P.3.c.006 Life satisfaction, psychopathology and functional level in chronic schizophrenia undergoing antipsychotic treatment

2009 ◽  
Vol 19 ◽  
pp. S514
Author(s):  
H. Jung ◽  
S. Hwang ◽  
J. Yi ◽  
Y. Kim ◽  
Y. Kim
CNS Spectrums ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 557-563 ◽  
Author(s):  
Ira D. Glick ◽  
Daisy Zamora ◽  
Danielle Kamis ◽  
John M. Davis

ObjectiveBecause ethically and practically a randomized control trial of antipsychotics will never be done, we recently conducted and reported a 8- to 50-year, naturalistic follow-up from an academic clinic of patients with chronic schizophrenia on antipsychotic medication. We found that better medication adherence was a statistically significant predictor of better long-term global outcome and life satisfaction. Because there were important limitations on our findings, we now in this communication, using similar methodology, detail outcomes for a very different sample—inner city patients with chronic schizophrenia with a long past history of antipsychotic treatment, who were enrolled in clinical trials for new medications for schizophrenia.MethodsThis is a retrospective, naturalistic, longitudinal 6- to 49-years antipsychotic treatment (mean average, 20) follow-up of a consecutive series of patients volunteering for screening for studies with schizophrenia. Lifetime data were collected on (1) their medication adherence, (2) long-term global outcome, and (3) life satisfaction. Outcomes were rated by 2 different clinicians, 1 with information on medication adherence (nonblind rater) and 1 without (blind rater). We used linear regression models adjusted for age, family support, substance use disorder, race, marital status, and number of years in treatment to estimate the association between adherence and each outcome.ResultsA total of 34 patients were assessed. Medication adherence was positively associated with the blind clinician’s rating of global outcome (P value=0.03) and the global assessment of functioning (P value=0.05). In the nonblinded clinician rating, medication adherence was unrelated to global outcome (P value=0.26) and to patients’ report of life satisfaction (P value=0.54).ConclusionThis replication study, like our previous study, is not inconsistent with the recommendation for continuous, long-term treatment for chronic schizophrenia unless medically contraindicated.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Bo Tao ◽  
Yuan Xiao ◽  
Hengyi Cao ◽  
Wenjing Zhang ◽  
Chengmin Yang ◽  
...  

Abstract Background The corpus callosum (CC) deficits have been well documented in chronic schizophrenia. However, the long-term impacts of antipsychotic monotherapies on callosal anatomy remain unclear. This cross-sectional study sought to explore micro- and macro-structural characteristics of the CC in never-treated patients and those with long-term mono-antipsychotic treatment. Methods The study included 23 clozapine-treated schizophrenia patients (CT-SCZ), 19 risperidone-treated schizophrenia patients (RT-SCZ), 23 never-treated schizophrenia patients (NT-SCZ), and 35 healthy controls (HCs). High resolution structural images and diffusion tensor imaging (DTI) data for each participant were obtained via a 3.0 T MR scanner. FreeSurfer was used to examine the volumes and fractional anisotropy (FA) values of the CC for each participant. Results There were significant deficits in the total and sub-regional CC volume and white matter integrity in NT-SCZ in comparison with healthy subjects. Compared with NT-SCZ, both CT-SCZ and RT-SCZ showed significantly increased FA values in the anterior CC region, while only RT-SCZ showed significantly increased volume in the mid-anterior CC region. Moreover, the volume of the mid-anterior CC region was significantly smaller in CT-SCZ compared to HCs. No correlations of clinical symptoms with callosal metrics were observed in schizophrenia patients. Conclusions Our findings provide insight into micro- and macro-structural characteristics of the CC in chronic schizophrenia patients with or without antipsychotics. These results suggest that the pathology itself is responsible for cerebral abnormalities in schizophrenia and that chronic exposure to antipsychotics may have an impact on white matter structure of schizophrenia patients, especially in those with risperidone treatment.


2019 ◽  
Vol 42 (4) ◽  
pp. 117-122 ◽  
Author(s):  
Chanoch Miodownik ◽  
Vladimir Lerner ◽  
Natalie Kudkaeva ◽  
Paul P. Lerner ◽  
Artashez Pashinian ◽  
...  

2016 ◽  
Vol 33 (S1) ◽  
pp. s264-s264
Author(s):  
K. Szymona ◽  
H. Karakuła-Juchnowicz ◽  
M. Flis ◽  
T. Kocki ◽  
A. Urbanska ◽  
...  

IntroductionDeficit of glutamatergic transmission and aberrant function of kynurenine pathway, with disturbed synthesis of glutamate receptors antagonist, kynurenic acid (KYNA) and neurotoxic metabolite of kynurenine, 3-hydroxykynurenine (3-OH-KYN) have been implicated in the pathogenesis of schizophrenia.ObjectivesDemonstrated by others higher level of KYNA in the brain may cause relative deficiency of glutamate-mediate transmission with resulting behavioural and cognitive changes.AimsSearch for predictors of satisfactory response to antipsychotic treatment based on the analysis of KYNA and 3-OH-KYN serum levels.MethodsFifty-three patients with chronic schizophrenia and 46 healthy individuals were enrolled in the study. Quantitative analyses of KYNA and 3-OH-KYN were performed using high-pressure liquid chromatography (HPLC) and electrochemical detection, respectively. Clinical assessments (PANSS, SANS, SAPS) and blood analyses were conducted at 3 time-points: during the active phase of disease, after 4 weeks of modified pharmacotherapy, and after reaching remission.ResultsIn schizophrenia group, lower levels of KYNA (P = 0.002) and non-altered levels of 3-OH-KYN (p = 0.195), as compared to control, were detected during active phase of disease. Despite clinical improvement, no significant changes in the level of studied metabolites were observed later on. The initial level of 3-OH-KYN correlated negatively (r = –0.368; Spearman's rank) with clinical improvement (negative symptoms) (P < 0.05).Conclusions1. The peripheral dysregulation of kynurenine pathway metabolites in chronic schizophrenia manifests as relative increase in the ratio between neurotoxic 3-OH-KYN and neuroprotective KYNA. 2. The higher serum level of 3-OH-KYN during relapse of schizophrenia seems to predict poor response to antipsychotic treatment.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2021 ◽  
Author(s):  
Haidong Yang ◽  
Wen Pan ◽  
Wenhuan Xiao ◽  
Man Yang ◽  
Jianchun Xu ◽  
...  

Abstract Background: Neuregulin1 (NRG1) plays a role in neuronal migration, regulation of synaptic plasticity, and neural survival, and has been considered to be among the candidate genes for schizophrenia. This study focused on the variations in serum NRG1b1 levels following antipsychotic treatment and the relationship between NRG1b1 level and improvements in psychotic symptoms in first-episode drug-naïve (FEDN) patients and chronic schizophrenia.Methods: A total of 100 patients with schizophrenia were recruited and compared with 79 matched healthy controls. All patients had been drug-naïve for at least four weeks. Serum NRG1b1 levels and positive and negative syndrome scale (PANSS) scores were measured at the baseline and after four weeks. Serum NRG1b1 levels were measured using sandwich enzyme-linked immunosorbent assays (ELISA).Results: Baseline NRG1b1 levels were significantly lower in the patients with schizophrenia compared with the healthy controls. NRG1b1 levels increased significantly following antipsychotic treatment. NRG1b1 levels gradually increased with declining PANSS scores and its three subscales during antipsychotic therapy. The levels of NRG1b1 increased significantly in responders after four weeks of treatment, although non-responders showed no such effect. Correlation analyses showed that the levels of NRG1b1 were negatively correlated with the duration of illness and positively correlated with improvement in symptoms.Conclusion: The levels of serum NRG1b1 and the therapeutic effects gradually increased following treatment, indicating that NRG1b1 may be an indicator of therapy, and that it may also be associated with the pathophysiological mechanism causing schizophrenia, although this possible pathway requires further investigation. Antipsychotic drugs increase Neuregulin1b1 serum levels in first-episode drug-naïve patients and chronic schizophrenia with suggestions for improving the treatment of psychotic symptoms


2020 ◽  
Vol 34 (5) ◽  
pp. 540-547
Author(s):  
Masayuki Takase ◽  
Hisoshi Kimura ◽  
Nobuhisa Kanahara ◽  
Yusuke Nakata ◽  
Masaomi Iyo

Background: Patients with first-episode psychosis respond well to initial antipsychotic treatment, but among patients experiencing a relapse of psychosis, the response rate falls to approximately 30%. The mechanism of this discrepancy has not been clarified, but the development of dopamine supersensitivity psychosis with the underlying up-regulation of post-synaptic dopamine D2 receptors could be involved in this lesser response. It is uncertain whether elevated dopamine synthesis and release occurs in patients with dopamine supersensitivity psychosis, in contrast to those with first-episode psychosis. Patients and methods: We examined a first-episode psychosis group ( n=6) and a chronic schizophrenia group, i.e. patients experiencing relapse ( n=23) including those who relapsed due to dopamine supersensitivity psychosis ( n=18). Following the initiation of treatment, we measured the patients’ blood concentrations of homovanillic acid and 3-methoxy-4-hydroxyphenylglycol at two weeks and four weeks after the baseline measurements. Results: The first-episode psychosis group tended to show decreased homovanillic acid, accompanied by an improvement of symptoms. The chronic schizophrenia group showed no alteration of homovanillic acid or 3-methoxy-4-hydroxyphenylglycol over the treatment period. These results were the same in the dopamine supersensitivity psychosis patients alone. Conclusions: Our findings suggest that unlike first-episode psychosis, the release of dopamine from presynaptic neurons did not increase in relapse episodes in the patients with dopamine supersensitivity psychosis. This indirectly indicates that the development of supersensitivity of post-synapse dopamine D2 receptor is involved in relapse in dopamine supersensitivity psychosis patients.


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