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(searched for: doi:10.1016/0006-3223(91)90002-4)
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Jin-Hui Wang
Published: 11 September 2019
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Christian S Legind, Brian V Broberg, Rachel Brouwer, René C W Mandl, Bjørn H Ebdrup, Simon J Anhøj, Maria H Jensen, Rikke Hilker, Birgitte Fagerlund, , et al.
Schizophrenia Bulletin, Volume 45, pp 1231-1241; https://doi.org/10.1093/schbul/sbz007

Abstract:
Whether aberrant cerebral blood flow (CBF) in schizophrenia is affected by genetic influences, and consequently a potential marker for genetic susceptibility, is unknown. Our aims were to determine the heritability of CBF in thalamic, frontal, and striatal areas, and to ascertain if associations with disease were under genetic influence. Monozygotic (MZ) twin pairs concordant (n = 2) or discordant (n = 20) for schizophrenia spectrum disorders (ICD-10 F2x.x), matched on sex and age with dizygotic (DZ; n = 20) and healthy control pairs (MZ: n = 27; DZ: n = 18; total: n = 181 individuals), were recruited via the National Danish Twin Register. CBF in thalamus, frontal lobes, and putamen was measured with pseudo-continuous arterial spin labeling on a 3 T magnetic resonance scanner. Twin statistics were performed with structural equation modeling. CBF in the frontal lobes was heritable (h2 = 0.44, 95% CI [0.22–0.60]) but not correlated to disease. CBF correlated to schizophrenia spectrum disorders in the left thalamus (r = 0.17, [0.03–0.31]; P = 0.02), as well as in the left putamen (r = 0.19, [0.05–0.32]; P = 0.007) and the right putamen (r = 0.18, [0.03–0.32]; P = 0.02). When restricting the sample to schizophrenia (F20.x) only, shared genetic influences between CBF in the left putamen and schizophrenia liability (phenotypic correlation = 0.44, [0.28–0.58], P < 0.001) were found. Our results provide heritability estimates of CBF in the frontal lobes, and we find CBF in thalamus and putamen to be altered in schizophrenia spectrum disorders. Furthermore, shared genetic factors influence schizophrenia liability and striatal perfusion. Specifically, higher perfusion in the left putamen may constitute a marker of genetic susceptibility for schizophrenia.
Topics in Magnetic Resonance Imaging, Volume 19, pp 111-130; https://doi.org/10.1097/rmr.0b013e3181808140

Abstract:
Cerebral perfusion imaging using magnetic resonance imaging (MRI) is widely used in the research and clinical fields to assess the profound changes in blood flow related to ischemic events such as acute stroke, chronic steno-occlusive disease, vasospasm, and abnormal vessel formations from congenital conditions or tumoral neovascularity. With continuing improvements in the precision of MRI-based perfusion techniques, it is increasingly feasible to use this tool in the study of the subtle brain perfusion changes occurring in psychiatric illnesses. This article aims to review the existing literature on applications of perfusion MRI in psychiatric disorder and substance abuse research. The article also provides a brief introductory overview of dynamic susceptibility contrast MRI and arterial spin labeling techniques. An outlook of necessary steps to bring perfusion MRI into the realm of clinical psychiatry as a diagnostic tool is brought forth. Opportunities for research in unexplored disorders and with higher field strengths are briefly examined.PubMed, ISI Web of Knowledge & Scopus were used to search the literature and cross reference several neuropsychiatric disorders with a search term construct, including "magnetic resonance imaging," "dynamic susceptibility contrast," "arterial spin labeling," perfusion or "cerebral blood flow" or "cerebral blood volume" or "mean transit time." The list of disorders used in the search included schizophrenia, depression and bipolar disorder, dementia and Alzheimer's disease, Parkinson's disease, posttraumatic stress disorder, autism, Asperger disease, attention deficit, Tourette syndrome, obsessive-compulsive disorder, Huntington's disease, bulimia nervosa, anorexia nervosa, and substance abuse. For each disorder for which perfusion MRI studies were found, a brief overview of the disorder symptoms, treatment, prevalence, and existing models is provided, and previous findings from nuclear medicine-based perfusion imaging are overviewed. Findings of perfusion MRI studies are then summarized, and overlap of findings are discussed. Overarching conclusions are made, or an outlook for future work in the area is offered, where appropriate.Despite the now fairly broad availability of perfusion MRI, only a limited number of studies were found using this technology. The search produced 13 studies of schizophrenia, 7 studies in major depression, 12 studies in Alzheimer's disease, and 2 studies in Parkinson's disease. Drug abuse and other disorders have mainly been studied with nuclear medicine-based perfusion imaging. The literature concerning the use of perfusion imaging in psychiatry has not been reviewed in the last 5 years or more. The use of MRI for perfusion measurements in psychiatry has not been reviewed in 10 years.Although MRI-based perfusion imaging in psychiatry has mainly been used as a research tool, a path is progressively being cleared for its application in clinical diagnostic and treatment monitoring. The precision of perfusion MRI methods now rivals that of nuclear medicine-based perfusion imaging techniques. Because of their noninvasive nature, arterial spin labeling methods have gained popularity in studies of neuropsychiatric disorders such as schizophrenia, depression, Alzheimer's, and Parkinson's diseases. Perfusion imaging measurements have yet to be included within the diagnostic criteria of neuropsychiatric disorders despite having shown to have great discriminant power in specific disorders. As this young methodology continues to improve and research studies demonstrate the correlation of measured perfusion abnormalities to microcirculatory abnormalities and neuropsychiatric symptomatology, the idea of including such a test within diagnostic criteria for certain mental illnesses becomes increasingly plausible.
Published: 1 December 2007
Neuropathology, Volume 27, pp 604-608; https://doi.org/10.1111/j.1440-1789.2007.00798.x

Abstract:
The neuropathology of schizophrenia remains obscure despite the fact that many neuropathologists have investigated this area for over 100 years. While remarkable progress has been made in the neuropathological study of neurodegenerative diseases including Alzheimer's disease, progress in studying the neuropathological entity of schizophrenia has not kept pace; the phrase "schizophrenia is the graveyard of neuropathologists" has been stated in the field. Since the 1980s, the morphological or functional abnormalities in the brains of schizophrenia patients have been reported by means of CT or MRI and with advanced functional brain image technology such as positron emission tomography or single photon emission computed tomography. Results from such imaging studies have led to neuropathological examination of the post mortem brains of schizophrenia patients being undertaken again. These neuroimaging studies have influenced the neuropathological investigation of the schizophrenic brain. Not only the classical microscopic observation of neuropathology, but also measurement and statistical analysis using computer imaging software or using immunohistological techniques has been performed. Based on the neuropathological studies of schizophrenia over the last 20 years, it is clear that schizophrenia is not a pure functional disease without organic factors. Reports of neuropathological abnormalities in the post mortem schizophrenic brain indicated they were found in almost all areas of the brain, but there are more reports describing the temporal lobe and frontal lobe compared to those describing other areas of the brain. These observed neuropathological abnormalities are explained rationally by the hypothesis of a neurodevelopmental disorder in this disease. In recent molecular biology studies, several putative candidate genes were reported, and some of these genes might have the function of neurodevelopment or making neuronal networks. It is important to consider together these findings with morphometric studies in neuropathological observation, neuroimaging studies and genome studies to pursue the etiology of schizophrenia from various perspectives.
, , Takami Yagyu, Sachi Morita, , , Masafumi Yoshimura, Gaku Okugawa, Kenji Nobuhara, Toshihiko Kinoshita
Published: 1 January 2006
Neuropsychobiology, Volume 54, pp 134-139; https://doi.org/10.1159/000098264

Abstract:
To explore brain functions in schizophrenic patients, the global analytic strategy of multichannel EEG was performed that combines measures of global complexity (Ω), total power (Σ) and generalized frequency (Φ), and EEG microstate analysis was applied to multichannel EEG data for 24 nonmedicated patients and 24 healthy subjects. The patients had higher Ω and Σ values, and lower Φ values compared with healthy subjects. Three topographical classes were obtained from all EEG data by EEG microstate analysis. The mean duration of one topographical class in the patients was shortened compared to healthy subjects. These results indicated looser cooperativity, or decreased connectivity of the active brain process and deviant brain information processing in schizophrenic patients.
, D. R. Weinberger
Published: 1 January 2001
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A. Heinz, D. R. Weinberger
Published: 1 January 2000
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Annett Höse, H.-P. Volz,
Published: 1 January 2000
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Noriomi Kuroki, Masaaki Matsushita
Published: 1 June 1998
Neuropathology, Volume 18, pp 235-241; https://doi.org/10.1111/j.1440-1789.1998.tb00106.x

The publisher has not yet granted permission to display this abstract.
Daniel T. Mattson, , Marilyn D. Lucas
The Journal of Genetic Psychology, Volume 158, pp 487-494; https://doi.org/10.1080/00221329709596685

Abstract:
The symptoms of schizophrenia are frequently divided into positive and negative subtypes. It has been suggested that the negative symptoms are similar to those seen with prefrontal lobe cortical dysfunction. Several neuropsychological investigations of that hypothesis have been carried out, but none have directly compared a negative symptom group with a positive symptom group on the same test battery. In the present study, the Positive and Negative Syndrome Scale (PANSS; Kay, Fiszbein, & Opler, 1987) was used to distinguish two groups of 20 patients with schizophrenia with predominant positive or negative symptoms. A battery of 7 neuropsychological tests considered capable of isolating prefrontal lobe dysfunction was administered. A significant group difference was noted on 6 of the tests; the negative symptom group performed much worse than the positive symptom group. The results of this study support the hypothesis that a relationship exists between the negative symptoms of schizophrenia and prefrontal lobe dysfunction.
Jerry J. Sweet, Cynthia Westergaard
Published: 1 January 1997
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Jair C. Soares, J. John Mann
Published: 1 January 1997
Biological Psychiatry, Volume 41, pp 86-106; https://doi.org/10.1016/s0006-3223(96)00006-6

Abstract:
The structural neuroimaging findings in mood disorders were reviewed, to evaluate evidence for a neuroanatomic model of pathophysiology, involving the prefrontal cortex, the basal ganglia, the amygdala-hippocampus complex, thalamus, and connections among these structures. Global atrophy is not consistently found. The best replicated finding is an increased rate of white matter and periventricular hyperintensities. A smaller frontal lobe, cerebellum, caudate, and putamen appear present in unipolar depression. A larger third ventricle, and smaller cerebellum and perhaps temporal lobe appear present in bipolar disorder. These localized structural changes involve regions that may be critical in the pathogenesis of mood disorders. Generalized and localized anatomic alterations may be related to age or vascular disease. The clinical and biological correlates of these changes need to be investigated to allow development of a more complete model of pathophysiology of mood disorders.
Laura Marsh, John Lauriello, Edith V. Sullivan, Adolf Pfefferbaum
Published: 1 January 1996
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Ralph E. Hoffman, Jill Rapaport, Rezvan Ameli, Thomas H. McGlashan, Diane Harcherik, David Servan-Schreiber
Journal of Cognitive Neuroscience, Volume 7, pp 479-496; https://doi.org/10.1162/jocn.1995.7.4.479

Abstract:
The mechanism of hallucinated speech, a symptom commonly reported by schizophrenic patients, is unknown. The hypothesis that these hallucinations arise from pathologically altered working memory underlying speech perception was explored. A neural network computer simulation of contextually guided sequential word detection based on Elman (1990a,b) was studied. Pruning anatomic connections or reducing neuronal activation in working memory caused word “percepts” to emerge spontaneously (i.e., in the absence of external “speech inputs”), thereby providing a model of hallucinated speech. These simulations also demonstrated distinct patterns of word detection impairments when inputs were accompanied by varying levels of noise. In a parallel human study, the ability to shadow noisecontaminated, connected speech was assessed. Schizophrenic patients reporting hallucinated speech demonstrated a pattern of speech perception impairments similar to a simulated neural network with reduced anatomic connectivity and enhanced neuronal activation. Schizophrenic patients not reporting this symptom did not demonstrate these speech perception impairments. Neural network simulations and human empirical data, when considered together, suggested that the primary cause of hallucinated “voices” in schizophrenia is reduced neuroanatomic connectivity in verbal working memory.
Denis Lacroix, Yves Chaput, Jean-Pierre Rodriguez, Michel Filion, Denis Morrison, Pierre St-Denis, Jean-Marie Albert
Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 19, pp 861-876; https://doi.org/10.1016/0278-5846(95)00116-d

Abstract:
1. The authors conducted a retrospective exploratory computerized EEG study on the effect of clozapine in treatment-refractory schizophrenics, 10 high-responders (HRs) and 10 low-responders (LRs), in an attempt to correlate amplitude but especially coherence changes with a positive clinical response to clozapine. 2. EEGs with eyes closed were obtained before and during a clozapine treatment. Both groups had a similar drug profile with regards to non-clozapine medication. Probability maps were computed to illustrate changes of amplitude and coherence (for all combinations of paired electrodes) for 4 frequency bands (theta, alpha, beta 1 and 2). 3. The effect on AMPLITUDE was a generalized increase in lower bands and a decrease in anterior regions in higher bands of both HRs and LRs. Considerable changes of COHERENCE were observed on a wide set of paired electrodes in most frequency bands with some electrodes involved in HRs but uninvolved or differently involved in LRs suggesting differences in selected brain regions. 4. Changes of coherence but not amplitude were correlated with changes on the BPRS, thus to clinical improvement, and concerned mostly the right anterior-medial temporal (T4) and central (C4) electrodes paired with prefrontal electrodes, left central (C3), temporal (T3) and parietal (P3) electrodes in the theta band. 5. Clozapine has both generalized and regional effects as can be suspected considering its effect on many subtypes of brain receptors. A brain dysfunction centralized on the right anterior-medial temporal region may characterize treatment-refractory schizophrenics.
, Yn-Ho Huang, Lin-Sung Chang, Yu-Chih Yang, Cho-Boon Sim
Published: 29 June 1995
Psychiatry Research, Volume 57, pp 65-73; https://doi.org/10.1016/0165-1781(95)02496-j

Abstract:
The 2-deoxyglucose (2-DG) method was used to study regional metabolic changes in rats following chronic d-amphetamine treatment without subsequent challenges. Four groups of rats were pretreated (intraperitoneal administration) with d-amphetamine (0, 1, 5, or 10 mg/kg) once per day for 14 days. After a 7-day abstinence period without further challenge, the 2-DG method was used to measure the rates of local cerebral glucose utilization (LCGU). Significant metabolic changes among the four groups were found in five brain regions, including the nucleus accumbens and the lateral habenular nucleus. Another four groups of rats with the same pretreatment regimens, challenged with 5 mg/kg d-amphetamine, were used for behavioral testing. The results showed intense stereotyped behaviors in the 5 mg/kg and the 10 mg/kg groups. In the steady state, however, there were no significant glucose utilization changes in the nigrostriatal system, which is thought to be related to stereotyped behaviors. During steady state, metabolic changes were found in a limited number of brain regions. No difference in LCGU was found in the sensitization-related regions. Further challenges with stimulants may be necessary to investigate the metabolic responses after sensitization.
R. McClure, M. Keshavan, N. J. Minshew, K. Panchalingam, J. W. Pettegrew
Published: 1 January 1995
The publisher has not yet granted permission to display this abstract.
Matcheri S. Keshavan, Stewart Anderson, Jay W. Pettergrew
Published: 30 June 1994
Journal of Psychiatric Research, Volume 28, pp 239-265; https://doi.org/10.1016/0022-3956(94)90009-4

Abstract:
Several lines of evidence support the notion that a substantial reorganization of cortical connections, involving a programmed synaptic pruning, takes place during adolescence in humans. A review of neurobiological abnormalities in schizophrenia indicates that the neurobiological parameters that undergo peripubertal regressive changes may be abnormal in this disorder. An excessive pruning of the prefrontal corticocortical, and corticosubcortical synapses, perhaps involving the excitatory glutamatergic inputs to pyramidal neurons, may underlie schizophrenia. A reciprocal failure of pruning in certain subcortical structures, such as lenticular nuclei, may also occur. Several developmental trajectories, related to early brain insults as well as genetic factors affecting postnatal neurodevelopment, could lead to the illness. These models would have heuristic value and may be consistent with several known facts of the schizophrenic illness, such as its onset in adolescence and the gender differences in its onset and natural course. The relationship between these models and other etiological models of schizophrenia are summarized and approaches to test relevant hypotheses are discussed.
Felix Strumwasser
Journal of the Experimental Analysis of Behavior, Volume 61, pp 307-317; https://doi.org/10.1901/jeab.1994.61-307

Abstract:
Neuroscience seeks to understand how the human brain, perhaps the most complex electrochemical machine in the universe, works, in terms of molecules, membranes, cells and cell assemblies, development, plasticity, learning, memory, cognition, and behavior. The human behavioral sciences, in particular psychiatry and clinical psychology, deal with disorders of human behavior and mentation. The gap between neuroscience and the human behavioral sciences is still large. However, some major advances in neuroscience over the last two decades have diminished the span. This article reviews the major advances of neuroscience in six areas with relevance to the behavioral sciences: (a) evolution of the nervous system; (b) visualizing activity in the human brain; (c) plasticity of the cerebral cortex; (d) receptors, ion channels, and second/third messengers; (e) molecular genetic approaches; and (f) understanding integrative systems with networks and circadian clocks as examples.
Minda R. Lynch
Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 16, pp 797-832; https://doi.org/10.1016/0278-5846(92)90102-k

Abstract:
Negative symptoms have been associated with structural impairment in the PFC, and hypothesized to arise from a central hypodopaminergic substrate. Corticofugal PFC neurons, which are inhibited by VTA DA innervation, exert a tonic excitatory modulation on DA activity in the NAS. Lesions of ascending DA forebrain projections "uncouple" the functional link between D1 and D2 receptors, permitting independent activation of D1 sites in generating behavioral output. A previously identified absence of this D1/D2 link in schizophrenic brain suggests that functional activation of PFC D1 receptors may induce hyperinhibition of descending corticofugal efferents to the NAS. Consequent hypoactivity of DA in the NAS is proposed to give rise to negative symptoms of schizophrenia, and low dose DA agonist treatments may mimic behavioral features of this symptom profile via direct PFC D1 stimulation. It follows that clozapine's efficacy for negative symptoms may be attributable, in part, to blockade of PFC D1 receptors, with subsequent enhancement of glutamate-facilitated NAS DA activity.
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