Psychopharmacology bulletin最新文献

The first monoamine oxidase inhibitors (MAOIs) used for the treatment of depression in the 1950-60s were credited with treating severe melancholic depression (MeD) successfully and greatly reducing the need for electroconvulsive therapy (ECT). Following the hiatus caused by the then ill-understood cheese reaction, MAOI use was relegated to atypical and treatment-resistant depressions only, based on data from insufficiently probing research studies suggesting their comparatively lesser effectiveness in MeD. The siren attraction of new 'better' drugs with different mechanisms amplified this trend. Following a re-evaluation of the data, we suggest that MAOIs are effective in MeD. Additionally, the broad unitary conceptualisation of major depressive disorder (MDD) in the DSM model diminished the chance of demonstrating distinctive responses to different antidepressant drugs (ADs) such as SSRIs, TCAs, and MAOIs, thereby further reducing the interest in MAOIs. More reliable categorical distinction of MeD, disentangling it from MDD, may be possible if more sensitive measuring instruments (CORE, SMPI) are used. We suggest these issues will benefit from re-appraisement via an inductive reasoning process within a binary (rather than a unitary) model for defining the different depressive disorders, allowing for the use of more reliable diagnostic criteria for MeD in particular. We conclude that MAOIs remain essential for, inter alia, TCA-resistant MeD, and should typically be used prior to ECT; additionally, they have a role in maintaining remission in cases treated with ECT (and ketamine/esketamine). We suggest that MAOIs should be utilized earlier in treatment algorithms and with greater regularity than is presently the case.

Authors report on an interesting case of a teenager with attention-deficit/hyperactivity disorder and comorbid generalized anxiety disorder, who developed takotsubo cardiomyopathy subsequent to pharmacokinetic and pharmacodynamic interactions between atomoxetine, a selective norepinephrine reuptake inhibitor, and the antidepressant duloxetine. Clinicians should be mindful of the potential for cardiovascular adverse effects when prescribing agents that target noradrenergic receptors.

Introduction The purpose of this guide is to provide convenient and useful information on about Alzheimer's disease and dementias of late life. The information includes selected facts, diagnostic criteria tables, descriptions of selected tests and screens, guidelines, clinical pharmacological data and references. This guide is divided into several sections: Background factsDiagnostic aids and criteria for dementia diagnosesMedications used for Alzheimer's disease and dementia Basic information on marketed treatments is provided although the treatment may not be FDA approved for this use. Approved cholinesterase inhibitors, memantine, and monoclonal antibodies are listed. No treatment is recommended or endorsed, however. This guide does not address the evidence base for the efficacy of the treatments listed. Caveats: Except for treatments above, discussions of medications for people with dementia nearly always involve off label use. For example, antidepressants and antipsychotics are indicated in the FDA-approved prescribing information for major depression and schizophrenia, and not for depressive symptoms or the delusions or hallucinations occurring within the context of dementia with two exceptions. In these instances, the doses listed are for reference only and should not be considered as recommendations or appropriate use. Physicians should consult the product package labeling for any drug mentioned.

This study aimed to explore the relationship between Captagon usage and the development of delusions of infidelity. The study sample; 101 male patients, was recruited from patients admitted to Eradah Complex for Mental Health and addiction, Jeddah, Saudi Arabia, with the diagnosis of amphetamine (Captagon) induced psychosis during the period from September 2021 to March 2022. All patients underwent an extensive psychiatric interview; including interview with patients' families; a demographic sheet, a drug use questionnaire, the structured clinical interview for DSM-IV (SCID 1), routine medical investigation, and urine screening for drugs. Patients' ages ranged from 19 to 46 years old with Mean ± SD 30.87 ± 6.58. 57.4 % were single, 77.2% have finished their high school, and 22.8% had no work. Captagon using age ranged from 14-40 years old, and regular daily dose ranged from 1-15 tablet, while maximum daily dose ranged from 2-25 tablets. Twenty-six patients (25.7%) of the study group have developed infidelity delusions. A higher divorce rate was present among patients who developed infidelity delusions (53.8%) in comparison to patients who developed other types of delusions (6.7%). Infidelity delusions are common among patients diagnosed with Captagon induce psychosis, and they harmfully influence their social lives.

Background: Memenatine is USFDA approved for dementia of Alzheimer's disease. Apart from this indication, trend of its use in psychiatry is on the rise addressing a multitude of disorders.

Study question: Memantine remains one of only few psychotropic drugs with antiglutamate activity. This might impart it a therapeutic potential in treatment-resistant major psychiatric disorders characterized by neuroprogression. We reviewed memantine basic pharmacology and its diversifying clinical indications while examining the extant evidence.

Methods: EMBASE, Ovid MEDLINE, PubMed, Scopus, Web of Science, and Cochrane Database of Systemic Reviews were searched for all relevant studies up to date of November, 2022.

Results: Sound evidence supports use of memantine for major neuro-cognitive disorder due to Alzheimer's disease and severe vascular dementia, obsessive-compulsive disorder, treatment-resistant schizophrenia, and, ADHD. Modicum evidence supports use of memantine for PTSD, GAD and pathological gambling. Less compelling evidence is present for use in catatonia. No evidence supports use for core symptoms of autism spectrum disorder.

Conclusions: Memantine is an important addition to the psychopharmacological armamentarium. Level of evidence supporting the use of memantine in these off-label indications is highly variable, and hence, sound clinical judgment is necessary for its proper use and placement in real-life psychiatric practice and psychopharmacotherapy algorithms.

No single neurotransmitter aberration could explain the heterogeneity of schizophrenia syndrome and thus, treatment strategies capitalizing solely on a single neurotransmitter system (e.g., DA blockade) is less likely to be fully successful on clinical grounds. Hence, there is a pressing need to develop newer antipsychotics above and beyond DA antagonism. In this regard, authors brief on five agents that sound pretty promising and might usher in a new sparkle in the psychopharmacotherapy of schizophrenia. This paper is a sequel for authors' previous article on future of schizophrenia psychopharmacotherapy.

Introduction: Cognitive deficits within the first years of Parkinson's disease (PD) diagnosis are commonly reported, and progression to dementia greatly impacts independence. Identifying measures sensitive to early changes is critical for trials of symptomatic therapies and neuroprotection.

Methods: A sample of 253 newly diagnosed PD patients and 134 Health Controls (HC) completed a brief cognitive battery annually over a 5-year period through the Parkinson's Progression Markers Initiative (PPMI). The battery included standardized measures of memory, visuospatial functions, processing speed, working memory, and verbal fluency. Inclusion criterion for HCs was performance above a cutoff for possible Mild Cognitive Impairment (pMCI) on cognitive screening (MoCA ⩾ 27) The PD sample was therefore divided to match HCs on baseline cognitive testing (PD-normal n = 169; PD-pMCI n = 84). The multivariate approach to repeated measures examined rates of change between groups on cognitive measures.

Results: An interaction indicating slightly greater decline over time in PD-normal relative to HCs was observed on a measure of working memory: letter-number sequencing. Differential rates of change were not observed on any other measures. Motor symptoms on the dominant right upper extremity accounted for performance differences on a test with writing demands (Symbol-Digit Modality Test). PD-pMCI performed worse than PD-normal on all cognitive measures at baseline, but did not decline faster.

Discussion: Working memory appears to decline slightly faster in early PD compared to HCs, while other domains remain similar. Within PD, faster decline was not associated with lower baseline cognition. These findings have implications for clinical trial outcome selection and study design.

Objectives: Literature on ADHD has taken long strides recently as heaps of new data are pouring in through countless papers. Here, authors try to outline changing paradigms in ADHD practice. DSM-5 changes regarding the typology and diagnostic criteria are highlighted. Overview of co-morbidities, associations, developmental trajectories, and syndromic continuity across lifespan is outlined. Recent insights into aetiology and diagnostic tools are briefly discussed. New medications in the pipeline are also described.

Methods: EMBASE, Ovid MEDLINE, PubMed, Scopus, Web of Science, and Cochrane Database of Systemic Reviews were searched for all relevant updates in ADHD literature as of June, 2022.

Results: DSM-5 brought about changes to the diagnostic criteria of ADHD. These included replacing types with presentations, pushing age to 12, and, incorporating adult diagnostic criteria. In the same vein, DSM-5 allows now for diagnosing concurrent ADHD and ASD. Associations of ADHD to allergy, obesity, sleep disorders, and, epilepsy have been demonstrated in recent literature. Neurocircuity underlying ADHD has been extended beyond frontal-striatal to include CTC as well as DMN accounting for ADHD heterogeneity. NEBA was FDA-approved to differentiate ADHD from hyperkinetic ID. Atypical antipsychotics use to address behavioural facets in ADHD is on the rise with no solid evidence-base. α-2 agonists are FDA-approved as monotherapy or adjunctive to stimulants. Pharmacogenetic testing is readily available for ADHD. Different formulations of stimulants abound on the market widening clinicians' repertoire. Stimulant-related exacerbation of anxiety and tics were challenged in recent studies. Drugs for ADHD in the pipeline include-dasotraline, armodafinil, tipepidine, edivoxetine, metadoxine, and memantine.

Conclusions: Literature on ADHD keeps expanding towards advancing our understanding of the complex and heterogeneous intricacies of this commonplace neurodevelopmental disorder and hence informing better decisions on how best to manage its diverse cognitive, behavioural, social and medical facets.

Objective: There is an increased risk for depression in the offspring of depressed parents. This is in part mediated by maladaptive parenting. Females are more vulnerable to parenting behavior and were found to be at increased risk of depression compared to male offspring of depressed parents. Previous work suggested a reduced risk for depression in the offspring of parents with remitted depression. Offspring gender differences in this association were rarely considered. Here, we are examining the hypothesis that female offspring are more likely to benefit from treating parental depression using data from the U.S. National Comorbidity Survey Replication (NCS-R).

Method: The NCS-R is a nationally representative household survey of adults 18 years and older carried out between February 2001 and April 2003. The World Health Organization World Mental Health Composite International Diagnostic Interview (WHO WMH-CIDI) was used to assess DSM-IV Major Depressive Disorder (MDD). Multiple logistic regressions were used to assess the association between parental treatment and offspring risk for MDD. An interaction term was added to study the effect of offspring's gender on this risk.

Results: The age-adjusted odds ratio for treatment of parental depression was 1.15 (95% CI: 0.78, 1.72). There was no effect modification by gender (p = 0.42). Surprisingly, treatment of parental depression did not reduce their offspring's risk for depression.

Conclusion: Gender of the offspring had no effect on the risk of depression in the adult offspring of treated versus untreated depressed parents. A focus on mediators like parenting behavior and its gender specific effect needs to be explored in future studies.