Structural Abnormalities In Schizophrenia Research Articles

Orbitofrontal volume deficit in schizophrenia and thought disorder.

Orbitofrontal Cortex (OFC) structural abnormality in schizophrenia has not been well characterized, probably due to marked anatomical variability and lack of consistent definitions. We previously reported OFC sulcogyral pattern alteration and its associations with social disturbance in schizophrenia, but OFC volume associations with psychopathology and cognition have not been investigated. We compared chronically treated schizophrenia patients with healthy control (HC) subjects, using a novel, reliable parcellation of OFC subregions and their association with cognition, especially the Iowa Gambling Task (IGT), and with schizophrenic psychopathology including thought disorder. Twenty-four patients with schizophrenia and 25 age-matched HC subjects underwent MRI. OFC Regions of Interest (ROI) were manually delineated according to anatomical boundaries: Gyrus Rectus (GR); Middle Orbital Gyrus (MiOG); and Lateral Orbital Gyrus (LOG). The OFC sulcogyral pattern was also classified. Additionally, MiOG probability maps were created and compared between groups in a voxel-wise manner. Both groups underwent cognitive evaluations using the IGT, Wisconsin Card Sorting Test, and Trail Making Test (TMT). An 11% bilaterally smaller MiOG volume was observed in schizophrenia, compared with HC (F(1,47) = 17.4, P = 0.0001). GR and LOG did not differ, although GR showed a rightward asymmetry in both groups (F(1,47) = 19.2, P < 0.0001). The smaller MiOG volume was independent of the OFC sulcogyral pattern, which differed in schizophrenia and HC (chi2 = 12.49, P = 0.002). A comparison of MiOG probability maps suggested that the anterior heteromodal region was more affected in the schizophrenia group than the posterior paralimbic region. In the schizophrenia group, a smaller left MiOG was strongly associated with worse 'positive formal thought disorder' (r = -0.638, P = 0.001), and a smaller right MiOG with a longer duration of the illness (r = -0.618, P = 0.002). While schizophrenics showed poorer performance than HC in the IGT, performance was not correlated with OFC volume. However, within the HC group, the larger the right hemisphere MiOG volume, the better the performance in the IGT (r = 0.541, P = 0.005), and the larger the left hemisphere volume, the faster the switching attention performance for the TMT, Trails B (r = -0.608, P = 0.003). The present study, applying a new anatomical parcellation method, demonstrated a subregion-specific OFC grey matter volume deficit in patients with schizophrenia, which was independent of OFC sulcogyral pattern. This volume deficit was associated with a longer duration of illness and greater formal thought disorder. In HC the finding of a quantitative association between OFC volume and IGT performance constitutes, to our knowledge, the first report of this association.

Duration of illness and treatment effects on hippocampal volume in male patients with schizophrenia

Reduced hippocampal volume is a consistently described structural abnormality in schizophrenia but its cause and timing are not known. To examine the relationship of duration of schizophrenic illness and treatment effects with hippocampal volumes. Quantitative 1.5 T magnetic resonance imaging brain scans of young male patients in the early stage of schizophrenic illness were compared with those of chronically ill older patients. Scans were also acquired for controls matched to both patient groups for age and handedness. Duration of illness was recorded and severity of symptoms assessed with the Positive and Negative Syndrome Scale. The patients with schizophrenia had smaller hippocampal volumes than the controls. The volume reduction was larger in older patients than in young, compared with age-matched controls. In the early illness group atypical antipsychotics rather than haloperidol were associated with larger hippocampal volumes even after controlling for differences in illness severity. The greater reduction of hippocampal volume in people with chronic v. early illness, after controlling for illness severity and age, supports the hypothesis of progressive hippocampal reduction in males with schizophrenia. Atypical antipsychotics early in illness may protect against this.

Shape changes in prefrontal, but not parieto-occipital regions: brains of schizophrenic patients come closer to a circle in coronal and sagittal view

There is some evidence for prefrontal (PF) lobe changes in schizophrenia while the parieto-occipital (PO) region seems to be unaffected. This magnetic resonance imaging (MRI) study was performed to examine shape differences as part of the spectrum of structural abnormalities in schizophrenia. The measurements were done on families affected with schizophrenia to identify the influence of genetic and environmental factors on these changes. The sample under study consisted of 164 subjects including 45 family members (FM) suffering from schizophrenia, 27 FM with other psychiatric disorders and 51 FM without psychiatric disorders based on ICD-10 criteria. In addition, 41 nonpsychiatric control subjects were included in the study. On defined planes at the corpus callosum boundary of the PF and the PO, brain width, height and length were measured on coronal slices. Ratios of these linear measurements were also calculated based on the idea that a plane can be approximated by a circle if the concerning ratio comes close to 1. It was hypothesized that these relative brain shape parameters, especially the PF ratio width/height, would show differences between schizophrenic patients and control subjects. For all members from families with schizophrenia compared with control subjects, there were significant differences in the PF, but not in the PO region. PF height was increased. PF ratios of width/height and height/(2×length) were closer to 1 in affected families than in control subjects. The results can be interpreted as an indication for PF brain shape changes in subjects with a disposition for schizophrenia. On coronal and sagittal planes situated at the corpus callosum, their PF could be approximated by a circle better than in control subjects. As the frontal lobe takes shape late in brain development, underlying genetic mechanisms may be dysregulated in schizophrenic patients and subjects at risk to develop the disorder.

Anterior and posterior hippocampal volumes in schizophrenia

Background While the evidence for hippocampal structural abnormalities in schizophrenia is now well accepted, whether there is differentially greater volume loss within specific subregions of the hippocampus remains a matter of some debate. Here we present volume estimates of anterior and posterior hippocampal volumes using a novel morphometric protocol. Methods We studied 25 male patients with schizophrenia and 25 age-matched male control subjects. Hippocampal volumes were estimated using a three-dimensional morphometric protocol for the analysis of high-resolution structural magnetic resonance images (MRI). Anterior hippocampal volumes were differentiated from posterior hippocampal volumes by the presence of the uncus in coronal slices. Results While the patients with schizophrenia had significantly smaller overall hippocampal volumes relative to the control group, there was no evidence for a topographically specific pattern of volume loss along the anterior–posterior hippocampal axis. Conclusions These results confirm the presence of overall hippocampal volume decreases in patients with schizophrenia, but do not confirm a topographically specific localization of this effect. It appears that the hippocampal volume deficit in schizophrenia is diffuse, a finding that has important consequences for understanding the underlying pathophysiologic mechanisms in schizophrenia.

Rightward cerebral asymmetry in subtypes of schizophrenia according to Leonhard's classification and to DSM-IV: a structural MRI study

Although well documented, brain structural abnormalities in schizophrenia are non-specific, and morphometric parameters show significant overlap between patients and healthy controls. Such inconsistencies in neuroimaging findings could represent different levels of severity along a single pathogenic process or distinct clinical and etiopathological psychoses within a schizophrenic spectrum. The aim of the present study was the investigation of distinct brain abnormalities in different subtypes of schizophrenia. Forty patients were classified according to DSM-IV and Leonhard's classifications. Psychopathology was assessed by the Positive and Negative Syndrome Scale (PANSS) and the Negative Symptom Rating Scale (NSRS). Patients were compared to 20 healthy volunteers on volumetric measures of cerebral structures (hemisphere, hippocampus and planum temporale) and ventricular–brain ratio (VBR) obtained by magnetic resonance imaging. Patients showed rightward asymmetry of cerebral hemispheres and increased VBR. Rightward asymmetry correlated with severity of negative symptoms and prevailed in the systematic forms of Leonhard, suggesting a distinct pattern of left hemisphere abnormality in this subgroup of psychoses. Increased VBR values showed a single normal distribution in the subgroups, indicating that ventricular enlargement is not restricted to a subgroup but is present to a certain degree in all cases.

Thalamic and caudate volumes in monozygotic twins discordantfor schizophrenia.

The thalamus and caudate nucleus are key subcortical structures in the fronto-striato-thalamic pathways that have been implicated in the pathogenesis of schizophrenia. Previous studies have been inconsistent in identifying structural and functional abnormalities in these structures. However, methodologies in these studies have been unreliable and some have not adequately matched patients and controls. Using algebraically-manipulated double-echomagnetic resonance (MR) images, we developed a reliable method to estimate caudate and thalamic volumes in a group of 13 monozygotic(MZ) twins; eight discordant for schizophrenia and five normal.Initially, volumes were measured on four image types: proton density(PD), T2-weighted, summed (PD + T2) and subtracted (PD-T2) to determine the most reliable method. There was a significant method by region interaction, where caudate volumes measured on PD images were significantly larger than those measured on T2-weighted images, while the opposite was found for thalamic volumes. However, there was no interaction of method by diagnosis. Test-retest reliability was highest for the summed images. Using summed images to measure the volumes of the caudate and thalamus in each twin, we found significantly increased caudate volumes in affected twins compared to their unaffected cotwins,but no significant difference in thalamic volume. Our results in a small sample of MZ twins discordant for schizophrenia do not support the presence of structural abnormalities in the thalamus. The findings in the caudate are consistent with previously reported effects of antipsychotic medication. We also report a reliable method for assessing the volumes of subcortical structures. However, volumetric estimates of brain structures may be dependent on which method is used and the structure being assessed. Such interactions need to be considered in future studies investigating brain structural abnormalities in schizophrenia and other disorders.

Disorders of Brain and Mind

Back to table of contents Previous article Next article Book Forum: Neuropsychiatry and NeurologyFull AccessDisorders of Brain and MindCONSTANTINE G. LYKETSOS, M.D., M.H.S., CONSTANTINE G. LYKETSOSSearch for more papers by this author, M.D., M.H.S., Baltimore, Md.Published Online:1 Apr 2001https://doi.org/10.1176/appi.ajp.158.4.671AboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail The recent increase in appreciation of the role that the brain plays in psychiatry, coupled with advances in neuroscience, brain imaging, and pharmacology, has led to an explosion of information on the interplay of brain and mind in the expression of psychiatric disorders. Pertinent research over the past two decades has been of two types. On the one hand is study of the psychiatric and psychological manifestations of coarse brain diseases or damage to specific brain regions as well as conditions closely linked to the brain, such as cognitive disorders and amnesia. On the other hand is careful study of the brains of patients with major psychiatric illnesses, particularly schizophrenia and the mood disorders, using a variety of modalities.Disorders of Brain and Mind is a compilation of much of the research in these areas. The book contains seven sections, each with two chapters. The first section is on frontal lobes and neuropsychiatry. Its chapters are on the neuropsychology of the frontal lobes and on frontal lobe structural abnormalities in schizophrenia. The second section is on basal ganglia in neuropsychiatry; the first chapter is on the neuropsychology of basal ganglia disorders, and the second is on the behavioral pharmacology of brain dopamine systems with implications for schizophrenia. The next section is on memory and its disorders. Once again, there is a chapter on neuropsychology of memory and amnesia. The second chapter in this section is on clinical neuropsychological studies of patients with amnestic disorders. Next is a section on brain disease and mental illness, which has one chapter on the psychiatric manifestations of demonstrable brain disease and one on structural brain imaging and the psychoses. The section that follows is on epilepsy; one chapter is on behavior in chronic experimental epilepsies and the other is a conceptual paper regarding the behavior disorders of epilepsy. A section on schizophrenia follows with both chapters expanding on the neurodevelopmental hypothesis of schizophrenia. The final section, Imaging Brain and Mind: Old and New Approaches, includes one chapter that discusses magnetic resonance spectroscopy in neuropsychiatry and another that discusses the hallucination as a disorder of brain and mind.Overall, this book is quite well written, thorough, and well founded empirically. In fact, the reference lists at the end of each chapter are very comprehensive. The chapters are all well balanced in their strengths, but the chapter by David and Busatto on the hallucination is an especially well-written integration of psychiatric phenomenology and neuroscience. It nicely illustrates the complex reasoning that will be necessary in future explorations of the relationship between brain and mind.Disorders of Brain and Mind is a very important book, despite its small weaknesses in conceptualization and integration of the topic and the occasional duplication or even slight contradiction in content, typical of an edited book. Its major strength is that it is a comprehensive “state of the field” review of the interface between brain and mind. Although the philosophical issues of the mind-brain problem are not addressed directly, the book’s empirical nature is quite satisfying. The book is also presented in a way that helps the reader appreciate the complexities of the issues at hand as well as some of the advances that have recently occurred. For any psychiatrist, both clinical or academic, interested in the interface of brain and mind, this is a valuable book that can be read through quite easily as an update and can also be referred to from time to time. For students new to psychiatry, this volume might also serve as an introductory text. Neuroscientists who are looking for a rather thorough review of brain-behavior relationships in select disorders will also find this book of interest.Edited by Maria A. Ron and Anthony S. David. New York, Cambridge University Press, 1998, 373 pp., $90.00; $44.95 (paperback published 2000). FiguresReferencesCited byDetailsCited ByNone Volume 158Issue 4 April 2001Pages 671-671 Metrics History Published online 1 April 2001 Published in print 1 April 2001

A review of MRI studies of progressive brain changes in schizophrenia.

In the early twentieth century, when Kraepelin first described ‘dementia praecox’ which eventually evolved into the concept of schizophrenia, he proposed that dementia praecox was probably an unknown organic brain disease. However, in contrast to the case of Alzheimer’s disease and Huntington’s disease, subsequent pathological studies of the brain failed to establish the neuropathology of schizophrenia. As a result, it had been generally accepted that schizophrenia would be a functional psychosis with neurochemical aberrations but without organic abnormalities. In 1976, Johnstone et al first reported the computerassisted tomography (CT) finding of lateral ventricular enlargement in patients with schizophrenia. This finding has been replicated in a number of CT studies and has been recognized as representing brain structural abnormalities in schizophrenia. Magnetic resonance imaging (MRI) enables more detailed and quantitative assessments of the fine brain structures, providing considerable evidence for the view that schizophrenia is a brain disorder with structural brain abnormalities.

Evidence for progression of brain structural abnormalities in schizophrenia: beyond the neurodevelopmental model.

Clinical, neuroimaging, neuropathological and neuropsychological evidence suggests that, in schizophrenia, there is structural and functional disturbance of the hippocampus. The purpose of this paper is to present published findings concerning the nature, timing and course of these putative disturbances of hippocampal function and the pathophysiological mechanisms involved, and to explore whether schizophrenia is a disorder of neurodevelopment, neurodegeneration or a combination of both processes. The available cross-sectional and longitudinal evidence for hippocampal involvement in schizophrenia is reviewed and a model of hippocampal involvement in this disorder, which derives from our own cross-sectional and longitudinal hippocampal imaging data, is described. We propose a three-hit model in which an early neurodevelopmental lesion renders the hippocampus vulnerable to further insult later in life during the transition phase to active illness. The available evidence suggests that the left hippocampus is particularly vulnerable during these early stages, while further insult involving the hippocampus bilaterally occurs in those who develop a chronic form of the illness. Intervention strategies should target the most vulnerable stages of the illness, in particular the transition phase to psychosis, when novel treatments may prevent the illness or ameliorate its effects.

Evidence for progression of brain structural abnormalities in schizophrenia: beyond the neurodevelopmental model

Evidence for progression of brain structural abnormalities in schizophrenia: beyond the neurodevelopmental model

163. Third ventricle enlargement and developmental delay in first episode schizophrenia

Enlargement of the lateral ventricles provides the most consistent evidence of structural brain abnormality in schizophrenia. The third ventricle has been studied to a lesser extent. The causes, effects, timing and course of ventricular pathology remain unclear. Establishing the processes underlying ventricular enlargement in schizophrenia will contribute to unraveling it’s aetiology. Detailed information on childhood development was collected from the mothers of 21 patients experiencing their first episode of schizophrenia, schizoaffective disorder or schizophreniform psychosis. T1-weighted images were obtained in 1.5 mm contiguous sections for the whole brain in the axial plane. Volumes were calculated for ventricular CSF, whole brain, prefrontal, premotor, sensorimotor, occipitoparietal regions including grey matter. There was a significant correlation between third ventricle volume and developmental score (r = 0.709, p < 0.0001). 7 patients with developmental delay had significantly larger third and lateral ventricles than the 14 without. The groups were comparable for age, gender, height, handedness, education and socio-economic status. There were no other differences in whole brain volume adjusted measures between the groups. Patients with first episode schizophrenia with a history of developmental delay have larger ventricles. The presence of developmental delay may discriminate between ventricular pathology and other structural abnormality in schizophrenia. These findings are in keeping with a developmental model of schizophrenia.

Development of novel antipsychotic drugs

The development of the current generation of antipsychotics has depended on animal, biochemical and pharmacological models of the action of drugs discovered serentipidously. They have focused on the dopamine hypothesis of schizophrenia. More recent studies of the structural abnormalities in schizophrenia, coupled with an understanding of the genetics and developmental biology of brain development, point to a new generation of novel medicines and therapies for patients with this disorder.

Evidence for Progression of Brain Structural Abnormalities in Schizophrenia: Beyond the Neurodevelopmental Model

ObjectiveClinical, neuroimaging, neuropathological and neuropsychological evidence suggests that, in schizophrenia, there is structural and functional disturbance of the hippocampus. The purpose of this paper is to present published findings concerning the nature, timing and course of these putative disturbances of hippocampal function and the pathophysiological mechanisms involved, and to explore whether schizophrenia is a disorder of neurodevelopment, neurodegeneration or a combination of both processes.MethodThe available cross-sectional and longitudinal evidence for hippocampal involvement in schizophrenia is reviewed and a model of hippocampal involvement in this disorder, which derives from our own cross-sectional and longitudinal hippocampal imaging data, is described.ResultsWe propose a three-hit model in which an early neurodevelopmental lesion renders the hippocampus vulnerable to further insult later in life during the transition phase to active illness. The available evidence suggests that the left hippocampus is particularly vulnerable during these early stages, while further insult involving the hippocampus bilaterally occurs in those who develop a chronic form of the illness.ConclusionsIntervention strategies should target the most vulnerable stages of the illness, in particular the transition phase to psychosis, when novel treatments may prevent the illness or ameliorate its effects.

Cerebral ventricular asymmetry in schizophrenia: a high resolution 3D magnetic resonance imaging study

Lateral ventricular volume asymmetries in schizophrenia were studied using high resolution 3D magnetic resonance imaging in conjunction with segmentation and quantitation techniques. Comparisons were made between two clinical syndromes that have been associated with opposite patterns of functional hemispheric activation, namely an active and a withdrawn syndrome. Ratios of both left to right ventricular volume and left to right ventricle-to-brain ratios differed significantly between the two groups. These results primarily reflected differences in the left ventricular volume, in keeping with previous reports which have usually implicated left hemispheric structural abnormalities in schizophrenia. It is suggested that a syndromal approach might help to resolve some of the inconsistencies in the existing literature on lateralised neuroanatomical differences in schizophrenia.

Investigation of frontal lobe subregions in first-episode schizophrenia

The evidence for frontal lobe structural abnormalities in schizophrenia using magnetic resonance (MR) imaging has been mixed, but most studies used either single slice measures or total volumes of a single frontal region, neither of which is sensitive to potential volume differences in more specific subregions. This study employed reliable methods for parcellation of the frontal lobes from MR images based on the sulcal anatomy. Following a cytoarchitectonic theory that distinguishes dorsomedial (archicortically derived) from ventrolateral (paleocortically derived) frontal subregions, we measured the superior frontal gyrus, anterior cingulate gyrus, and orbital frontal region in 19 first-episode schizophrenia patients and 26 healthy comparison subjects. Results indicated that male patients had significantly larger right orbital frontal volume compared to their left orbital frontal volume and compared to healthy men. Among male patients larger right orbital frontal volume was significantly correlated with smaller right `archicortical' (i.e. anterior cingulate and superior frontal gyri) volume. Furthermore, the ratio of right orbital frontal to right `archicortical' volume was significantly and positively correlated with level of delusions among male patients. These findings suggest that there may be reciprocal controls on `archicortical' and `paleocortical' neurodevelopment among men with schizophrenia, and that larger paleocortical relative to archicortical volumes may be associated with increased delusions.

Schizophrenia and anteroventral thalamic nucleus: selective decrease of parvalbumin-immunoreactive thalamocortical projection neurons

This study was designed to examine possible anatomical changes of thalamocortical circuits in schizophrenics. Previous immunocytochemical studies have shown that parvalbumin, a calcium-binding protein, occurs in thalamocortical projection neurons, but not in GABAergic interneurons in the anteroventral thalamic nucleus (AN). Using parvalbumin-immunocytochemistry we investigated the densities of thalamocortical projection neurons in the AN of schizophrenic cases ( n=12) and controls ( n=14). The densities of all neurons in the AN were estimated by Nissl-staining. The majority of thalamocortical projection neurons in AN were identified by parvalbumin-immunoreaction. Significantly reduced densities of thalamocortical projection neurons were estimated in the right ( P=0.003) and left AN ( P=0.018) in schizophrenic subjects. The densities of all neurons in right and left AN were also diminished in schizophrenics; however, these decreases did not reach statistical significance. The reductions of parvalbumin-positive thalamocortical projection neurons were not correlated with the length of disease, this finding supporting the neurodevelopmental etiology of structural abnormalities in schizophrenia.

Clinical and structural abnormalities in schizophrenia

Clinical and structural abnormalities in schizophrenia

Psychopathology: the evolving science of mental disorder

List of contributors Preface Steven Matthysse Part I. Brain Mechanisms: 1. Editor's introduction: from controversy to connectivity Francine M. Benes 2. The functional parcellation of dorsolateral prefrontal cortex and the heterogeneous facets of schizophrenia Patricia Goldman-Rakic 3. Components of working memory deficit in schizophrenia Sohee Park and Gillian O'Driscoll 4. Temporal lobe structural abnormalities in schizophrenia: a selective review and presentation of new magnetic resonance findings Martha E. Shenton 5. Location, location, location: the pathway from behavior to brain locus in schizophrenia Deborah L. Levy 6. The defects of affect and attention in schizophrenia: a possible neuroanatomical substrate Francine M. Benes Part II. Development: 7. Editor's introduction: methods in the developmental study of madness Jerome Kagan 8. Developmental psychopathology: from attribution toward information Sheldon H. White Comments Philip S. Holzman 9. A paradoxical partnership: some historical and contemporary referents linking adult schizophreniform disorder and resilient children under stress Norman Garmezy 10. A look at the evolution of developmental models of schizophrenia L. Erlenmeyer-Kimling 11. Developmental theory: lessons from the study of risk and psychopathology Dante Cicchetti 12. The return of the ancients: on temperament and development Jerome Kagan Part III. Thinking: 13. Editor's introduction: Upward toward phenomenology m downward toward physiology Steven Matthysse 14. The psychometric assessment of schizophrenia proneness Jean P. Chapman and Loren J. Chapman 15. Politeness in schizophrenia Roger Brown Comments Philip S. Holzman 16. Neuroleptic treatment effects in relation to psychotherapy, social skills training and social withdrawal in schizophrenics Herbert E. Spohn Comments Philip S. Holzman 17. Familial factors in the impairment of attention in schizophrenia: data from Ireland, Israel and the District of Columbia Allan F. Mirsky 18. Parsing cognitive processes: psychopathological and neurophysiological constraints Anne Sereno 19. Cognitive psychopathology in schizophrenia: explorations in language, memory, associations and movements Brendan A. Maher Part IV. Genetics: 20. Editor's introduction: contemporary issues in the genetics of psychopathological disorders Deborah L. Levy, Steven Matthysse and Philip S. Holzman 21. Genetic and environmental factors in the etiology of schizophrenia Seymour S. Kety 22. Problems and paradoxes in research on the etiology of schizophrenia Einar Kringlen Comments Philip S. Holzman and Steven Matthysse 23. Epistemological issues in psychiatric research Josef Parnas 24. Searching for major genes in schizophrenia Kenneth K. Kidd 25. The Drosophila eye and the genetics of schizophrenia Steven Matthysse Part V. Response and Reflections: 26. Reflections on the developing science of psychopathology Philip S. Holzman Author index Subject index.

P300 lateral asymmetries in schizophrenic syndromes

Lateral ventricular volume asymmetries in schizophrenia were studied using high resolution 3D magnetic resonance imaging in conjunction with segmentation and quantitation techniques. Comparisons were made between two clinical syndromes that have been associated with opposite patterns of functional hemispheric activation, namely an active and a withdrawn syndrome. Ratios of both left to right ventricular volume and left to right ventricle-to-brain ratios differed significantly between the two groups. These results primarily reflected differences in the left ventricular volume, in keeping with previous reports which have usually implicated left hemispheric structural abnormalities in schizophrenia. It is suggested that a syndromal approach might help to resolve some of the inconsistencies in the existing literature on lateralised neuroanatomical differences in schizophrenia.

Normal planum temporale asymmetry in familial schizophrenia: A volumetric MRI study

Although well documented, brain structural abnormalities in schizophrenia are non-specific, and morphometric parameters show significant overlap between patients and healthy controls. Such inconsistencies in neuroimaging findings could represent different levels of severity along a single pathogenic process or distinct clinical and etiopathological psychoses within a schizophrenic spectrum. The aim of the present study was the investigation of distinct brain abnormalities in different subtypes of schizophrenia. Forty patients were classified according to DSM-IV and Leonhard's classifications. Psychopathology was assessed by the Positive and Negative Syndrome Scale (PANSS) and the Negative Symptom Rating Scale (NSRS). Patients were compared to 20 healthy volunteers on volumetric measures of cerebral structures (hemisphere, hippocampus and planum temporale) and ventricular–brain ratio (VBR) obtained by magnetic resonance imaging. Patients showed rightward asymmetry of cerebral hemispheres and increased VBR. Rightward asymmetry correlated with severity of negative symptoms and prevailed in the systematic forms of Leonhard, suggesting a distinct pattern of left hemisphere abnormality in this subgroup of psychoses. Increased VBR values showed a single normal distribution in the subgroups, indicating that ventricular enlargement is not restricted to a subgroup but is present to a certain degree in all cases.