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(searched for: doi:10.1007/bf00381351)
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Published: 27 March 2021
The publisher has not yet granted permission to display this abstract.
Published: 27 March 2021
The publisher has not yet granted permission to display this abstract.
, Henrik Dobrowolny, Bernhard Bogerts, Gerburg Keilhoff,
Published: 16 May 2018
Cell and Tissue Research, Volume 375, pp 243-258; https://doi.org/10.1007/s00441-018-2849-3

Abstract:
The past decades have witnessed an explosion of knowledge on brain structural abnormalities in schizophrenia and depression. Focusing on the hypothalamus, we try to show how postmortem brain microscopy has contributed to our understanding of mental disease-related pathologic alterations of this brain region. Gross anatomical abnormalities (volume changes of the third ventricle, the hypothalamus, and its nuclei) and alterations at the cellular level (loss of neurons, increased or decreased expression of hypothalamic peptides such as oxytocin, vasopressin, corticotropin-releasing hormone, and other regulatory factors as well as of enzymes involved in neurotransmitter and neuropeptide metabolism) have been reported in schizophrenia and/or depression. While histologic research has mainly concentrated on neurons, little is currently known about the impact of non-neuronal cells for hypothalamus pathology in mental disorders. Their study would be a rewarding task for the future.
Frontiers in Neuroscience, Volume 10; https://doi.org/10.3389/fnins.2016.00202

Abstract:
Schizophrenia is a complex psychiatric disorder characterized by the presence of positive, negative and cognitive symptoms that lacks a unifying neuropathology. In the present paper, we will review the current understanding of molecular dysregulation in schizophrenia, including genetic and epigenetic studies. In relation to the latter, basic research suggests that normal cognition is regulated by epigenetic mechanisms and its dysfunction occurs upon epigenetic misregulation, providing new insights into missing heritability of complex psychiatric diseases, referring to the discrepancy between epidemiological heritability and the proportion of phenotypic variation explained by DNA sequence difference. In schizophrenia the absence of consistently replicated genetic effects together with evidence for lasting changes in gene expression after environmental exposures suggest a role of epigenetic mechanisms. In this review we will focus on epigenetic modifications as a key mechanism through which environmental factors interact with individual's genetic constitution to affect risk of psychotic conditions throughout life.
Kang Ik K. Cho, Martha E. Shenton, Marek Kubicki, Wi Hoon Jung, , Kim Sung Nyun, Sung Nyun Kim,
Schizophrenia Bulletin, Volume 42, pp 723-731; https://doi.org/10.1093/schbul/sbv169

Abstract:
Disrupted thalamo-cortical connectivity is regarded as a core psychopathology in patients diagnosed with schizophrenia. However, whether the thalamo-cortical white matter connectivity is disrupted before the onset of psychosis is still unknown. To determine this gap in knowledge, the strength of thalamo-cortical white matter anatomical connectivity in subjects at clinical-high risk for psychosis (CHR) was compared to that of first-episode psychosis (FEP) and healthy controls. A total of 37 CHR, 21 FEP, and 37 matched healthy controls underwent diffusion-weighted magnetic resonance imaging to examine the number of probabilistic tractography “counts” representing thalamo-cortical white matter connectivity. We also investigated the relationship with psychopathology. For FEP, the connectivity between the thalamus and parietal cortex was significantly increased (F = 5.65, P< .05) compared to that of healthy controls. However, the connectivity between thalamus and orbitofrontal cortex was significantly reduced compared to both healthy controls (F = 11.86, P< .005) and CHR (F = 6.63, P< .05). Interestingly, CHR exhibited a similar pattern as FEP, albeit with slightly reduced magnitude. Compared to healthy controls, there was a significant decrease (F = 4.16, P< .05) in CHR thalamo-orbitofrontal connectivity. Also, the strength of the thalamo-orbitofrontal connectivity was correlated with the Global Assessment of Functioning score in CHR (r = .35, P< .05). This observed pattern of white matter connectivity disruptions in FEP and in CHR suggests that this pattern of disconnectivity not only highlights the involvement of thalamus but also might be useful as an early biomarker for psychosis.
Anne-Marie Gagné, Marc Hébert, Michel Maziade
Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 62, pp 29-34; https://doi.org/10.1016/j.pnpbp.2015.04.007

Abstract:
This review highlights morphological and functional anomalies found along the entire visual pathway in schizophrenia, from the retina to the cortex. Based on the evidence of widespread anatomical and functional visual abnormalities, we posited that a neurodevelopmental anomaly occurring early in life was likely to explain those. Incidentally, support to the neurodevelopmental theory of schizophrenia is strongly emerging from many neurobiological domains. In vertebrates, the first visual structures migrate toward the orbit position at the end of the fourth week of gestation. A neurodevelopmental defect around that time on these embryonic structures could account for the visual anomalies in schizophrenia. Retinol activity might be involved in the process. Future research in schizophrenia should focus on early visual testing, on trials combining multiple visual anomaly assessments and a closer look to retinol activity during the pregnancy.
, C. Atriano-Mendieta, R. Carrillo-Meza,
Published: 1 February 2013
Neurocase, Volume 19, pp 22-26; https://doi.org/10.1080/13554794.2011.654211

Abstract:
Thalamic dysfunction has been associated with schizophrenia and other psychotic disorders. We describe an adult patient with a lacunar infarct in the posterior region of the right thalamus exhibiting a paranoid schizophrenia-like psychosis as the only clinical manifestation. Neuropsychological assessment showed alterations in visuospatial memory and executive functions at follow up. This case highlights the role of information processing by the thalamus in the development of delusions. We suggest that dysfunction of the right mediodorsal and pulvinar thalamic nuclei disrupts both thalamic sensory processing and thalamo-prefrontal circuits mediating belief evaluation, leading to delusional beliefs.
Published: 1 January 2013
Frontiers in Psychology, Volume 4; https://doi.org/10.3389/fpsyg.2013.00088

Abstract:
Compared to unaffected observers patients with schizophrenia (SZ) show characteristic differences in visual perception, including a reduced susceptibility to the influence of context on judgments of contrast – a manifestation of weaker surround suppression (SS). To examine the generality of this phenomenon we measured the ability of 24 individuals with SZ to judge the luminance, contrast, orientation, and size of targets embedded in contextual surrounds that would typically influence the target’s appearance. Individuals with SZ demonstrated weaker SS compared to matched controls for stimuli defined by contrast or size, but not for those defined by luminance or orientation. As perceived luminance is thought to be regulated at the earliest stages of visual processing our findings are consistent with a suppression deficit that is predominantly cortical in origin. In addition, we propose that preserved orientation SS in SZ may reflect the sparing of broadly tuned mechanisms of suppression. We attempt to reconcile these data with findings from previous studies.
Published: 15 January 2011
Biological Psychiatry, Volume 69, pp 113-126; https://doi.org/10.1016/j.biopsych.2010.04.030

Abstract:
The challenges involved in identifying the neuropathological substrates of the clinical syndrome recognized as schizophrenia are well known. Stereological sampling provides a means to obtain accurate and precise quantitative estimates of components of neural circuits and thus offers promise of an enhanced capacity to detect subtle alterations in brain structure associated with schizophrenia. In this review, we 1) consider the importance and rationale for robust quantitative measures of brain abnormalities in postmortem studies of schizophrenia; 2) provide a brief overview of stereological methods for obtaining such measures; 3) discuss the methodological details that should be reported to document the robustness of a stereological study; 4) given the constraints of postmortem human studies, suggest how to approach the limitations of less robust designs; and 5) present an overview of methodologically sound stereological estimates from postmortem studies of schizophrenia.
H.-J. Möller, A. Schaub, M. Riedel
Published: 1 January 2011
The publisher has not yet granted permission to display this abstract.
Paul J. Harrison, , Joel E. Kleinman Md
Published: 10 December 2010
The publisher has not yet granted permission to display this abstract.
, Ilaria Spoletini, Carlo Caltagirone,
Published: 31 October 2010
Schizophrenia Research, Volume 123, pp 1-14; https://doi.org/10.1016/j.schres.2010.07.007

Abstract:
Although several structural MRI studies report significant thalamus volume reduction in patients with schizophrenia, many other studies do not. Therefore, the present meta-analyses aimed to clarify whether a reduction in thalamic volume characterizes patients diagnosed with schizophrenia by considering first-episode and chronic phases of the illness and right and left thalamus separately
Raúl Alelú-Paz, José Manuel Giménez-Amaya
Published: 1 November 2008
Journal of Psychiatry and Neuroscience, Volume 33, pp 489-98

Abstract:
The mediodorsal nucleus of the human thalamus is in a crucial position that allows it to establish connections with diverse cerebral structures, particularly the prefrontal cortex. The present review examines existing neurobiologic studies of the brains of people with and without schizophrenia that indicate a possible involvement of the mediodorsal nucleus in this psychiatric disorder. Studies at synaptic and cellular levels of the neurobiology of the mediodorsal nucleus, together with a better anatomic understanding of this diencephalic structure owing to neuroimaging studies, should help to establish a more deep and solid pathophysiologic model of schizophrenia.
, Damira Caric, Ramin Saghafi, Wei Zhang, Allan R. Sampson, David A. Lewis
Published: 19 July 2008
Acta Neuropathologica, Volume 117, pp 369-384; https://doi.org/10.1007/s00401-008-0410-2

Abstract:
Subjects with schizophrenia show deficits in visual perception that suggest changes predominantly in the magnocellular pathway and/or the dorsal visual stream important for visiospatial perception. We previously found a substantial 25% reduction in neuron number of the primary visual cortex (Brodmann’s area 17, BA17) in postmortem tissue from subjects with schizophrenia. Also, many studies have found reduced volume and neuron number of the pulvinar—the large thalamic association nucleus involved in higher-order visual processing. Here, we investigate if the lateral geniculate nucleus (LGN), the visual relay nucleus of the thalamus, has structural changes in schizophrenia. We used stereological methods based on unbiased principles of sampling (Cavalieri’s principle and the optical fractionator) to estimate the total volume and neuron number of the magno- and parovocellular parts of the left LGN in postmortem brains from nine subjects with schizophrenia, seven matched normal comparison subjects and 13 subjects with mood disorders. No significant schizophrenia-related structural differences in volume or neuron number of the left LGN or its major subregions were found, but we did observe a significantly increased total volume of the LGN, and of the parvocellular lamina and interlaminar regions, in the mood group. These findings do not support the hypothesis that subjects with schizophrenia have structural changes in the LGN. Therefore, our previous observation of a schizophrenia-related reduction of the primary visual cortex is probably not secondary to a reduction in the LGN.
Hans-Jürgen Möller, A. Deister, A. Schaub, M. Riedel
Published: 1 January 2008
The publisher has not yet granted permission to display this abstract.
, Joseph N. Pierri, Qiang Wu, Allan R. Sampson,
Published: 16 January 2007
Journal of Comparative Neurology, Volume 501, pp 290-301; https://doi.org/10.1002/cne.21243

The publisher has not yet granted permission to display this abstract.
Maja Abitz, Rune Damgaard Nielsen, Edward G. Jones, Henning Laursen, Niels Graem,
Published: 11 January 2007
Cerebral Cortex, Volume 17, pp 2573-2578; https://doi.org/10.1093/cercor/bhl163

Abstract:
The aim of this study was to quantify the total number of neurons and glial cells in the mediodorsal nucleus of the thalamus (MD) of 8 newborn human brains, in comparison to 8 adult human brains. The estimates of the cell numbers were obtained using the stereological principles of the optical fractionator. In the case of the adults, the total number of neurons in the entire MD was an average of 41% lower than in the newborn, which was statistically highly significant (P< 0.001). The estimated average total number of neurons in MD thalamus of the newborns was 11.2 million (coefficient of variation [CV] = standard deviation/mean = 0.16), compared with the adults' 6.43 million (CV = 0.15). The glial cell numbers were substantially higher in the adult brains, with an increase of almost 4 times from 10.6 million at birth to 36.3 million in the fully developed adult brain. This is the first demonstration of a higher number of human neurons in the brain of newborns compared with the adult.
, Andrea Schmidt, Bruno Baumann, Hans-Gert Bernstein, Georg Northoff, Renate Stauch, Dieter Krell, Bernhard Bogerts
Published: 30 December 2005
Psychiatry Research: Neuroimaging, Volume 140, pp 281-289; https://doi.org/10.1016/j.pscychresns.2005.09.005

Abstract:
Previous neuropathological studies on the mediodorsal thalamic nucleus (MD) in schizophrenia have yielded conflicting results. While some studies suggested that patients with schizophrenia have a pronounced reduction of the volume and neuron number in the MD, more recent data have not found anatomical alterations in this thalamic nucleus. However, most studies have considerable methodological shortcomings. In the present study, we investigated the volume, neuron density and neuron number in the left and right MD in patients with schizophrenia (n = 20) and normal control subjects without neuropsychiatric disorders (n = 18). Patients with schizophrenia showed no significant difference in neuron density and total neuron number in the MD. Compared with the control group, patients with schizophrenia had a smaller MD volume in both hemispheres, a difference that approached significance in the left MD (− 7.3%) when the whole brain volume was included as a covariate. No significant main group effect of diagnosis was found for the right MD volume. There were no significant correlations between MD volume, neuron density, total neuron number and the duration of illness or the age of the patients. Taken together, the present results suggest that schizophrenia is associated with a moderate volume reduction in the left mediodorsal thalamic nucleus, while the neuron density and the total neuron number are unchanged.
, T. Cullen, D. Ongur, S. Heckers
Published: 27 October 2005
Journal of Neural Transmission, Volume 113, pp 907-928; https://doi.org/10.1007/s00702-005-0363-8

The publisher has not yet granted permission to display this abstract.
U.W. Preuss, T. Zetzsche, M. Jäger, C. Groll, , R. Bottlender, G. Leinsinger, , K. Hahn, H.J. Möller, et al.
Published: 1 February 2005
Schizophrenia Research, Volume 73, pp 91-101; https://doi.org/10.1016/j.schres.2004.09.019

The publisher has not yet granted permission to display this abstract.
, Maria T. Panayotacopoulou, Joop J. van Heerikhuize, Unga A. Unmehopa, Dimitra P. Kontostavlaki,
Published: 1 January 2005
Neuroendocrinology, Volume 82, pp 63-69; https://doi.org/10.1159/000090981

Abstract:
Dysfunction in water intake and metabolism has frequently been reported in schizophrenia. The general population of schizophrenics under neuroleptic treatment secretes lower amounts of vasopressin than controls at comparable values of plasma osmolality. The purpose of the present study was to investigate the synthetic activity of vasopressin neurons of the dorsolateral supraoptic nucleus in schizophrenia on postmortem material using a battery of histochemical activity markers. Our material consisted of formalin-fixed and paraffin-embedded hypothalami from 5 schizophrenic patients under neuroleptic treatment and from 5 matched controls, obtained from The Netherlands' Brain Bank. DSM-III or DSM-IV criteria were used for the clinical diagnosis. The histochemical markers used to study the neuronal activity of the magnocellular vasopressin-synthesizing neurons were: cell size, size of the Golgi apparatus, and expression of vasopressin and tyrosine hydroxylase mRNA by in situ hybridization. Morphometric evaluation and statistical analysis (Mann-Whitney U test) were performed. Our results showed no statistically significant differences in any of the neuronal activity markers between schizophrenic patients and controls. Therefore, the neurosecretory activity of vasopressin neurons of the dorsolateral part of the supraoptic nucleus does not appear to be changed in schizophrenic patients under medication. Since our sample did not include patients with reported polydipsia or hyponatremia, prospective investigation is needed to evaluate the above-mentioned neuronal activity markers in such a particular subgroup of schizophrenic patients.
, H H Holcomb
Published: 31 August 2004
Molecular Psychiatry, Volume 10, pp 27-39; https://doi.org/10.1038/sj.mp.4001563

The publisher has not yet granted permission to display this abstract.
, Gerburg Keilhoff, Alicja Bukowska, Anke Ziegeler, Sieglinde Funke, Henrik Dobrowolny, Dimitrios Kanakis, Bernhard Bogerts, Uwe Lendeckel
Published: 1 December 2003
Journal of Neuroscience Research, Volume 75, pp 353-360; https://doi.org/10.1002/jnr.10858

The publisher has not yet granted permission to display this abstract.
, , Thomas Zetzsche, Gerda Leinsinger, Klaus Maag, , Klaus Hahn, Hans-Jürgen Möller
Published: 28 August 2002
Psychiatry Research: Neuroimaging, Volume 115, pp 127-135; https://doi.org/10.1016/s0925-4927(02)00044-6

Abstract:
Absence of the adhesio interthalamica (AI) in schizophrenic first episode patients is suggestive for another marker of early developmental neuropathologic changes. Moreover, findings suggest that schizophrenic patients without AI are characterised by more severe negative symptoms. The study aims to investigate the presence vs. absence of AI in relation to brain measurements and clinical features. Presence or absence of AI and volumetric brain measurements were assessed in 50 patients with schizophrenia and 50 matched controls. No differences in the incidence of AI were found between the groups. Patients without AI revealed a strong trend towards a larger third ventricle and significantly higher scores for negative symptoms. Interestingly, the subgroup of healthy controls without AI also had larger third ventricles. The absence of AI may represent another early developmental marker of cerebral malformation in a clinical subgroup of schizophrenic patients.
Peter Danos, Bruno Baumann, Andrea Krämer, Hans-Gert Bernstein, Renate Stauch, Dieter Krell, , Bernhard Bogerts
Published: 9 June 2002
Schizophrenia Research, Volume 60, pp 141-155; https://doi.org/10.1016/s0920-9964(02)00307-9

The publisher has not yet granted permission to display this abstract.
T.J Cullen, M.A Walker, , R Craven, T.J Crow, M.M Esiri,
Published: 16 May 2002
Schizophrenia Research, Volume 60, pp 157-166; https://doi.org/10.1016/s0920-9964(02)00297-9

The publisher has not yet granted permission to display this abstract.
, Theo G. M. Van Erp, Isabelle M. Rosso, Matti Huttunen, Jouko Lönnqvist, Tiia Pirkola, Oili Salonen, , Veli-Pekka Poutanen, Carl-Gustav Standertskjöld-Nordenstam
Archives of General Psychiatry, Volume 59, pp 35-41; https://doi.org/10.1001/archpsyc.59.1.35

Abstract:
STRUCTURAL BRAIN abnormalities are robust correlates of schizophrenia, but their causes have not been conclusively established.1-3 Neuromotor and cognitive deficits in preschizophrenic children4-6 and cortical laminar neuron displacement in schizophrenic patients at autopsy7-10 suggest that at least some of the anatomical changes associated with schizophrenia are neurodevelopmental in origin.11 Genetic influences in schizophrenia are substantial,12 but the mode of inheritance is complex. It involves at least several genes13 and certain neurally disruptive environmental exposures, such as obstetric complications (OCs).14-27 Of the many types of OCs found to predict schizophrenia, fetal hypoxia has shown the strongest association, accounting for a greater proportion of liability than exposure to infections during gestation, fetal growth retardation, and other obstetric factors.27 Because no study using objective birth records has found that hypoxic OCs are more frequent in the first-degree relatives of schizophrenic patients than in the general population,17-24 these complications do not appear to be consequences of genetic liability to schizophrenia. It is also unlikely that these early influences cause schizophrenia on their own because more than 90% of individuals who experience fetal hypoxia, even in its severe form, do not develop schizophrenia.17,18,25,26 Hypoxic OCs must thus act additively or interactively with genetic factors in influencing disease liability.27
Lisa C Konick, Lee Friedman
Published: 1 January 2001
Biological Psychiatry, Volume 49, pp 28-38; https://doi.org/10.1016/s0006-3223(00)00974-4

Abstract:
Background: This article presents a meta-analysis of thalamic size reduction in schizophrenia. Methods: Reviewed studies were based on magnetic resonance imaging or postmortem material and included measures of thalamic volume or thalamic area in schizophrenic patients and comparison subjects. Meta-analysis I was based on absolute thalamic values (not controlled for overall brain size), and Meta-analysis II evaluated thalamic size adjusted for brain size. Results: Meta-analysis I included data from 15 studies (485 schizophrenic subjects and 500 control subjects). Twelve (80%) of the studies had negative effect sizes, which is consistent with the hypothesis that thalamic size is smaller in schizophrenic subjects compared to control subjects. The composite effect size was −0.29 (p < .0001; without outliers: −0.41, p < .0001). Meta-analysis II included data from 11 studies (313 schizophrenic patients and 434 control subjects). Ten (91%) of the studies had negative effect sizes. The composite effect size was −0.35 (p < .0001; without outlier: −0.30, p < .0001). Conclusions: Both meta-analyses indicate a statistically significant, small-to-moderate effect size for thalamic size reduction in schizophrenia; however, the effect size for thalamic size reduction is modest in comparison to that of other structural abnormalities noted in schizophrenia.
B. Bogerts, P. Falkai
Published: 1 January 2001
The publisher has not yet granted permission to display this abstract.
H. Beckmann
Published: 1 January 2001
The publisher has not yet granted permission to display this abstract.
Gregory J. Popken, William E. Bunney, ,
Proceedings of the National Academy of Sciences, Volume 97, pp 9276-9280; https://doi.org/10.1073/pnas.150243397

Abstract:
The hypoactivity of dorsolateral prefrontal cortex in schizophrenics is well known. One cause of this hypoactivity may be defective corticocortical or thalamocortical connections. Recent imaging studies of the thalamus suggest reductions in volume of the whole thalamus and reduced activity in the medial group of thalamic nuclei, which may indicate loss of functional input to the cortex. Using stereological techniques in six pairs of individually matched brains from schizophrenics and controls, we measured the volumes and obtained estimates of the number of neurons in the three subnuclei (parvocellular, pc; densocellular, dc; magnocellular, mc) of the mediodorsal nucleus (MD) and from the ventral posterior medial nucleus. There was a significant reduction in total neuron number in MD as a whole but this neuron loss was largely restricted to MDpc and MDdc [−30.9 and −24.5%, respectively ( P ≤ 0.01)]. MDmc and the control ventral posterior medial nucleus showed no significant changes in cell number. Because the subnuclei of MD have different connections and project to different areas of the frontal cortex, the specific loss of neurons in MDpc and MDdc has implications for the functional defects observed in schizophrenia.
Eric Falke, Li-Ying Han,
Published: 16 March 2000
Psychiatry Research, Volume 93, pp 103-110; https://doi.org/10.1016/s0165-1781(00)00104-9

Abstract:
The cognitive and functional deterioration observed in many ‘poor-outcome’ patients with schizophrenia suggests an ongoing neurodegenerative process. Diagnostic neuropathologic studies have excluded known neurodegenerative diseases as the cause of this dementia, and in a previous quantitative investigation of neurodegeneration and neural injury in this population we found no abnormalities in the cerebral cortex. However, it is possible that the deterioration observed in these patients could be due to subcortical neurodegenerative processes. Neurodegeneration and neural injury in the caudate nucleus and mediodorsal nucleus of the thalamus were investigated in a postmortem study of 11 prospectively accrued, clinically well-characterized elderly people with schizophrenia, 11 elderly control subjects with no neuropsychiatric illness, and 12 subjects with Alzheimer's disease. Traditional and immunohistochemical staining and unbiased computerized counting methods were used to quantify common markers of neurodegeneration and neural injury (neuron loss, neurofibrillary tangles, astrocytosis, microgliosis). No statistically significant differences were found between schizophrenia and control subjects for the densities of any markers. There is no evidence that abnormal neurodegeneration occurs in these two important subcortical structures.
H. Beckmann
Published: 1 January 2000
The publisher has not yet granted permission to display this abstract.
Meena Dasari, , John Jesberger, Traci A Stuve, Robert L Findling, Thomas P Swales, S.Charles Schulz
Published: 19 October 1999
Psychiatry Research: Neuroimaging, Volume 91, pp 155-162; https://doi.org/10.1016/s0925-4927(99)00028-1

Abstract:
The purpose of this study was to compare thalamic size in adolescent patients with either schizophrenia or bipolar disorder and healthy controls. T2-weighted axial magnetic resonance images were used to manually define the area of the thalamus for 20 schizophrenia patients, 15 bipolar patients and 16 normal control subjects, all of whom were adolescents. Two orthogonal planned contrasts were tested: Contrast 1, patients with schizophrenia vs. patients with bipolar disorder; and Contrast 2, both patient groups taken as a single group compared to controls. Contrast 1 was not statistically significant for right or left thalamic area. Contrast 2 was statistically significant and indicated reductions in thalamic area in the patients as compared to controls. The same pattern of results emerged after adjustment for total brain volume. Our results indicate that thalamic abnormalities reported in adult schizophrenic and bipolar patients are also observed in adolescent patients. Our findings also add to the evidence implicating the thalamus in the pathophysiology of schizophrenia and bipolar disorder.
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