Predictors for early‐onset psychotic symptoms in patients newly diagnosed with Parkinson's disease without psychosis at baseline: A 5‐year cohort study
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SUBMITTER: Chen J
PROVIDER: S-EPMC10909617 | biostudies-literature | 2024 Mar
REPOSITORIES: biostudies-literature
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Project description:ObjectiveEpidemiological studies suggest that patients with attention-deficit/hyperactivity disorder (ADHD) treated with amphetamines have an increased risk of newly diagnosed psychosis. This risk in youth is poorly understood. This investigation studied the potential risk of newly diagnosed psychotic symptoms associated with exposure to 4 classes of ADHD medications.MethodThis retrospective study used a medical records-linkage system from a cohort of youth (age 6-18 years) with diagnosed ADHD who were prescribed amphetamines, methylphenidate, atomoxetine, or α-2 agonists. Cohort members with any diagnosis of psychosis before their first ADHD medication were excluded. The primary outcome was newly diagnosed psychotic symptoms. The risk for psychotic symptoms for each medication (vs the remaining medication classes combined) was estimated using a multivariable time-varying covariate Cox proportional hazard regression model that adjusted for sex and age at ADHD diagnosis.ResultsOf 5,171 youth (68.6% male), 134 (2.6 %) had newly diagnosed psychotic symptoms. Exposure to amphetamine (vs amphetamine nonexposure, hazard ratio 1.41, 95% CI 1.15-2.26) and atomoxetine (vs atomoxetine nonexposure, hazard ratio 2.01, 95% CI 1.38-2.92) was associated with increased risk of newly diagnosed psychotic symptoms. Secondary analysis showed that the frequency of newly diagnosed psychotic symptoms was higher with atomoxetine/stimulant lifetime combination therapy (12.5% with amphetamines, 7.7% with methylphenidate) than atomoxetine monotherapy (1.2%).ConclusionRisk of newly diagnosed psychotic symptoms was low. These results suggest that cumulative exposure to amphetamines or atomoxetine/stimulant lifetime combination therapy may be associated with an increased risk of newly diagnosed psychotic symptoms in youth with ADHD.Diversity & inclusion statementWe worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way. We worked to ensure sex and gender balance in the recruitment of human participants. One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented racial and/or ethnic groups in science. One or more of the authors of this paper received support from a program designed to increase minority representation in science. We actively worked to promote sex and gender balance in our author group. We actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our author group. While citing references scientifically relevant for this work, we also actively worked to promote sex and gender balance in our reference list. While citing references scientifically relevant for this work, we also actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our reference list. The author list of this paper includes contributors from the location and/or community where the research was conducted who participated in the data collection, design, analysis, and/or interpretation of the work.
| S-EPMC11562438 | biostudies-literature
Project description:Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. Determining structural imaging biomarkers associated with prodromal Parkinson's disease dementia may allow for the earlier identification of those at risk, and allow for targeted disease modifying therapies. One hundred and five non-demented subjects with newly diagnosed idiopathic Parkinson's disease and 37 healthy matched controls had serial 3 T structural magnetic resonance imaging scans with clinical and neuropsychological assessments at baseline, which were repeated after 18 months. The Movement Disorder Society Task Force criteria were used to classify the Parkinson's disease subjects into Parkinson's disease with mild cognitive impairment (n = 39) and Parkinson's disease with no cognitive impairment (n = 66). Freesurfer image processing software was used to measure cortical thickness and subcortical volumes at baseline and follow-up. We compared regional percentage change of cortical thinning and subcortical atrophy over 18 months. At baseline, cases with Parkinson's disease with mild cognitive impairment demonstrated widespread cortical thinning relative to controls and atrophy of the nucleus accumbens compared to both controls and subjects with Parkinson's disease with no cognitive impairment. Regional cortical thickness at baseline was correlated with global cognition in the combined Parkinson's disease cohort. Over 18 months, patients with Parkinson's disease with mild cognitive impairment demonstrated more severe cortical thinning in frontal and temporo-parietal cortices, including hippocampal atrophy, relative to those with Parkinson's disease and no cognitive impairment and healthy controls, whereas subjects with Parkinson's disease and no cognitive impairment showed more severe frontal cortical thinning compared to healthy controls. At baseline, Parkinson's disease with no cognitive impairment converters showed bilateral temporal cortex thinning relative to the Parkinson's disease with no cognitive impairment stable subjects. Although loss of both cortical and subcortical volume occurs in non-demented Parkinson's disease, our longitudinal analyses revealed that Parkinson's disease with mild cognitive impairment shows more extensive atrophy and greater percentage of cortical thinning compared to Parkinson's disease with no cognitive impairment. In particular, an extension of cortical thinning in the temporo-parietal regions in addition to frontal atrophy could be a biomarker in therapeutic studies of mild cognitive impairment in Parkinson's disease for progression towards dementia.
| S-EPMC4671477 | biostudies-literature
Project description:ObjectiveCurrent research does not provide a clear explanation for why some patients with Parkinson's Disease (PD) develop psychotic symptoms. The 'aberrant salience hypothesis' of psychosis has been influential and proposes that dopaminergic dysregulation leads to inappropriate attribution of salience to irrelevant/non-informative stimuli, facilitating the formation of hallucinations and delusions. The aim of this study is to investigate whether non-motivational salience is altered in PD patients and possibly linked to the development of psychotic symptoms.MethodsWe investigated salience processing in 14 PD patients with psychotic symptoms, 23 PD patients without psychotic symptoms and 19 healthy controls. All patients were on dopaminergic medication for their PD. We examined emotional salience using a visual oddball fMRI paradigm that has been used to investigate early stages of schizophrenia spectrum psychosis, controlling for resting cerebral blood flow as assessed with arterial spin labelling fMRI.ResultsWe found significant differences between patient groups in brain responses to emotional salience. PD patients with psychotic symptoms had enhanced brain responses in the striatum, dopaminergic midbrain, hippocampus and amygdala compared to patients without psychotic symptoms. PD patients with psychotic symptoms showed significant correlations between the levels of dopaminergic drugs they were taking and BOLD signalling, as well as psychotic symptom scores.ConclusionOur study suggests that enhanced signalling in the striatum, dopaminergic midbrain, the hippocampus and amygdala is associated with the development of psychotic symptoms in PD, in line with that proposed in the 'aberrant salience hypothesis' of psychosis in schizophrenia.
| S-EPMC7298672 | biostudies-literature
Project description:Background: Subjective cognitive complaints (SCCs) and mild cognitive impairment (MCI) are common among patients with Parkinson's disease (PD). However, the relationship between SCCs and MCI is not well understood. Herein, we aimed to investigate whether there are any differences in the prevalence and risk factors of SCCs between early PD patients with and without MCI. Methods: Overall, 108 newly diagnosed, untreated PD patients underwent comprehensive neuropsychological assessments. PD patients with mild cognitive impairment (PD-MCI) were diagnosed according to the MCI level II criteria. Furthermore, SCCs were measured with the Cognitive Complaints Interview (CCI). Logistic regression analysis, after adjusting for confounding variable, was performed in order to investigate risk factors of SCCs in PD-MCI patients and PD patients with normal cognition (PD-NC). Results: Furthermore, 42 (42.3%) participants reported SCCs and 53 (53.5%) participants were diagnosed with PD-MCI. The prevalence of SCCs in PD-MCI and PD-NC participants was 30.3% and 12.1%, respectively. Logistic regression analyses revealed that the presence of SCCs in PD-MCI group was significantly associated with Non-Motor Symptoms Questionnaire (NMSQ) score (OR = 1.340, 95%CI = 1.115-1.610, p = 0.002), while the presence of SCCs in PD-NC group was significantly associated with time of Stroop Color-Word Test card C (OR = 1.050, 95%CI = 1.009-1.119, p = 0.016). Conclusion: SCCs are frequent among patients with early PD. The prevalence and risk factor of SCCs are distinct in PD with and without MCI. These findings suggest that SCCs in early PD with different cognitive status appear to have different pathogenicity.
| S-EPMC8651703 | biostudies-literature
Project description:Several recent publications described algorithms to identify subjects with Parkinson's disease (PD). In creating the "PREDIGT Score", we previously developed a hypothesis-driven, simple-to-use formula to potentially calculate the incidence of PD. Here, we tested its performance in the 'De Novo Parkinson Study' (DeNoPa) and 'Parkinson's Progression Marker Initiative' (PPMI); the latter included participants from the 'FOllow Up persons with Neurologic Disease' (FOUND) cohort. Baseline data from 563 newly diagnosed PD patients and 306 healthy control subjects were evaluated. Based on 13 variables, the original PREDIGT Score identified recently diagnosed PD patients in the DeNoPa, PPMI + FOUND and the pooled cohorts with area-under-the-curve (AUC) values of 0.88 (95% CI 0.83-0.92), 0.79 (95% CI 0.72-0.85), and 0.84 (95% CI 0.8-0.88), respectively. A simplified version (8 variables) generated AUC values of 0.92 (95% CI 0.89-0.95), 0.84 (95% CI 0.81-0.87), and 0.87 (0.84-0.89) in the DeNoPa, PPMI, and the pooled cohorts, respectively. In a two-step, screening-type approach, self-reported answers to a questionnaire (step 1) distinguished PD patients from controls with an AUC of 0.81 (95% CI 0.75-0.86). Adding a single, objective test (Step 2) further improved classification. Among seven biological markers explored, hyposmia was the most informative. The composite AUC value measured 0.9 (95% CI 0.88-0.91) in DeNoPa and 0.89 (95% CI 0.84-0.94) in PPMI. These results reveal a robust performance of the original PREDIGT Score to distinguish newly diagnosed PD patients from controls in two established cohorts. We also demonstrate the formula's potential applicability to enriching for PD subjects in a population screening-type approach.
| S-EPMC9338052 | biostudies-literature
Project description:ObjectivesAlthough depression symptoms are common among patients with Parkinson's disease (PD), the medical literature still reports underrecognition of depression in patients with PD. Our main objective is to examine the trend of depression recognition during the first year of PD diagnosis using large population data.MethodsWe conducted a population-based study of residents in Wales, using the Secure Anonymized Information Linkage (SAIL) Databank. We included newly diagnosed patients with PD aged 40 years or older with a first PD diagnosis between 2000 and 2015. Depression and antidepressants related data were extracted from SAIL. A series of multilevel logistic regressions were run to determine the factors affecting depression recognition. The results were presented using odds ratios (ORs) with 95% confidence intervals (CI).ResultsThe study included 6596 patients with PD. About 38% of patients had a recorded code of antidepressants, depression diagnosis, or both within the first year of PD diagnosis. There was a significant association of depression diagnosis, antidepressant use, or both with the year of PD diagnosis (OR 0.972, 95% CI 0.962-0.983). We also found that patients who used monoamine oxidase inhibitors (MAO-B inhibitors) were associated with a lower depression diagnosis, use antidepressants, or both, compared to those who did not use MAO-B inhibitors (OR 0.769, 95% CI 0.627-0.943).ConclusionThere is a slight decrease in depression recognition in PD patients between 2000 and 2015, which could be due to an increase in depression recognition during the prodromal phase of PD.
| S-EPMC8413829 | biostudies-literature
Project description:In the literature, there have been several attempts to develop prediction models for youth who are at clinical high risk (CHR) of developing psychosis. Although there are no specific clinical or demographic variables that seem to consistently predict the later transition to psychosis in those CHR youth, in addition to attenuated psychotic symptoms, the most commonly occuring predictors tend to be poor social functioning and certain cognitive tasks. Unfortunately, there has been little attempt to replicate alogorithms. A recently published article by Cornblatt et al suggested that, for individuals with attentuated psychotic symptoms (APS), disorganized communication, suspiciousness, verbal memory, and a decline in social functioning were the best predictors of later transition to psychosis (the RAP model). The purpose of this article was to first test the prediction model of Cornblatt et al with a new sample of individuals with APS from the PREDICT study. The RAP model was not the best fit for the PREDICT data. However, using other variables from PREDICT, it was demonstrated that unusual thought content, disorganized communication, baseline social functioning, verbal fluency, and memory, processing speed and age were predictors of later transition to psychosis in the PREDICT sample. Although the predictors were different in these 2 models, both supported that disorganized communication, poor social functioning, and verbal memory, were good candidates as predictors for later conversion to psychosis.
| S-EPMC5216866 | biostudies-literature
Project description:Childhood trauma (CT) has been identified as a potential risk factor for the onset of psychotic disorders. However, to date, there is limited consensus with respect to which symptoms may ensue after exposure to trauma in early life, and whether specific pathways may account for these associations. The aim of the present study was to use the novel network approach to investigate how different types of traumatic childhood experiences relate to specific symptoms of psychotic disorders and to identify pathways that may be involved in the relationship between CT and psychosis. We used data of patients diagnosed with a psychotic disorder (n = 552) from the longitudinal observational study Genetic Risk and Outcome of Psychosis Project and included the 5 scales of the Childhood Trauma Questionnaire-Short Form and all original symptom dimensions of the Positive and Negative Syndrome Scale. Our results show that all 5 types of CT and positive and negative symptoms of psychosis are connected through symptoms of general psychopathology. These findings are in line with the theory of an affective pathway to psychosis after exposure to CT, with anxiety as a main connective component, but they also point to several additional connective paths between trauma and psychosis: eg, through poor impulse control (connecting abuse to grandiosity, excitement, and hostility) and motor retardation (connecting neglect to most negative symptoms). The results of the current study suggest that multiple paths may exist between trauma and psychosis and may also be useful in mapping potential transdiagnostic processes.
| S-EPMC5216845 | biostudies-literature
Project description:ObjectiveThis study investigated the neural correlates of psychotic-like experiences in youths during tasks involving inhibitory control, reward anticipation, and emotion processing. A secondary aim was to test whether these neurofunctional correlates of risk were predictive of psychotic symptoms 2 years later.MethodFunctional imaging responses to three paradigms-the stop-signal, monetary incentive delay, and faces tasks-were collected in youths at age 14, as part of the IMAGEN study. At baseline, youths from London and Dublin sites were assessed on psychotic-like experiences, and those reporting significant experiences were compared with matched control subjects. Significant brain activity differences between the groups were used to predict, with cross-validation, the presence of psychotic symptoms in the context of mood fluctuation at age 16, assessed in the full sample. These prediction analyses were conducted with the London-Dublin subsample (N=246) and the full sample (N=1,196).ResultsRelative to control subjects, youths reporting psychotic-like experiences showed increased hippocampus/amygdala activity during processing of neutral faces and reduced dorsolateral prefrontal activity during failed inhibition. The most prominent regional difference for classifying 16-year-olds with mood fluctuation and psychotic symptoms relative to the control groups (those with mood fluctuations but no psychotic symptoms and those with no mood symptoms) was hyperactivation of the hippocampus/amygdala, when controlling for baseline psychotic-like experiences and cannabis use.ConclusionsThe results stress the importance of the limbic network's increased response to neutral facial stimuli as a marker of the extended psychosis phenotype. These findings might help to guide early intervention strategies for at-risk youths.
| S-EPMC5951182 | biostudies-literature
Project description:ObjectiveThe way in which parental posttraumatic stress symptoms (PTSS) unfold in the first year after a cancer diagnosis in their child is poorly understood. The aims of this study were to identify parental PTSS trajectories and to examine couple-related predictors (dyadic coping and we-disease appraisals), sociodemographic predictors (education and sex), and medical predictors (child's physical impairment) of trajectory membership.MethodA 1-year prospective study was conducted, and 157 parents of children newly diagnosed with cancer were assessed. PTSS was measured with the Posttraumatic Diagnostic Scale for DSM-5 (PDS-5) at 3-6 weeks (T1), 6 months (T2), and 12 months (T3) after the diagnosis. The trajectories were identified with Latent Class Growth Analysis, the predictors were explored with binomial logistic regression.ResultsTwo distinct trajectories were found. The majority of parents (86.0%) followed a low PTSS trajectory, characterized by initially low scores that slightly decreased over 12 months. In contrast, 14.0% of parents displayed a stable, high PTSS trajectory. A high trajectory of child's physical impairment and low scores in parental dyadic coping were significantly associated with the likelihood of a high parental PTSS trajectory.ConclusionsThe findings provide new insights into the critical period of the first year after a child's cancer diagnosis. While most parents display a resilient, low PTSS trajectory, a minority consistently experience high PTSS levels. Child's physical impairment and dyadic coping should be considered as predictors for early identification of vulnerable parents. Incorporating dyadic coping in parental support following a childhood cancer diagnosis could be beneficial for parental mental health.
| S-EPMC11554108 | biostudies-literature