Electrophysiology of the prefrontal cortex in healthy controls and schizophrenic patients: a review

2001 ◽  
Vol 108 (6) ◽  
pp. 679-694 ◽  
Author(s):  
A. J. Fallgatter
2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Xiaoxiao Shan ◽  
Rongyuan Liao ◽  
Yangpan Ou ◽  
Yudan Ding ◽  
Feng Liu ◽  
...  

Background. Previous studies have revealed the abnormalities in homotopic connectivity in schizophrenia. However, the relationship of these deficits to antipsychotic treatment in schizophrenia remains unclear. This study explored the effects of antipsychotic therapy on brain homotopic connectivity and whether the homotopic connectivity of these regions might predict individual treatment response in schizophrenic patients. Methods. A total of 21 schizophrenic patients and 20 healthy controls were scanned by the resting-state functional magnetic resonance imaging. The patients received olanzapine treatment and were scanned at two time points. Voxel-mirrored homotopic connectivity (VMHC) and pattern classification techniques were applied to analyze the imaging data. Results. Schizophrenic patients presented significantly decreased VMHC in the temporal and inferior frontal gyri, medial prefrontal cortex (MPFC), and motor and low-level sensory processing regions (including the fusiform gyrus and cerebellum lobule VI) relative to healthy controls. The VMHC in the superior/middle MPFC was significantly increased in the patients after eight weeks of treatment. Support vector regression (SVR) analyses revealed that VMHC in the superior/middle MPFC at baseline can predict the symptomatic improvement of the positive and negative syndrome scale after eight weeks of treatment. Conclusions. This study demonstrated that olanzapine treatment may normalize decreased homotopic connectivity in the superior/middle MPFC in schizophrenic patients. The VMHC in the superior/middle MPFC may predict individual response for antipsychotic therapy. The findings of this study conduce to the comprehension of the therapy effects of antipsychotic medications on homotopic connectivity in schizophrenia.


2011 ◽  
Vol 26 (S2) ◽  
pp. 942-942
Author(s):  
R. Martínez de Velasco Soriano ◽  
F. Pando Velasco ◽  
M. Serrano Díaz de Otálora ◽  
J. Gómez-Arnau Ramírez ◽  
C. Riaza Bermudo-Soriano

IntroductionN-acetil-aspartate (NAA) is located inside the soma and dendrites. Its believed to be an indirect indicator of the metabolic activity of these cells. Phosphomonoesters (PME) are involved in synthesis of neuronal membranes and phosphodiesters (PDE) in its degradation. Glutamine, an aminoacid produced by glial cells, is transported into the neurone for its transformation into glutamate and gamma aminobutyric acid.MethodsReview clinical trials performed on schizophrenic patients with SF-MRI, with 31P y 1H, to measure concentration of NAA, PME, PDE and glutamine.ObjectivesDetecting chemichal alterations that could be used as indicators in schizophrenia.ResultsNAA concentration in temporal and frontal cortex of schizophrenic patients, are significantly lower than in healthy controls. In other trials, differences in NAA concentration (measured in prefrontal cortex) have not been found, comparing patients during their first psychotic episode and healthy controls. Lowered concentrations of PME and increased ones of PDE in prefrontal cortex of schizophrenic patients have been found. Glutamine levels are increased in schizophrenic patients, being directely correlated with the duration of the process. These levels are reduced when antipsychotic drugs are used.ConclusionsThe decrease on NAA levels at schizophrenia onset and on healthy relatives remark its value as an endophenotypical indicator, but not as an illness indicator. Changes on PME and PDE concentrations cannot be used as illness indicators. The increase on glutamine synthesis could be due to glutamatergic hypofunction in schizophrenic patients, but there are other factors that may cause it, so it cannot be used as an indicator.


2014 ◽  
Vol 24 (6) ◽  
pp. 283-284
Author(s):  
Afke F. Terwisscha van Scheltinga ◽  
Steven C. Bakker ◽  
Neeltje E.M. van Haren ◽  
Heleen B.M. Boos ◽  
Hugo G. Schnack ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
Pingping Guo ◽  
Siyuan Lang ◽  
Muliang Jiang ◽  
Yifeng Wang ◽  
Zisan Zeng ◽  
...  

Background: Brain functional alterations have been observed in children with congenital sensorineural hearing loss (CSNHL). The purpose of this study was to assess the alterations of regional homogeneity in children with CSNHL.Methods: Forty-five children with CSNHL and 20 healthy controls were enrolled into this study. Brain resting-state functional MRI (rs-fMRI) for regional homogeneity including the Kendall coefficient consistency (KCC-ReHo) and the coherence-based parameter (Cohe-ReHo) was analyzed and compared between the two groups, i.e., the CSNHL group and the healthy control group.Results: Compared to the healthy controls, children with CSNHL showed increased Cohe-ReHo values in left calcarine and decreased values in bilateral ventrolateral prefrontal cortex (VLPFC) and right dorsolateral prefrontal cortex (DLPFC). Children with CSNHL also had increased KCC-ReHo values in the left calcarine, cuneus, precentral gyrus, and right superior parietal lobule (SPL) and decreased values in the left VLPFC and right DLPFC. Correlations were detected between the ReHo values and age of the children with CSNHL. There were positive correlations between ReHo values in the pre-cuneus/pre-frontal cortex and age (p < 0.05). There were negative correlations between ReHo values in bilateral temporal lobes, fusiform gyrus, parahippocampal gyrus and precentral gyrus, and age (p < 0.05).Conclusion: Children with CSNHL had RoHo alterations in the auditory, visual, motor, and other related brain cortices as compared to the healthy controls with normal hearing. There were significant correlations between ReHo values and age in brain regions involved in information integration and processing. Our study showed promising data using rs-fMRI ReHo parameters to assess brain functional alterations in children with CSNHL.


Lupus ◽  
2019 ◽  
Vol 28 (14) ◽  
pp. 1678-1689 ◽  
Author(s):  
E Papadaki ◽  
E Kavroulakis ◽  
G Bertsias ◽  
A Fanouriakis ◽  
D Karageorgou ◽  
...  

The study examined the hypothesis that hypoperfusion in brain areas known to be involved in emotional disturbances in primary psychiatric disorders is also linked to emotional difficulties in systemic lupus erythematosus (SLE) and that these are not secondary to the physical and social burden incurred by the disease. Nineteen SLE patients without overt neuropsychiatric manifestations (non-NPSLE), 31 NPSLE patients, and 23 healthy controls were examined. Dynamic susceptibility contrast MRI was used and cerebral blood flow and cerebral blood volume values were estimated in six manually selected regions of interest of brain regions suspected to play a role in anxiety and depression (dorsolateral prefrontal cortex, ventromedial prefrontal cortex, anterior cingulate cortex, hippocampi, caudate nuclei and putamen). NPSLE patients reported high rates of anxiety and depression symptomatology. Significantly reduced cerebral blood flow and cerebral blood volume values were detected in the NPSLE group compared to healthy controls in the dorsolateral prefrontal cortex and ventromedial prefrontal cortex, bilaterally. Within the NPSLE group, anxiety symptomatology was significantly associated with lower perfusion in frontostriatal regions and in the right anterior cingulate gyrus. Importantly, the latter associations appeared to be specific to anxiety symptoms, as they persisted after controlling for depression symptomatology and independent of the presence of visible lesions on conventional MRI. In conclusion, hypoperfusion in specific limbic and frontostriatal regions is associated with more severe anxiety symptoms in the context of widespread haemodynamic disturbances in NPSLE.


Epigenomics ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 251-265 ◽  
Author(s):  
Beatriz Garcia-Ruiz ◽  
Lorena Moreno ◽  
Gerard Muntané ◽  
Vanessa Sánchez-Gistau ◽  
Alfonso Gutiérrez-Zotes ◽  
...  

Aim: To investigate DDR1 methylation in blood and brain DNA in psychosis and its relationship with stress markers. Materials & methods: Saliva cortisol, blood neutrophil and lymphocyte counts, leukocyte DNA and psychological variables were collected from 60 patients with nonaffective psychosis and 40 healthy controls (HC). Brain dorsolateral prefrontal cortex DNA from 35 patients with schizophrenia and 34 HC was studied. DDR1 methylation at 43 CpG sites was measured using the MassARRAY EpiTYPER platform. Results: We describe leukocyte DDR1 hypermethylation in patients with psychosis compared with HC; this hypermethylation is associated with psychological stress, neutrophil-to-lymphocyte ratios, and, in the dorsolateral prefrontal cortex, DDR1 methylation correlated with DDR1 isoform expression. Conclusion: We confirmed a relationship between stress and blood and brain DDR1 methylation in psychosis.


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