Schizophrenia - what does structural MRI show?

Tidsskrift for den Norske laegeforening 04/2013; 133(8):850-853. DOI: 10.4045/tidsskr.12.1084
Source: PubMed


Schizophrenia is a serious mental disorder that affects several brain functions. MRI technology has enabled in vivo studies of brain anatomy in patients with schizophrenia aimed at understanding more about the disorder.

This article is based on a search in PubMed on «schizophrenia MRI» and on the authors' own research and experience. We included structural MRI studies, carried out on humans, written in English. Here we present a selection of studies that we believe are representative of the field.

In patients with schizophrenia, MR imaging shows a smaller total brain volume and enlarged ventricles. Specific subcortical regions are affected, with reduced hippocampal and thalamic volumes, and an increase in the volume of the globus pallidus. In the cortex can be seen changes in folding patterns and a reduction in cortical volume and thickness, most pronounced in the frontal and temporal lobes. These findings are at group level--there is a high degree of overlap between sick and healthy individuals, and the effect sizes are medium to small. Several of the changes are present at onset of the disorder; this supports the theory that schizophrenia may be related to abnormal neurodevelopment. Longitudinal anatomical changes are reported, but it is uncertain what these changes represent.

The research literature shows that schizophrenia has neuroanatomical correlates that can be seen at group level by studying MR images. Structural MRI cannot currently be used to identify schizophrenia at the level of the individual.

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    • "ORIGINAL ARTICLE of these illnesses. Structural imaging has consistently shown cortical grey-matter deficits in the frontal lobes in SZ (reviewed in Haukvik et al. 2014), and network models suggest disconnectivity in the frontal lobes is a key problem (Curčić-Blake et al. 2013). WM connectivity within and between the frontal lobes is also thought to be critical in depressive disorders (Bracht et al. 2012; Ozalay et al. 2013), and the extent of frontal cortical thickness has been related to severity of depressive symptoms (Riederer et al. 2012; Wagner et al. 2012). "
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    ABSTRACT: Abnormalities in the anterior inter-hemispheric connectivity have previously been implicated in major depressive disorder. Disruptions in fractional anisotropy in the callosum and fornix have been reported in schizophrenia and major depressive disorder. Oligodendrocyte density and overall size of the callosum and fornix show no alteration in either illness, suggesting that gross morphology is unchanged but more subtle organizational disruption may exist within these brain regions in mood and affective disorders. Using high-resolution oil-immersion microscopy we examined the cross-sectional area of the nerve fibre and the axonal myelin sheath, and using standard high-resolution light microscopy we measured the density of myelinated axons. These measurements were made in the genu of the corpus callosum and the medial body of the fornix at its most dorsal point. Measures were taken in the sagittal plane in the callosal genu and in the coronal plane at the most dorsal part of the fornix body. Cases of major depressive disorder had significantly greater mean myelin cross-sectional area (p = 0.017) and myelin thickness (p = 0.004) per axon in the genu than in control or schizophrenia groups. There was no significant change in the density of myelinated axons, and no changes observed in the fornix. The results suggest a clear increase of myelin in the axons of the callosal genu in MDD, although this type of neuropathological study is unable to clarify whether this is caused by changes during life or has a developmental origin.
    Psychological Medicine 02/2015; 45(10):1-11. DOI:10.1017/S0033291715000136 · 5.94 Impact Factor
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    • "Here, we apply this framework to the question of global cognitive deficit vs. specific executive impairments in schizophrenia. As in various psychiatric conditions, cognitive deficits in schizophrenia have been commonly explained in terms of frontal dysfunction (e.g., Lewis and González-Burgos, 2008; Lewis, 2012), and in anatomical terms, a range of frontal abnormalities have been described (Ellison-Wright et al., 2008; Haukvik et al., 2013). Importantly, some recent factor analytic studies have described a single principal component that accounts for much of the variance of patients' cognitive performance (e.g., Dickinson et al., 2006, 2008; Keefe et al., 2006; Harvey et al., 2011, 2013). "
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    ABSTRACT: An enduring question is unity vs. separability of executive deficits resulting from impaired frontal lobe function. In previous studies, we have asked how executive deficits link to a conventional measure of fluid intelligence, obtained either by standard tests of novel problem-solving, or by averaging performance in a battery of novel tasks. For some classical executive tasks, such as the Wisconsin Card Sorting Test (WCST), Verbal Fluency, and Trail Making Test B (TMTB), frontal deficits are entirely explained by fluid intelligence. However, on a second set of executive tasks, including tests of multitasking and decision making, deficits exceed those predicted by fluid intelligence loss. In this paper we discuss how these results shed light on the diverse clinical phenomenology observed in frontal dysfunction, and present new data on a group of 15 schizophrenic patients and 14 controls. Subjects were assessed with a range of executive tests and with a general cognitive battery used to derive a measure of fluid intelligence. Group performance was compared and fluid intelligence was introduced as a covariate. In line with our previous results, significant patient-control differences in classical executive tests were removed when fluid intelligence was introduced as a covariate. However, for tests of multitasking and decision making, deficits remained. We relate our findings to those of previous factor analytic studies describing a single principal component, which accounts for much of the variance of schizophrenic patients' cognitive performance. We propose that this general factor reflects low fluid intelligence capacity, which accounts for much but not all cognitive impairment in this patient group. Partialling out the general effects of fluid intelligence, we propose, may clarify the role of additional, more specific cognitive impairments in conditions such as schizophrenia.
    Frontiers in Behavioral Neuroscience 02/2014; 8:46. DOI:10.3389/fnbeh.2014.00046 · 3.27 Impact Factor
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    ABSTRACT: Temporal lobe epilepsy in both animals and humans is characterized by abnormally integrated hippocampal dentate granule cells. Among other abnormalities, these cells make axonal connections with inappropriate targets, grow dendrites in the wrong direction, and migrate to ectopic locations. These changes promote the formation of recurrent excitatory circuits, leading to the appealing hypothesis that these abnormal cells may by epileptogenic. While this hypothesis has been the subject of intense study, less attention has been paid to the possibility that abnormal granule cells in the epileptic brain may also contribute to comorbidities associated with the disease. Epilepsy is associated with a variety of general findings, such as memory disturbances and cognitive dysfunction, and is often comorbid with a number of other conditions, including schizophrenia and autism. Interestingly, recent studies implicate disruption of common genes and gene pathways in all three diseases. Moreover, while neuropsychiatric conditions are associated with changes in a variety of brain regions, granule cell abnormalities in temporal lobe epilepsy appear to be phenocopies of granule cell deficits produced by genetic mouse models of autism and schizophrenia, suggesting that granule cell dysmorphogenesis may be a common factor uniting these seemingly diverse diseases. Disruption of common signaling pathways regulating granule cell neurogenesis may begin to provide mechanistic insight into the cooccurrence of temporal lobe epilepsy and cognitive and behavioral disorders. This article is part of a Special Issue entitled "NEWroscience 2013".
    Epilepsy & Behavior 01/2014; 38. DOI:10.1016/j.yebeh.2013.12.022 · 2.26 Impact Factor
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