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REVIEW ON LONGITUDINAL BRAIN VOLUME CHANGES IN HEALTHY INDIVIDUALS
Abstracts
subject. Information on OCs was collected from original birth records and scored blindly according to the McNeil-Sjöström scale. Both a continuous measure and a cut-off measure for severe OCs were analysed in patients and control subjects separately. Age was co-varied for in the statistical analyses. A false discovery rate (FDR) of 0.05 was applied to control for multiple comparisons. Results: There were no differences between patients and control subjects regarding number or severity of OCs. Schizophrenia patients with severe OCs demonstrated higher as well as lower lGI in scattered areas across both hemispheres when compared to patients without severe OCs (p < 0.05, uncorrected). In patients, increasing number of OCs was related to lower lGI in a large cluster in the left medial posterior temporal lobe, and in a smaller cluster in the left inferior frontal sulcus and gyrus (p < 0.05, uncorrected). Control subjects with severe OCs displayed higher lGI as well as lower lGI in scattered areas across both hemispheres (p < 0.05, uncorrected) compared to controls without severe OCs. Continuous OCs scores in controls were related to lower lGI in the left inferior frontal and precentral sulci and gyri (p < 0.05); for this area, there was a similar inverse relationship between OCs-scores and lGI in patients and control subjects (albeit for a larger area in the control subjects). None of the findings remained significant after correction for multiple testing. Discussion: The results of the present study are suggestive of an association between OCs and cortical folding. The uncorrected results displayed scattered areas in which the findings from schizophrenia patients and control subjects differ. However, the inverse relationship between increasing number of OCs and cortical folding in the left inferior frontal sulcus and gyrus is present in both patients and controls. If replicated, the findings suggest that a relationship between OCs and cortical folding may be caused by factors shared between schizophrenia patients and healthy controls rather than factors related to schizophrenia alone.
doi:10.1016/j.schres.2010.02.331
Poster 104 REVIEW ON LONGITUDINAL BRAIN VOLUME CHANGES IN HEALTHY INDIVIDUALS Anna M. Hedman, Neeltje E.M. van Haren, Hugo H.G. Schnack, René S. Kahn, Hilleke E. Hulshoff Pol UMC Utrecht, Rudolf Magnus Institute of Neuroscience Utrecht, Utrecht, Netherlands Background: Longitudinal Magnetic Resonance Imaging (MRI) studies provide us with the unique opportunity to study brain development within subjects over time. Usually, these studies included subjects whose ages span only several years of the human life span. Evidence begins to show that plastic changes are not limited to childhood and adolescence but continuing during adulthood. Here we review and integrate the findings of longitudinal MRI studies in healthy subjects that investigated the volume of the whole brain and that have been published until October 1st 2009. Methods: A systematic search was conducted at PUBMED for relevant studies followed by a search in cross-references. A total of 51 studies were included on change over time in whole brain volume. A total of 1886 healthy individuals were included. The number of participants per study varied between 7 and 120. The interval of follow-up varied between 12 weeks and 10 years. Percentage whole brain volume change per year was extracted from the studies. The formula for this calculation was as follows: ((T2-T1/T1)*100)/follow-up interval in years) with T1 being whole
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brain volume at inclusion and T2 being whole brain volume at follow-up measurement. Three studies presented their findings as trajectories (whole brain volume development during childhood). Results: Our findings show that whole brain volume change is an ongoing process throughout the full lifespan with pronounced increase in childhood followed by rapid decreases in volume change by the age of approximately 15 years. Thereafter, in adolescent and adulthood whole brain volume is relative stable, showing a mild decrease over time of approximately 0.3% per year. Between the ages of 35 and 55 years the decrease becomes more pronounced and the loss accelerates after the age of 55 years. Discussion: Brain development with ongoing changes in the whole brain volume is a life long process. Underlying factors for these changes in the healthy brain might be neurodevelopmental processes, synaptic pruning, hormonal influences and/or agerelated neurodegeneration. Our findings may help understanding the underlying mechanisms of normal brain changes, and may contribute in distinguishing psychiatric and neurodegenerative diseases from healthy aging processes.
doi:10.1016/j.schres.2010.02.332
Poster 105 FRONTAL CORTICAL THICKNESS IS ASSOCIATED WITH CLINICAL IMPROVEMENT OF NEGATIVE SYMPTOMS IN MALE ADOLESCENTS WITH EARLY-ONSET FIRST-EPISODE PSYCHOSIS Margarita Amador1, Joost Janssen1,2, Santiago Reig2, Mara Parellada1, Dolores Moreno1, Carmen Moreno1, Maria Mayoral1, Montserrat Graell3, Manuel Desco2, Celso Arango1 1 Hospital Universitario Gregorio Marañón, Department of Psychiatry, and Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM) Madrid, Madrid, Spain; 2Hospital Universitario Gregorio Marañón, Department of Experimental Surgery and Medicine, and CIBERSAM Madrid, Madrid, Spain; 3Hospital Universitario Infantil Niño Jesús, Department of Psychiatry Madrid, Madrid, Spain Background: First-episode psychosis in adults and adolescents is associated with volume deficits in the frontal cortex. It is unclear if deficits in cortical thickness and/or cortical surface and/or cortical gyrification underlie the patient-control differences in cortical volume. In addition, in adult and adolescent patients with psychosis it's not evident if cortical structural brain abnormalities are related to change in clinical symptoms over time. The current study was designed to compare frontal cortical thickness, surface, and gyrification between male adolescents with early-onset first-episode psychosis (EOP) and healthy controls. Within patients, the relationship between frontal cortical morphology and change in clinical symptoms over a two-year clinical follow up period was investigated. Methods: Baseline Magnetic Resonance Imaging (MRI) brain scans were obtained from 49 adolescent EOP patients, and 34 healthy controls. Mean age was 15 years for patients and controls, and all patients had less than six months of psychotic symptoms at study enrollment. All patients had a baseline and a two-year clinical follow up assessment which included the Positive and Negative Syndrome Scale (PANSS). Change in symptoms was defined as the difference in PANSS score at baseline and follow up (follow up – baseline). At baseline, all patients were on antipsychotic medication, the mean daily chlorpromazine equivalent (CPE) dose of the patient sample was 401. FreeSurfer software was used to generate intracranial volume, frontal cortical thickness, frontal cortical surface, and frontal cortical gyrification from the baseline MRI brain scans. Results: After controlling for age and intracranial volume, patients had a significantly thinner frontal cortex (means for controls and patients:
subject. Information on OCs was collected from original birth records and scored blindly according to the McNeil-Sjöström scale. Both a continuous measure and a cut-off measure for severe OCs were analysed in patients and control subjects separately. Age was co-varied for in the statistical analyses. A false discovery rate (FDR) of 0.05 was applied to control for multiple comparisons. Results: There were no differences between patients and control subjects regarding number or severity of OCs. Schizophrenia patients with severe OCs demonstrated higher as well as lower lGI in scattered areas across both hemispheres when compared to patients without severe OCs (p < 0.05, uncorrected). In patients, increasing number of OCs was related to lower lGI in a large cluster in the left medial posterior temporal lobe, and in a smaller cluster in the left inferior frontal sulcus and gyrus (p < 0.05, uncorrected). Control subjects with severe OCs displayed higher lGI as well as lower lGI in scattered areas across both hemispheres (p < 0.05, uncorrected) compared to controls without severe OCs. Continuous OCs scores in controls were related to lower lGI in the left inferior frontal and precentral sulci and gyri (p < 0.05); for this area, there was a similar inverse relationship between OCs-scores and lGI in patients and control subjects (albeit for a larger area in the control subjects). None of the findings remained significant after correction for multiple testing. Discussion: The results of the present study are suggestive of an association between OCs and cortical folding. The uncorrected results displayed scattered areas in which the findings from schizophrenia patients and control subjects differ. However, the inverse relationship between increasing number of OCs and cortical folding in the left inferior frontal sulcus and gyrus is present in both patients and controls. If replicated, the findings suggest that a relationship between OCs and cortical folding may be caused by factors shared between schizophrenia patients and healthy controls rather than factors related to schizophrenia alone.
doi:10.1016/j.schres.2010.02.331
Poster 104 REVIEW ON LONGITUDINAL BRAIN VOLUME CHANGES IN HEALTHY INDIVIDUALS Anna M. Hedman, Neeltje E.M. van Haren, Hugo H.G. Schnack, René S. Kahn, Hilleke E. Hulshoff Pol UMC Utrecht, Rudolf Magnus Institute of Neuroscience Utrecht, Utrecht, Netherlands Background: Longitudinal Magnetic Resonance Imaging (MRI) studies provide us with the unique opportunity to study brain development within subjects over time. Usually, these studies included subjects whose ages span only several years of the human life span. Evidence begins to show that plastic changes are not limited to childhood and adolescence but continuing during adulthood. Here we review and integrate the findings of longitudinal MRI studies in healthy subjects that investigated the volume of the whole brain and that have been published until October 1st 2009. Methods: A systematic search was conducted at PUBMED for relevant studies followed by a search in cross-references. A total of 51 studies were included on change over time in whole brain volume. A total of 1886 healthy individuals were included. The number of participants per study varied between 7 and 120. The interval of follow-up varied between 12 weeks and 10 years. Percentage whole brain volume change per year was extracted from the studies. The formula for this calculation was as follows: ((T2-T1/T1)*100)/follow-up interval in years) with T1 being whole
227
brain volume at inclusion and T2 being whole brain volume at follow-up measurement. Three studies presented their findings as trajectories (whole brain volume development during childhood). Results: Our findings show that whole brain volume change is an ongoing process throughout the full lifespan with pronounced increase in childhood followed by rapid decreases in volume change by the age of approximately 15 years. Thereafter, in adolescent and adulthood whole brain volume is relative stable, showing a mild decrease over time of approximately 0.3% per year. Between the ages of 35 and 55 years the decrease becomes more pronounced and the loss accelerates after the age of 55 years. Discussion: Brain development with ongoing changes in the whole brain volume is a life long process. Underlying factors for these changes in the healthy brain might be neurodevelopmental processes, synaptic pruning, hormonal influences and/or agerelated neurodegeneration. Our findings may help understanding the underlying mechanisms of normal brain changes, and may contribute in distinguishing psychiatric and neurodegenerative diseases from healthy aging processes.
doi:10.1016/j.schres.2010.02.332
Poster 105 FRONTAL CORTICAL THICKNESS IS ASSOCIATED WITH CLINICAL IMPROVEMENT OF NEGATIVE SYMPTOMS IN MALE ADOLESCENTS WITH EARLY-ONSET FIRST-EPISODE PSYCHOSIS Margarita Amador1, Joost Janssen1,2, Santiago Reig2, Mara Parellada1, Dolores Moreno1, Carmen Moreno1, Maria Mayoral1, Montserrat Graell3, Manuel Desco2, Celso Arango1 1 Hospital Universitario Gregorio Marañón, Department of Psychiatry, and Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM) Madrid, Madrid, Spain; 2Hospital Universitario Gregorio Marañón, Department of Experimental Surgery and Medicine, and CIBERSAM Madrid, Madrid, Spain; 3Hospital Universitario Infantil Niño Jesús, Department of Psychiatry Madrid, Madrid, Spain Background: First-episode psychosis in adults and adolescents is associated with volume deficits in the frontal cortex. It is unclear if deficits in cortical thickness and/or cortical surface and/or cortical gyrification underlie the patient-control differences in cortical volume. In addition, in adult and adolescent patients with psychosis it's not evident if cortical structural brain abnormalities are related to change in clinical symptoms over time. The current study was designed to compare frontal cortical thickness, surface, and gyrification between male adolescents with early-onset first-episode psychosis (EOP) and healthy controls. Within patients, the relationship between frontal cortical morphology and change in clinical symptoms over a two-year clinical follow up period was investigated. Methods: Baseline Magnetic Resonance Imaging (MRI) brain scans were obtained from 49 adolescent EOP patients, and 34 healthy controls. Mean age was 15 years for patients and controls, and all patients had less than six months of psychotic symptoms at study enrollment. All patients had a baseline and a two-year clinical follow up assessment which included the Positive and Negative Syndrome Scale (PANSS). Change in symptoms was defined as the difference in PANSS score at baseline and follow up (follow up – baseline). At baseline, all patients were on antipsychotic medication, the mean daily chlorpromazine equivalent (CPE) dose of the patient sample was 401. FreeSurfer software was used to generate intracranial volume, frontal cortical thickness, frontal cortical surface, and frontal cortical gyrification from the baseline MRI brain scans. Results: After controlling for age and intracranial volume, patients had a significantly thinner frontal cortex (means for controls and patients: