ABSTRACT
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.
Subject(s)
Antipsychotic Agents , Attention Deficit Disorder with Hyperactivity , Central Nervous System Stimulants , Adult , Humans , Child , Anxiety , Anxiety DisordersABSTRACT
Avoidant/Restrictive Food Intake Disorder and misophonia seem to be overrepresented in autism spectrum disorder. Literature is mute on psychopharmacotherapy in these complex presentations. Here, authors report on a challenging case of low-functioning ASD child with comorbid ARFID and misophonia that responded favorably to a low-dose risperidone. This is followed by a brief discussion of purported pharmacodynamic mechanisms and relevant literature.
Subject(s)
Autism Spectrum Disorder , Autistic Disorder , Avoidant Restrictive Food Intake Disorder , Feeding and Eating Disorders , Autism Spectrum Disorder/complications , Autism Spectrum Disorder/drug therapy , Autistic Disorder/drug therapy , Child , Humans , RisperidoneABSTRACT
Cystic fibrosis (CF) is a potentially fatal genetic disease that causes serious lung damage. With time, researchers have a more complete understanding of the molecular-biological defects that underlie CF. This knowledge is leading to alternative approaches regarding the treatment of this condition. Trikafta is the third FDA-approved drug that targets the F508del mutation of the CFTR gene. The drug is a combination of three individual drugs which are elexacaftor (ELX), tezacaftor (TEZ), and ivacaftor (IVA). This trio increases the activity of the cystic fibrosis transmembrane conductance regulator (CFTR) protein and reduces the mortality and morbidity rates in CF patients. The effectiveness of Trikafta, seen in clinical trials, outperforms currently available therapies in terms of lung function, quality of life, sweat chloride reduction, and pulmonary exacerbation reduction. The safety and efficacy of CFTR modulators in children with CF have also been studied. Continued evaluation of patient data is needed to confirm its long-term safety and efficacy. In this study, we will focus on reviewing data from clinical trials regarding the benefits of CFTR modulator therapy. We address the impact of Trikafta on lung function, pulmonary exacerbations, and quality of life. Adverse events of the different CFTR modulators are discussed.
Subject(s)
Autistic Disorder , Endophenotypes , Autistic Disorder/genetics , Fathers , Humans , MaleSubject(s)
Autistic Disorder/psychology , Autistic Disorder/therapy , Child Behavior Disorders/psychology , Child Behavior Disorders/therapy , Electroconvulsive Therapy/methods , Child , Humans , Intellectual Disability/complications , Intellectual Disability/psychology , Male , Psychotropic Drugs/therapeutic use , Treatment OutcomeSubject(s)
Citalopram/adverse effects , Hematuria/chemically induced , Obsessive-Compulsive Disorder/drug therapy , Selective Serotonin Reuptake Inhibitors/adverse effects , Adolescent , Citalopram/administration & dosage , Humans , Male , Selective Serotonin Reuptake Inhibitors/administration & dosageSubject(s)
Child Behavior , Child Psychiatry/methods , Cognitive Reserve , Mental Disorders , Age of Onset , Child , Child Development , Diagnostic and Statistical Manual of Mental Disorders , Humans , International Classification of Diseases , Mental Disorders/diagnosis , Mental Disorders/epidemiology , Mental Disorders/psychology , Mental Disorders/therapy , Prognosis , PsychopathologyABSTRACT
Stimulants-related bruxism has been previously reported; both diurnal and nocturnal. Here, authors report on a case of methylphenidate (MPH)-treated attention-deficit/hyperactivity disorder that developed nocturnal bruxism and failed multiple pharmacologic trials. Add-on clonidine has successfully helped with bruxisms while augmenting MPH response. This was achieved with great tolerability. This remains a viable option to deploy in such unusual clinical scenarios.
