographic data, clinical data and SBM of frontal, cingulate, and entorhinal structures. Using all-subsets regression, a model comprising HAMD score at baseline and cortical thickness of the left rostral anterior cingulate gyrus explained most variance in the data (multiple R2 = 0.82). The data suggest that SBM provides powerful measures for identifying biomarkers for ECT response in TRD. Rostral anterior cingulate thickness and HAMD score at baseline showed the greatest predictive power of clinical response, in contrast to cortical complexity, cortical gyrification, or demographical data.

Aberrant brain structural large-scale connectome in Crohn's disease.

BACKGROUND: Disturbed brain-gut interactions and a bidirectional relationship between inflammation and psychiatric symptoms such as anxiety and depression are being discussed in patients with inflammatory bowel diseases (IBD). Alterations of brain structure and function in IBD have been reported with heterogeneous results. Whether these changes reflect independent localized deficits or rather a systematic disruption in the anatomical organization of large-scale brain networks remains unclear. The present study investigated the gray matter structural connectome in patients with Crohn's disease (CD). METHODS: Sixty participants (30 with quiescent CD and 30 matched healthy controls [HC]) underwent high-resolution brain MRI at 3 Tesla. Well-established graph theoretical metrics were analyzed at the global and regional network level and compared between groups. KEY RESULTS: The networks in both groups followed a small-world organization, that is, an architecture that is simultaneously highly segregated and integrated. However, transitivity, a measure of global network segregation, was significantly reduced in patients (P = 0.003). Regionally, patients showed a reduction of nodal betweenness centrality in the right insula and cuneus and the left superior frontal cortex and reduced nodal degree within the left-hemispheric cingulate and the left lateral and right medial orbitofrontal cortex. CONCLUSION AND INFERENCES: These findings lend support to the hypothesis that CD is accompanied by alterations in both global network organization and regional connectivity. A deeper understanding of neural central networks in IBD may facilitate the development of complementary strategies in the treatment of "extraintestinal" comorbid conditions such as depression or anxiety.

The relevance of hippocampal subfield integrity and clock drawing test performance for the diagnosis of Alzheimer's disease and mild cognitive impairment.

OBJECTIVES: The clock drawing test (CDT) is one of the worldwide most used screening tests for Alzheimer's disease (AD). MRI studies have identified temporo-parietal regions being involved in CDT impairment. However, the contributions of specific hippocampal subfields and adjacent extrahippocampal structures to CDT performance in AD and mild cognitive impairment (MCI) have not been investigated so far. It is unclear whether morphological alterations or CDT score, or a combination of both, are able to predict AD. METHODS: 38 AD patients, 38 MCI individuals and 31 healthy controls underwent neuropsychological assessment and MRI at 3 Tesla. FreeSurfer 5.3 was used to perform hippocampal parcellation. We used a collection of statistical methods to better understand the relationship between CDT and hippocampal formation. We also tested the clinical feasibility of this relationship when predicting AD. RESULTS: Impaired CDT performance in AD was associated with widespread atrophy of the cornu ammonis, presubiculum, and subiculum, whereas MCI subjects showed CDT-related alterations of the CA4-dentate gyrus and subiculum. CDT correlates in AD and MCI showed regional and quantitative overlap. Importantly, CDT score was the best predictor of AD. CONCLUSIONS: Our findings lend support for an involvement of different hippocampal subfields in impaired CDT performance in AD and MCI. CDT seems to be more efficient than subfield imaging for predicting AD.

Electroconvulsive therapy induced gray matter increase is not necessarily correlated with clinical data in depressed patients.

BACKGROUND: Electroconvulsive therapy (ECT) and depression have been associated with brain volume changes, especially in the hippocampus and the amygdala. METHODS: In this retrospective study we collected data from individual pre-post ECT whole brain magnetic resonance imaging scans of depressed patients from six German university hospitals. Gray matter volume (GMV) changes were quantified via voxel-based morphometry in a total sample of 92 patients with major depressive episodes (MDE). Additionally, 43 healthy controls were scanned twice within a similar time interval. RESULTS: Most prominently longitudinal GMV increases occurred in temporal lobe regions. Within specific region of interests we detected significant increases of GMV in the hippocampus and the amygdala. These results were more pronounced in the right hemisphere. Decreases in GMV were not observed. GMV changes did not correlate with psychopathology, age, gender or number of ECT sessions. We ruled out white matter reductions as a possible indirect cause of the detected GMV increase. CONCLUSION: The present findings support the notion of hippocampus and amygdala modulation following an acute ECT series in patients with MDE. These results corroborate the hypothesis that ECT enables primarily unspecific and regionally dependent neuroplasticity effects to the brain.

Common and distinct patterns of abnormal cortical gyrification in major depression and borderline personality disorder.

Abnormal gray matter volume has been consistently reported in patients with major depressive disorder (MDD), but markers of cortical neurodevelopment have been rarely investigated. Also, it is unclear whether there exist common versus distinct spatial patterns of abnormal cortical development across different disorders presenting with negative emotions and deficient affective regulation. In this study, we used structural MRI at 3T to investigate the local gyrification index (LGI), a marker of fetal/infant neurodevelopment, in adult female patients with MDD (n = 22), in adult female patients with borderline personality disorder (BPD) (n = 17), and in controls (n = 22). Reduced cortical folding of the precuneus, the superior parietal gyrus and the parahippocampal gyrus was found in both MDD and BPD patients when compared to controls (p < 0.05, cluster-wise probability [CWP] corrected). MDD patients showed additional hypogyrification of the middle frontal gyrus and the fusiform gyrus when compared to both controls and BPD patients (p < 0.05, CWP corrected). In MDD patients, lower LGI of prefrontal regions was significantly associated with the age of disease onset and with the number of depressive episodes. In BPD patients, lower LGI of orbitofrontal regions was associated with impulsivity. Our findings suggest abnormal early cortical development in MDD, affecting brain regions that have been frequently implied in MDD pathophysiology. However, LGI abnormalities may not be specific for MDD, since MDD and BPD patients also exhibited common patterns of hypogyrification. Hypogyrification of cortical regions associated with higher-order cognition appears to be most pronounced in MDD. Abnormal early cortical neurodevelopment may mediate vulnerability to disorders of emotion.

Differential contributions of cortical thickness and surface area to trait impulsivity in healthy young adults.

BACKGROUND: Impulsivity is an essential human personality trait and highly relevant for the development of several mental disorders. There is evidence that impulsivity is heritable, yet little is known about neural correlates reflecting early brain development. Here, we address the question whether motor, attentional and non-planning components, as reflected by the Barratt Impulsiveness Scale (BIS-11), are distinctly associated with cortical thickness and surface area variations in young healthy individuals. METHOD: We investigated cortical thickness and surface area in 54 healthy volunteers (m/f = 30%/70%; age mean/SD = 24.9/4.02) using structural magnetic resonance imaging at 3 T together with surface-based analysis techniques. Impulsivity was examined on the Barratt impulsiveness scale (BIS-11) and related to the two distinct cortical measurements. RESULTS: Higher BIS-11 total scores were negatively associated with cortical thickness variations in the left lingual gyrus, left superior temporal gyrus, right cuneus, and right superior parietal gyrus (p < 0.05 cluster-wise probability [CWP] corrected). Higher BIS-11 nonplanning scores were negatively associated with cortical thickness variations in bilateral pericalcarine gyrus (p < 0.05 CWP corr.). In the orbitofrontal cortex, the association between impulsivity and cortical thickness differed significantly between males and females. CONCLUSION: These data suggest distinct neurodevelopmental trajectories underlying impulsivity in healthy subjects. Impulsivity total scores appear to be specifically related to cortical thickness variations, in contrast to variations of cortical surface area. Furthermore, our findings underscore the importance of better characterizing gender-specific structural correlates of impulsivity.

Neurological Soft Signs and Psychopathology in Chronic Schizophrenia: A Cross-Sectional Study in Three Age Groups.

As established in a wealth of studies subtle motor and sensory neurological abnormalities or neurological soft signs (NSS) are frequently found in patients with schizophrenia at any stage of their illness. However, the potential impact of chronicity and age on NSS was scarcely investigated. Therefore, we assessed NSS in 90 patients with subchronic (n = 22) or chronic (n = 68) schizophrenia and in 60 healthy controls who were assigned to three age groups (18-29, 30-49, and +50 years). NSS were measured on the Heidelberg Scale, psychopathological symptoms including apathy were rated on established instruments. As demonstrated by analysis of variance, NSS scores in patients were significantly (p < 0.05) increased relative to healthy controls. Significant age effects arose in all NSS subscores, with older subjects scoring well above the younger ones. These age effects were more pronounced in patients than controls, indicating that NSS in chronic schizophrenia exceed age-associated changes. Moreover, the NSS scores in patients were significantly associated with duration of illness, thought disturbance, positive symptoms, and apathy. These results were confirmed after age/duration of illness and years of education were partialed out and via regression analyses. Our findings conform to the hypothesis that NSS are associated with chronicity of the disorder as indicated by the correlations of NSS with both, duration of illness and apathy. The correlations between NSS and positive symptoms/thought disturbance correspond to the fluctuation of positive symptoms during the course of the disorder. The significantly more pronounced age effects on NSS in patients may either point to ongoing cerebral changes or to a greater susceptibility of patients toward physiological age effects, which may be mediated among other factors by a lower cognitive reserve.

Motor dysfunction as research domain in the period preceding manifest schizophrenia: A systematic review.

Schizophrenia is a severe behavioral syndrome of neurodevelopmental nature marked by primary or genuine motor abnormalities (GMA), which refer to spontaneous and medication-independent motor phenomena. Since motor dysfunction thus might be a consequence of events occurring during early childhood and adolescence, GMA can be detected in the period preceding manifest schizophrenia. However, the question whether motor system dysfunction might be a promising motor intermediate phenotype for schizophrenia remains unanswered. In this review, we systematically evaluate the evidence on GMA in healthy persons, individuals with schizotypal personality traits, persons at ultra-high risk for psychosis, and unaffected first-degree relatives of schizophrenia patients. What becomes evident is a continuum of GMA expression, which appears to be linked to abnormalities of cerebello-thalamo-cortical, fronto-parietal, and cortico-subcortical motor circuits. According to current evidence, motor dysfunction is a key aspect of the neurodevelopmental risk factor model of schizophrenia. Insights provided by this research will help promoting the RDoC Motor System construct and expand the clinical relevance of the motor domain in the period preceding manifest schizophrenia.

Cortical folding abnormalities in patients with schizophrenia who have persistent auditory verbal hallucinations.

In schizophrenia temporal cortical volume loss differs between patients presenting with persistent auditory verbal hallucinations (pAVH) in contrast to those without hallucinatory symptoms (nAVH). However, it is unknown whether this deficit reflects a neural signature of neurodevelopmental origin or if abnormal temporal cortical volume is reflective of factors which may be relevant at later stages of the disorder. Here, we tested the hypothesis that local gyrification index (LGI) in regions of the temporal cortex differs between patients with pAVH (n=10) and healthy controls (n=14), and that abnormal temporal LGI discriminates between pAVH and nAVH (n=10). Structural magnetic resonance imaging at 3T along with surface-based data analysis methods was used. Contrary to our expectations, patients with pAVH showed lower LGI in Broca´s region compared to both healthy persons and nAVH. Compared to nAVH, those individuals presenting with pAVH also showed lower LGI in right Broca's homologue and right superior middle frontal cortex, together with increased LGI in the precuneus and superior parietal cortex. Regions with abnormal LGI common to both patient samples were found in anterior cingulate and superior frontal areas. Inferior cortical regions exhibiting abnormal LGI in pAVH patients were associated with overall symptom load (BPRS), but not with measures of AVH symptom severity. The pattern of abnormal cortical folding in this sample suggests a neurodevelopmental signature in Broca's region, consistent with current AVH models emphasizing the pivotal role of language circuits and inner speech. Temporal cortical deficits may characterize patients with pAVH during later stages of the disorder.

Motor dysfunction as an intermediate phenotype across schizophrenia and other psychotic disorders: Progress and perspectives.

Primary motor abnormalities (PMA), as found in patients with schizophrenia, are quantitatively and qualitatively distinct markers of motor system abnormalities. PMA have been often referred to phenomena that are present across schizophrenia-spectrum disorders. A dysfunction of frontoparietal and subcortical networks has been proposed as core pathophysiological mechanism underlying the expression of PMA. However, it is unclear at present if such mechanisms are a common within schizophrenia and other psychotic disorders. To address this question, we review recent neuroimaging studies investigating the neural substrates of PMA in schizophrenia and so-called "nonschizophrenic nonaffective psychoses" (NSNAP) such as schizophreniform, schizoaffective, brief psychotic, and other unspecified psychotic disorders. Although the extant data in patients with schizophrenia suggests that further investigation is warranted, MRI findings in NSNAP are less persuasive. It is unclear so far which PMA, if any, are characteristic features of NSNAP or, possibly even specific for these disorders. Preliminary data suggest a relationship between relapsing-remitting PMA in hyper-/hypokinetic cycloid syndromes and neurodegenerative disorders of the basal ganglia, likely reflecting the transnosological relevance of subcortical abnormalities. Despite this evidence, neural substrates and mechanisms underlying PMA that are common in schizophrenia and NSNAP cannot be clearly delineated at this stage of research. PMA and their underlying brain circuits could be promising intermediate phenotype candidates for psychotic disorders, but future multimodal neuroimaging studies in schizophrenia and NSNAP patients and their unaffected first-degree relatives are needed to answer fundamental transnosologic questions.

Intrinsic Network Connectivity Patterns Underlying Specific Dimensions of Impulsiveness in Healthy Young Adults.

Impulsiveness is a central human personality trait and of high relevance for the development of several mental disorders. Impulsiveness is a multidimensional construct, yet little is known about dimension-specific neural correlates. Here, we address the question whether motor, attentional and non-planning components, as measured by the Barratt Impulsiveness Scale (BIS-11), are associated with distinct or overlapping neural network activity. In this study, we investigated brain activity at rest and its relationship to distinct dimensions of impulsiveness in 30 healthy young adults (m/f = 13/17; age mean/SD = 26.4/2.6 years) using resting-state functional magnetic resonance imaging at 3T. A spatial independent component analysis and a multivariate model selection strategy were used to identify systems loading on distinct impulsivity domains. We first identified eight networks for which we had a-priori hypotheses. These networks included basal ganglia, cortical motor, cingulate and lateral prefrontal systems. From the eight networks, three were associated with impulsiveness measures (p < 0.05, FDR corrected). There were significant relationships between right frontoparietal network function and all three BIS domains. Striatal and midcingulate network activity was associated with motor impulsiveness only. Within the networks regionally confined effects of age and gender were found. These data suggest distinct and overlapping patterns of neural activity underlying specific dimensions of impulsiveness. Motor impulsiveness appears to be specifically related to striatal and midcingulate network activity, in contrast to a domain-unspecific right frontoparietal system. Effects of age and gender have to be considered in young healthy samples.

Intrinsic neural network dysfunction in quiescent Crohn's Disease.

Psychological factors and comorbidities play an important role in inflammatory bowel diseases. Such comorbidity could be associated with a specific neural phenotype. Brain regions associated with emotion regulation and self-referential processing, including areas assigned to the "default mode network" (DMN), could be promising candidates in this regard. We investigated the functional integrity of multiple intrinsic neural networks in remitted patients with Crohn's disease (CD) and sought to establish relationships between neural network connectivity and psychiatric symptoms. Fifteen CD patients in remission and 14 controls were investigated. We employed resting-state functional magnetic resonance imaging (fMRI) at 3 Tesla followed by a spatial Independent Component Analysis for fMRI data. Abnormal connectivity in CD patients was observed in DMN subsystems only (p < 0.05, cluster-corrected). Increased connectivity was found in the anterior cingulate and left superior medial frontal gyrus (aDMN) and the middle cingulate cortex (pDMN). Middle cingulate activity showed a significant association with anxiety scores in patients (p = 0.029). This study provides first evidence of selectively disrupted intrinsic neural network connectivity in CD and suggests abnormalities of self-referential neural networks. An increased sensitivity to self-related affective and somatic states in CD patients could account for these findings and explain a higher risk for anxiety symptoms.

White matter microstructure variations contribute to neurological soft signs in healthy adults.

OBJECTIVE: Neurological soft signs (NSS) are core features of psychiatric disorders with significant neurodevelopmental origin. However, it is unclear whether NSS correlates are associated with neuropathological processes underlying the disease or if they are confounded by medication. Given that NSS are also present in healthy persons (HP), investigating HP could reveal NSS correlates, which are not biased by disease-specific processes or drug treatment. Therefore, we used a combination of diffusion MRI analysis tools to provide a framework of specific white matter (WM) microstructure variations underlying NSS in HP. METHOD: NSS of 59 HP were examined on the Heidelberg Scale and related to diffusion associated metrics. Using tract-based spatial statistics (TBSS), we studied WM variations in fractional anisotropy (FA) as well as radial (RD), axial (AD), and mean diffusivity (MD). Using graph analytics (clustering coefficient-CC, local betweenness centrality -BC), we then explored DTI-derived structural network variations in regions identified by previous MRI studies on NSS. RESULTS: NSS scores were negatively associated with RD, AD and MD in corpus callosum, brainstem and cerebellum (P < 0.05, corr.). NSS scores were negatively associated with CC and BC of the pallidum, the superior parietal gyrus, the precentral sulcus, the insula, and the cingulate gyrus (P < 0.05, uncorr.). CONCLUSION: The present study supports the notion that WM microstructure variations in subcortical and cortical sensorimotor regions contribute to NSS expression in young HP. Hum Brain Mapp 38:3552-3565, 2017. © 2017 Wiley Periodicals, Inc.

Hippocampal formation alterations differently contribute to autobiographic memory deficits in mild cognitive impairment and Alzheimer's disease.

Autobiographical memory (AM) is part of declarative memory and includes both semantic and episodic aspects. AM deficits are among the major complaints of patients with Alzheimer's disease (AD) even in early or preclinical stages. Previous MRI studies in AD patients have showed that deficits in semantic and episodic AM are associated with hippocampal alterations. However, the question which specific hippocampal subfields and adjacent extrahippocampal structures contribute to deficits of AM in individuals with mild cognitive impairment (MCI) and AD patients has not been investigated so far. Hundred and seven participants (38 AD patients, 38 MCI individuals and 31 healthy controls [HC]) underwent MRI at 3 Tesla. AM was assessed with a semi-structured interview (E-AGI). FreeSurfer 5.3 was used for hippocampal parcellation. Semantic and episodic AM scores were related to the volume of 5 hippocampal subfields and cortical thickness in the parahippocampal and entorhinal cortex. Both semantic and episodic AM deficits were associated with bilateral hippocampal alterations. These associations referred mainly to CA1, CA2-3, presubiculum, and subiculum atrophy. Episodic, but not semantic AM loss was associated with cortical thickness reduction of the bilateral parahippocampal and enthorinal cortex. In MCI individuals, episodic, but not semantic AM deficits were associated with alterations of the CA1, presubiculum and subiculum. Our findings support the crucial role of CA1, presubiculum, and subiculum in episodic memory. The present results implicate that in MCI individuals, semantic and episodic AM deficits are subserved by distinct neuronal systems.

Cortical signature of clock drawing performance in Alzheimer's disease and mild cognitive impairment.

It is unclear whether clock drawing test (CDT) performance relies on a widely distributed cortical network, or whether this test predominantly taps into parietal cortex function. So far, associations between cortical integrity and CDT impairment in Alzheimer's disease (AD) and mild cognitive impairment (MCI) largely stem from cortical volume analyses. Given that volume is a product of thickness and surface area, investigation of the relationship between CDT and these two cortical measures might contribute to better understanding of this cognitive screening tool for AD. 38 patients with AD, 38 individuals with MCI and 31 healthy controls (HC) underwent CDT assessment and MRI at 3 Tesla. The surface-based analysis via Freesurfer enabled calculation of cortical thickness and surface area. CDT was scored according to the method proposed by Shulman and related to the two distinct cortical measurements. Higher CDT scores across the entire sample were associated with cortical thickness in bilateral temporal gyrus, the right supramarginal gyrus, and the bilateral parietal gyrus, respectively (p < 0.001 CWP corr.). Significant associations between CDT and cortical thickness reduction in the parietal lobe remained significant when analyses were restricted to AD individuals. There was no statistically significant association between CDT scores and surface area (p < 0.001 CWP corr.). In conclusion, CDT performance may be driven by cortical thickness alterations in regions previously identified as "AD vulnerable", i.e. regions predominantly including temporal and parietal lobes. Our results suggest that cortical features of distinct evolutionary and genetic origin differently contribute to CDT performance.

Cerebellar volume change in response to electroconvulsive therapy in patients with major depression.

Electroconvulsive therapy (ECT) is remarkably effective in severe major depressive disorder (MDD). Growing evidence has accumulated for brain structural and functional changes in response to ECT, primarily within cortico-limbic regions that have been considered in current neurobiological models of MDD. Despite increasing evidence for important cerebellar contributions to affective, cognitive and attentional processes, investigations on cerebellar effects of ECT in depression are yet lacking. In this study, using cerebellum-optimized voxel-based analysis methods, we investigated cerebellar volume in 12 MDD patients who received right-sided unilateral ECT. 16 healthy controls (HC) were included. Structural MRI data was acquired before and after ECT and controls were scanned once. Baseline structural differences in MDD compared to HC were located within the "cognitive cerebellum" and remained unchanged with intervention. ECT led to gray matter volume increase of left cerebellar area VIIa crus I, a region ascribed to the "affective/limbic cerebellum". The effects of ECT on cerebellar structure correlated with overall symptom relief. These findings provide preliminary evidence that structural change of the cerebellum in response to ECT may be related to the treatment's antidepressant effects.

Cortical folding patterns are associated with impulsivity in healthy young adults.

Impulsivity is associated with distinct mental disorders but is also considered as a personality trait exhibited by healthy individuals. Current studies suggest that early stressful life events might cause higher impulsivity in the adulthood. Morphological features, which reflect early brain development, could provide valuable information regarding the origin of impulsive behavior. However, none of the previous MRI studies employed a methodology specifically designed to investigate the relationship between impulsivity and markers of brain development. In this regard, we aimed to investigate the relationship between cortical folding and the three distinct factors of impulsivity (attention, motor, and non-planning) in young healthy adults. Fifty-four right-handed healthy individuals were recruited for the study and underwent magnetic resonance imaging (MRI) at 3 Tesla. A surface-based analysis was used to calculate a local gyrification index (LGI). Impulsivity was examined by the Barratt Impulsiveness Scale (BIS-11) and related to LGI. Associations between LGI and BIS-11 scores were assessed using within-group correlations (p < 0.05, "cluster-wise probability" [CWP] corr.). BIS subscores were positively correlated with cortical folding in several distinct areas: Total and attention scores were positively correlated with LGI in the left postcentral gyrus, cingulate gyrus, precentral gyrus, pars opercularis of the inferior frontal gyrus, right middle temporal gyrus, superior parietal gyrus, pericalcarine gyrus, and lateral occipital gyrus (each p < 0.05 CWP corr.). BIS motor score was positively correlated with LGI in the left superior temporal, lingual and supramarginal gyrus (each p < 0.05 CWP corr.). BIS non-planning score showed a positive correlation with LGI in the pars opercularis of the right inferior frontal gyrus and the left middle temporal, precentral and superior parietal gyrus (each p < 0.05 CWP corr.). Furthermore, we found gender-specific differences in BIS-11-LGI-correlation in the middle and inferior frontal gyrus. Our findings illustrate the advantages of cortical folding as a marker of early brain development when investigating structural brain correlates of impulsivity in young adulthood. Further, they lend additional support to the notion that alterations in early neurodevelopment comprising fronto-temporo-parietal regions might give rise to higher impulsivity in healthy individuals.

Altered Markers of Brain Development in Crohn's Disease with Extraintestinal Manifestations - A Pilot Study.

BACKGROUND AND OBJECTIVE: Alterations of brain morphology in Crohn's disease have been reported, but data is scarce and heterogenous and the possible impact of disease predisposition on brain development is unknown. Assuming a systemic course of the disease, brain involvement seems more probable in presence of extraintestinal manifestations, but this question has not yet been addressed. The present study examined the relationship between Crohn's disease and brain structure and focused on the connection with extraintestinal manifestations and markers of brain development. METHODS: In a pilot study, brains of 15 patients with Crohn's disease (of which 9 had a history of extraintestinal manifestations, i.e. arthritis, erythema nodosum and primary sclerosing cholangitis) were compared to matched healthy controls using high resolution magnetic resonance imaging. Patients and controls were tested for depression, fatigue and global cognitive function. Cortical thickness, surface area and folding were determined via cortical surface modeling. RESULTS: The overall group comparison (i.e. all patients vs. controls) yielded no significant results. In the patient subgroup with extraintestinal manifestations, changes in cortical area and folding, but not thickness, were identified: Patients showed elevated cortical surface area in the left middle frontal lobe (p<0.05) and hypergyrification in the left lingual gyrus (p<0.001) compared to healthy controls. Hypogyrification of the right insular cortex (p<0.05) and hypergyrification of the right anterior cingulate cortex (p<0.001) were detected in the subgroup comparison of patients with against without extraintestinal manifestations. P-values are corrected for multiple comparisons. CONCLUSIONS: Our findings lend further support to the hypothesis that Crohn's disease is associated with aberrant brain structure and preliminary support for the hypothesis that these changes are associated with a systemic course of the disease as indicated by extraintestinal manifestations. Changes in cortical surface area and folding suggest a possible involvement of Crohn's disease or its predisposition during brain development.