Neurodevelopmental Disorders Research Articles

The Natural Course of Newborns with Transient Congenital Hypothyroidism.

The incidence of congenital hypothyroidism (CH) has increased worldwide over the last decades mainly due to the lowering of screening thresholds, resulting in an increased identification of newborns with transient CH. Several studies reported the prevalence and the predictive parameters of transient CH but reports on the long-term outcome are rare. This study aimed to assess the long-term course of neonates with transient CH. Neonates diagnosed with transient and permanent CH between the years 1998 to 2018 at the Pediatric Endocrine Institute of Ha'Emek Medical Center were enrolled in the study. Data were retrieved retrospectively from medical files. Included in the study were 76 newborns (45M,59%) with transient CH and 53 (25M,47%) with permanent CH. The major cause of transient CH was prematurity (29%) and subclinical hypothyroidism (30%). During retrospective follow-ups of up to 23 years, reinitiation of LT4 therapy was not required apart from four patients with underlying syndromic etiologies. Neurodevelopmental impairment occurred in 16% of children with transient CH compared with 29.4% in the permanent CH group. Transient CH is frequent among preterm infants but is limited to infancy. SCH frequently presents as overt hypothyroidism at birth but in most cases the requirement for LT4 supplemental therapy is limited to the first years of life, suggesting that long-term follow-up of thyroid function tests may be unnecessary for non-syndromic children. The high rate of neurodevelopmental impairment in newborns with transient CH emphasizes the need for neurodevelopmental monitoring in these patients.

NEUROCOGNITIVE EVALUATION OF PATIENTS WITH DIGEORGE SYNDROME

BackgroundDiGeorge syndrome (DGS), the most common microdeletion syndrome, affects multiple organs, including the heart, the nervous system, and the immune system. In this study, we aimed to evaluate the clinical, laboratory, brain MRI, and neurocognitive findings of our patients with DGS. MethodsClinical and laboratory data of fifty-two patients with DGS between June 2000- March 2022 were evaluated retrospectively. Brain MRI and neuropsychological tests were performed to assess the neurocognitive status of the patients. ResultsFifty-two patients (28 males and 24 females) were included in our study. Fifteen of them died during the follow-up. All 37 patients who are alive had partial DGS. The median age of patients was ten years and seven months, and the median age at diagnosis was five years and four months. Bilateral conduction deceleration in the anterior visual pathways in 6 (20%) of 30 patients was determined by the VEP (Visual Evoked Potentials). The auditory brainstem evoked potential test (BAEP) showed sensorineural hearing loss in 11 out of 30 (36.6%) patients. Brain MRI disclosed brain parenchymal abnormalities in 18 out of 25 (72%) patients. Impairments in executive functions, expressive language, and verbal memory were noted in 18 patients who were neuropsychologically assessed. ConclusionIt is important to keep in mind that patients with DiGeorge syndrome may be accompanied by neurocognitive findings. Awareness of the potential for underlying psychiatric and neurodevelopment disorders is key to anticipatory guidance, optimization of therapies, and maximizing life quality.

The Trials and Errors of Developing an Experimental Model to Study the Impact of Maternal Gut Microbiome Disruption on Perinatal Asphyxia.

Maternal gut microbiome impairment has garnered attention for its potential role in influencing neurodevelopmental outcomes in offspring, especially in situations that increase brain vulnerability such as perinatal asphyxia(PA). Maternal microbiome and fetal brain interplay emerge as a critical link between maternal health and offspring neurodevelopment. This study aims to generate a model to assess the impact of maternal dysbiosis triggered by gestational antibiotic administration and PA on offspring neurodevelopment. Wistar rats were subjected to antibiotics in drinking water from the 11th gestational day until birth. On the 6th postnatal day, pups were subjected to PA/normoxia, resulting in four experimental groups: control-normoxia, antibiotics-normoxia, control-asphyxia, and antibiotics-asphyxia. Early-life behavioral tests were conducted between postnatal days 7 and 9. The initial antimicrobial cocktail (ampicillin, vancomycin, neomycin, clindamycin, amphotericin-B) led to increased number of miscarriages, poor weight gain during pregnancy, reduced offspring weight, and changes in the maternal gut microbiome compared to control. Offspring presented impaired neurodevelopmental reflexes in both PA and antibiotic groups and increased hippocampal neuroinflammation. Due to these detrimental effects, a more pregnancy-safe antibiotic cocktail was used for a second experiment (ampicillin, vancomycin, neomycin, meropenem). This resulted in no miscarriages or pregnancy-weight loss but was still linked to gut microbiome disruption. PA impaired neurodevelopmental reflexes and increased neuroinflammation, effects amplified by antibiotic administration. These preliminary findings reveal the cumulative potential of maternal dysbiosis and PA on neurodevelopment impairment, emphasizing caution in gestational antimicrobial use. Further investigations should include offspring long-term follow-up and maternal behavior and integrate probiotics to counteract antibiotic effects.

Delay of Gratification in Preschoolers with Autism and Concerns for ADHD.

Self-regulation abilities in childhood are predictive of a range of challenges later in life, making it important to identify difficulties in this area as early as possible. Autistic children and those with attention-deficit/hyperactivity disorder (ADHD) often have difficulties with self-regulation, but little is known about the similarities and differences in such abilities across neurodevelopmental conditions. We examined self-regulation using a delay of gratification task in 36-month-old autistic children (n = 20), those showing clinically relevant concerns for ADHD (i.e. ADHD Concerns; n = 24), and Comparison children without these conditions (n = 130); early predictors of self-regulation were also assessed. Both the Autism and ADHD Concerns groups had greater difficulty waiting for a desired snack than the Comparison group. At the longest delay trial (30 seconds), a substantial percentage of autistic children (50%) and those with ADHD Concerns (35%) consumed the snack prematurely, in contrast to only 16% of the Comparison group. Parent-reported temperament-based impulsivity at 18 months and examiner-observed ADHD-like traits at 24 months were associated with increased self-regulation challenges at 36 months, regardless of group. Adjusting for verbal abilities attenuated some of these differences and associations, suggesting that language may be an important mechanism undergirding early self-regulatory abilities. Given possible links between preschool self-regulation and a range of critical functional outcomes, future studies may explore the efficacy of early interventions targeting impulsivity and regulatory behaviors in infants and toddlers at elevated likelihood for developing self-regulation challenges to potentially reduce the impact of these difficulties later in life.

260P NEUROMYODredger – 3 billion megaproject: expanding the accessibility of exome sequencing for the diagnosis of neurodevelopmental and neuromuscular disorders in nine countries

260P NEUROMYODredger – 3 billion megaproject: expanding the accessibility of exome sequencing for the diagnosis of neurodevelopmental and neuromuscular disorders in nine countries

FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

Fanconi anemia (FA) is a rare genetic disease characterized by congenital abnormalities and increased risk for bone marrow failure and cancer. Central nervous system defects, including acute and irreversible loss of neurological function and white matter lesions with calcifications, have become increasingly recognized among FA patients, and are collectively referred to as Fanconi Anemia Neurological Syndrome or FANS. The molecular etiology of FANS is poorly understood. In this study, we have used a functional integrative genomics approach to further define the function of the FANCD2 protein and FA pathway. Combined analysis of new and existing FANCD2 ChIP-seq datasets demonstrates that FANCD2 binds nonrandomly throughout the genome with binding enriched at transcription start sites and in broad regions spanning protein-coding gene bodies. FANCD2 demonstrates a strong preference for large neural genes involved in neuronal differentiation, synapse function, and cell adhesion, with many of these genes implicated in neurodevelopmental and neuropsychiatric disorders. Furthermore, FANCD2 binds to regions of the genome that replicate late, undergo mitotic DNA synthesis (MiDAS) under conditions of replication stress, and are hotspots for copy number variation. Our analysis describes an important targeted role for FANCD2 and the FA pathway in the maintenance of large neural gene stability.

Defective regulation of the eIF2-eIF2B translational axis underlies depressive-like behavior in mice and correlates with major depressive disorder in humans

Major depressive disorder (MDD) is a significant cause of disability in adults worldwide. However, the underlying causes and mechanisms of MDD are not fully understood, and many patients are refractory to available therapeutic options. Impaired control of brain mRNA translation underlies several neurodevelopmental and neurodegenerative conditions, including autism spectrum disorders and Alzheimer’s disease (AD). Nonetheless, a potential role for mechanisms associated with impaired translational control in depressive-like behavior remains elusive. A key pathway controlling translation initiation relies on the phosphorylation of the α subunit of eukaryotic initiation factor 2 (eIF2α-P) which, in turn, blocks the guanine exchange factor activity of eIF2B, thereby reducing global translation rates. Here we report that the expression of EIF2B5 (which codes for eIF2Bε, the catalytic subunit of eIF2B) is reduced in postmortem MDD prefrontal cortex from two distinct human cohorts and in the frontal cortex of social isolation-induced depressive-like behavior model mice. Further, pharmacological treatment with anisomycin or with salubrinal, an inhibitor of the eIF2α phosphatase GADD34, induces depressive-like behavior in adult C57BL/6J mice. Salubrinal-induced depressive-like behavior is blocked by ISRIB, a compound that directly activates eIF2B regardless of the phosphorylation status of eIF2α, suggesting that increased eIF2α-P promotes depressive-like states. Taken together, our results suggest that impaired eIF2-associated translational control may participate in the pathophysiology of MDD, and underscore eIF2-eIF2B translational axis as a potential target for the development of novel approaches for MDD and related mood disorders.

1.4 Development of Webcam-Collected and Artificial-Intelligence–Derived Social and Cognitive Performance Measures for Neurodevelopmental and Neurogenetic Conditions

1.4 Development of Webcam-Collected and Artificial-Intelligence–Derived Social and Cognitive Performance Measures for Neurodevelopmental and Neurogenetic Conditions

Challenges Faced by People with Learning Difficulties Two Years after the COVID-19 Outbreak

Abstract: Background: Learning difficulties are often accompanied by additional challenges in physical and mental health, as well as psychological, neurodevelopmental and medical conditions. In such a situation, crises such as the epidemic of COVID-19, which caused significant economic and social disparities can double the problems. To fully understand the wide-ranging impact of school closures, the transition to online education, and the recognition and support of mental health concerns, it is crucial that we carefully examine the lasting effects of the pandemic. Methods: The literature review played a crucial role in providing background information for this study. To gather academic literature, we extensively searched the PubMed and Scopus databases, including terms: “COVID-19” AND (“learning” OR “learning disorder” OR “learning disability”). From initially n = 173 studies only n = 64 studies remained for the literature review. Discussion: We present a comprehensive strategy to address the deleterious effects of Covid-19 on learning difficulties. The disparities faced by people with learning difficulties across different socio-economic groups increased after the pandemic. Individuals with learning difficulties often experience unique mental health challenges that require tailored support. Providing professional assistance is crucial to ensuring academic success for students with learning difficulties, as it allows us to fully consider the significant changes in education and tailor our support accordingly. This will empower them to surpass their obstacles and flourish in their efforts.

“People talk about FASD diagnosis but barely any young people are asked about it”: Diagnosis perspectives and disability identity in adolescents with FASD

PurposeYoung people with Fetal Alcohol Spectrum Disorder (FASD) are underrepresented in research and in public/professional discourse around the diagnosis and the impact of this disability. This study explores adolescents’ views about their self and disability identity, and knowledge and attitude towards the FASD diagnosis. MethodEight adolescents aged 12–19 years with an FASD diagnosis and in education, participated in this study. Data were collected online using Photovoice methodology and analysed using Interpretative Phenomenological Analysis. ResultsAdolescents expressed positive views of their FASD diagnosis in terms of its salience for self- understanding. They provided biological and causal explanations of FASD but there were no attributes of blame or shame towards biological parents. Adolescents primarily self-identified with personality traits and interests/hobbies but acknowledged FASD as part of their identity. As the adolescents developed their disability identity, parents and peers played different roles in the provision of information, support, and disclosure of the diagnosis. ConclusionThe views expressed by adolescents with FASD about the value and impact of the FASD diagnosis, and the disability identity process, were similar to other groups of young people with different neurodevelopmental and physical conditions. Self-understanding and advocacy relating to diagnosis and disability during adolescence can enhance wellbeing, access to supports and a positive self-identity. Professionals across different services can play a proactive role to develop the positive disability identity of adolescents with FASD.

Increasing Prevalence of Attention-Deficit/Hyperactivity Disorder in Patients With Borderline Personality Disorder.

While research has shown that the prevalence of ADHD in the general population has increased over time, there have been no studies focused on ADHD prevalence in patients with borderline personality disorder (BPD). This study compares two cohorts of adults with rigorously diagnosed BPD recruited nearly three decades apart (1992 vs. 2020). Participants from the 1992 McLean Study of Adult Development (MSAD) (N = 290) and the 2020 Flourishing study (N = 147) were assessed for ADHD using DSM-III-R and DSM-5 criteria respectively. Compared to MSAD subjects, the prevalence of ADHD among Flourishing subjects was significantly higher overall, and in female (but not male) subjects. This increased prevalence, which is likely due to the broadening of the DSM criteria over time, highlights what many observers believe to be a problematic expansion of the diagnostic criteria for ADHD that may have decoupled this criteria set from capturing a neurodevelopmental disorder that typically begins in childhood.

Pharmacological Treatment of Tourette Disorder in Children.

Background: Tourette disorder (TD) is a neurodevelopmental disorder characterized by childhood onset of tics lasting more than one year, with multiple motor tics and at least one phonic tic at some point during the course of the symptoms. Treatment of tics may include psychoeducation, non-pharmacologic treatment, or pharmacologic treatment. We review pharmacologic treatment here. Methods: We performed a literature review on pharmacologic treatments for TD. Results: There is no current evidence to suggest that medications impact the prognosis of tic disorders, so current clinical guidelines recommend reassurance of the patient and family and monitoring if there is no change in function or quality of life due to tics. If treatment is indicated, it must be chosen based on the needs of each individual patient. Comprehensive behavioral intervention for tics (CBIT) is considered first-line management for most individuals with bothersome tics, especially if they are mild to moderate in severity. Pharmacotherapy should be considered when tics are impairing daily functioning, causing social problems, accompanied by other neuropsychiatric symptoms, or when the patient is not likely to benefit from CBIT. Current recommended pharmacotherapy options include alpha-2 adrenergic agonists, dopamine modulators, GABAergic medications, dopamine depleters, and botulinum toxin injections. Additionally, there are other novel medications that are being studied in ongoing clinical trials. Conclusions: This review summarizes available pharmacotherapy options for TD in children. It provides an overview of new medications and offers guidance to physicians when selecting appropriate treatments. If medications are indicated for tic management, treatment should be chosen based on the needs of the individual patient.

Genome-wide association study meta-analysis of 9,619 cases with tic disorders

Despite the significant personal and societal burden of tic disorders (TD), treatment outcomes remain modest, necessitating a deeper understanding of their etiology. Family history is the biggest known risk factor and identifying risk genes could accelerate progress in the field. Expanding upon previous sample size limitations, we added 4,800 new TD cases and 971,560 controls, conducting a GWAS meta-analysis with 9,619 cases and 981,048 controls of European ancestry. We attempted to replicate the results in an independent deCODE Genetics GWAS (885 TD cases and 310,367 controls). To characterize GWAS findings, we conducted several post-GWAS gene-based and enrichment analyses. A genome-wide significant hit (rs79244681, p=2.27x10-08) within MCHR2-AS1 was identified, though it was not replicated. Post-GWAS analyses revealed a 13.8% SNP-heritability and three significant genes: BCL11B, NDFIP2, and RBM26. Common variant risk for TD was enriched within genes preferentially expressed in the cortico-striato-thalamo-cortical circuit (including the putamen, caudate, nucleus accumbens, and Brodman area 9) and five brain cell types (excitatory and inhibitory telencephalon-, inhibitory- di- and mesencephalon, hindbrain-, and medium spiny neurons). TD polygenic risk was enriched within loss-of-function intolerant genes (p=0.0017) and high-confidence neurodevelopmental disorder genes (p=0.0108). Of 112 genetic correlations, 43 were statistically significant, showing high positive correlations with most psychiatric disorders. Of the two SNPs previously associated with TD, one (rs2453763) replicated in an independent sub-sample of our GWAS (p=0.00018). This GWAS was still underpowered to identify high-confidence, replicable loci, but the results suggest imminent discovery of common genetic variants for TD.

Salubrious effects of proanthocyanidins on behavioral phenotypes and DNA repair deficiency in the BTBR mouse model of autism

Autism is a neurodevelopmental disorder distinguished by impaired social interaction and repetitive behaviors. Global estimates indicate that autism affects approximately 1.6% of children, with the condition progressively becoming more prevalent over time. Despite noteworthy progress in autism research, the condition remains untreatable. This serves as a driving force for scientists to explore new approaches to disease management. Autism is linked to elevated levels of oxidative stress and disturbances in the DNA repair mechanism, which may potentially play a role in its comorbidities development. The current investigation aimed to evaluate the beneficial effect of the naturally occurring flavonoid proanthocyanidins on the behavioral characteristics and repair efficacy of autistic BTBR mice. Moreover, the mechanisms responsible for these effects were clarified. The present findings indicate that repeated administration of proanthocyanidins effectively reduces altered behavior in BTBR animals without altering motor function. Proanthocyanidins decreased oxidative DNA strand breaks and accelerated the rate of DNA repair in autistic animals, as evaluated by the modified comet test. In addition, proanthocyanidins reduced the elevated oxidative stress and recovered the disrupted DNA repair mechanism in the autistic animals by decreasing the expressions of Gadd45a and Parp1 levels and enhancing the expressions of Ogg1, P53, and Xrcc1 genes. This indicates that proanthocyanidins have significant potential as a new therapeutic strategy for alleviating autistic features.

Altered sex differences related to food intake, hedonic preference, and FosB/deltaFosB expression within central neural circuit involved in homeostatic and hedonic food intake regulation in Shank3B mouse model of autism spectrum disorder.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder accompanied by narrow interests, difficulties in communication and social interaction, and repetitive behavior. In addition, ASD is frequently associated with eating and feeding problems. Although the symptoms of ASD are more likely to be observed in boys, the prevalence of eating disorders is more common in females. The ingestive behavior is regulated by the integrative system of the brain, which involves both homeostatic and hedonic neural circuits. Sex differences in the physiology of food intake depend on sex hormones regulating the expression of the ASD-associated Shank genes. Shank3 mutation leads to ASD-like traits and Shank3B -/- mice have been established as an animal model to study the neurobiology of ASD. Therefore, the long-lasting neuronal activity in the central neural circuit related to the homeostatic and hedonic regulation of food intake was evaluated in both sexes of Shank3B mice, followed by the evaluation of the food intake and preference. In the Shank3B +/+ genotype, well-preserved relationships in the tonic activity within the homeostatic neural network together with the relationships between ingestion and hedonic preference were observed in males but were reduced in females. These interrelations were partially or completely lost in the mice with the Shank3B -/- genotype. A decreased hedonic preference for the sweet taste but increased total food intake was found in the Shank3B -/- mice. In the Shank3B -/- group, there were altered sex differences related to the amount of tonic cell activity in the hedonic and homeostatic neural networks, together with altered sex differences in sweet and sweet-fat solution intake. Furthermore, the Shank3B -/- females exhibited an increased intake and preference for cheese compared to the Shank3B +/+ ones. The obtained data indicate altered functional crosstalk between the central homeostatic and hedonic neural circuits involved in the regulation of food intake in ASD.

NAD+ supplement relieved chronic sleep restriction (CSR)-induced microglial proinflammation in vivo and in vitro

Sleep insufficiency is a significant health problem worldwide and can induce multiple neurodevelopmental disorders in the central nervous system (CNS). Sleep deprivation (SD), especially chronic SD, leads to cognition and memory loss and worsens neurodegenerative disease liability. Microglia are the main inflammation-dominant glia and play a crucial role in SD-induced neurological impairments. Nicotinamide adenine dinucleotide (NAD+) is a redox reaction coenzyme that exerts anti-inflammatory and mitochondria-protective effects in microglia. Whether NAD+ mitigated SD-induced neurological disorders by regulating microglial functions is still unknown. In the current study, we designed an in vivo and in vitro model to evaluate the neuroprotective effect of NAD+ on chronic sleep restriction (CSR) and further investigate the underlying mechanisms. Behavioral tests and immunofluorescence staining were applied to investigate the cognition impairments and microglial activation. Biochemical experiments were tested to analyze the oxidative status and possible mechanism. In vitro data were used to verify the in vivo data. Our results displayed that NAD+ supplement mitigated CSR-induced cognitive decline and microglial activation response by suppressing the expression of pro-inflammatory cytokines in vivo. NAD+ administration also decreased oxidative stress and mitochondrial impairments in microglia. In vitro results showed that NAD+ treatment inhibited ROS production and prompted M1 conversion to M2 phenotype. cGAS-STING/NF-κB pathways were significantly activated but down-regulated by NAD+ administration. H151, a STING antagonist, was applied to validate that NAD+ treatment alleviates neuroinflammation partially by regulating cGAS-STING pathways in microglia. Our findings suggest that NAD+ supplement is a promising therapy for sleep disorders-induced neurological problems, and cGAS-STING pathway may act as a critical regulator in microglial proinflammation.

The Role of Parvalbumin Interneurons in Autism Spectrum Disorder.

As an important subtype of GABAergic interneurons, parvalbumin (PV) interneurons play a critical role in regulating cortical circuits and neural networks. Abnormalities in the development or function of PV interneurons have been linked to autism spectrum disorder (ASD), a neurodevelopmental disorder characterized by social and language deficits. In this review, we focus on the abnormalities of PV interneurons in ASD, including quantity and function and discuss the underlying mechanisms of impairments in PV interneurons in the pathology of ASD. Finally, we propose potential therapeutic approaches targeting PV interneurons, such as transplanting MGE progenitor cells and utilizing optogenetic stimulation in the treatment of ASD.

Chronic administration of low dose aspirin alleviates ASD-like behaviors and activates AMPK in valproic acid-exposed rats

BackgroundAutism Spectrum Disorder (ASD) is a neurodevelopmental disorder distinguished by deficits in social communication and the presence of restricted/repetitive behaviors. There has been a global increase in the prevalence of ASD, yet the underlying causes of ASD remain inadequately understood, and there is currently no pharmacological intervention for the core symptoms of ASD. However, recent studies have suggested that aspirin may have the potential for use in the treatment of ASD. MethodPregnant rats were administered either VPA or normal saline on gestational day 12.5. The male pups were administered a low dose of aspirin (1 mg/kg) or a vehicle control daily from postnatal day 23 to day 52. ASD-like behaviors were assessed by social interaction, spontaneous grooming test, open field test and light-dark transitions. The activity of AMP-activated protein kinase (AMPK) was quantified by measuring the level of p-AMPK using an immunoblotting assay. ResultsChronic administration of low dose aspirin resulted in significant improvements in social approach deficits, a reduction in repetitive grooming, and the alleviation of anxiety-like behavior in ASD rats. Furthermore, aspirin administration also led to the activation of AMPK in the hippocampus of rats exposed to VPA. ConclusionsThese results raise the question of the need for further investigation of agents with mechanisms related to aspirin in ASD.

Neurobiological Insights Into Cerebral Palsy: A Review of the Mechanisms and Therapeutic Strategies.

Cerebral palsy (CP) is a common neurodevelopmental disorder characterized by impaired mobility and posture caused by brain injury or abnormal development. CP relates to a variety of neurological mechanisms and pathways that impact the type and severity of motor disability, as well as comorbidities. The heterogeneity in clinical phenotype, pathogenesis, and etiology poses significant challenges for effective therapeutic intervention. The review aims to provide a comprehensive analysis of the neurobiological mechanisms underlying CP and evaluate current and prospective therapeutic strategies, highlighting the necessity for targeted interventions to address the disorder's multifaceted nature. A thorough literature review was conducted, focusing on studies published in peer-reviewed journals that explore the pathophysiological mechanisms, clinical interventions, and therapeutic strategies for CP. The pathogenesis of CP involves a complex interplay of genetic, environmental, and perinatal factors leading to brain injury. Inflammatory processes, oxidative stress, and excitotoxicity are critical in CP development. Current therapeutic approaches primarily focus on symptom management through physical and occupational therapy, as well as pharmacological interventions. Emerging therapies, including anti-inflammatory agents, antioxidants, and neuroprotective and neurotrophic agents, show potential but require further validation. Notably, although steroids provide anti-inflammatory benefits, their use in pediatric patients raises concerns regarding long-term adverse effects such as osteoporosis. Despite advances in understanding CP's neurobiological underpinnings, effective therapeutic targets remain elusive. A comprehensive approach addressing CP's heterogeneity is essential. Future research should emphasize in-depth evaluations of the efficacy and safety of therapeutic agents, particularly in pediatric populations, to develop targeted and effective treatments for CP.

Prevalence of Attention Deficit Hyperactivity Disorder among Primary School Children in Hyderabad, South India

Purpose: Attention deficit hyperactivity disorder (ADHD) is among the most prevalent neurodevelopmental disorders in childhood, and its incidence has increased in recent years. However, the frequency of ADHD varies significantly across different countries and regions. This study aimed to determine the prevalence of ADHD among primary school children in Hyderabad, India, as well as to raise awareness about ADHD among teachers.Methods: This descriptive cross-sectional study included 700 school-aged children between 5 and 12 years old, selected according to specific inclusion and exclusion criteria. The teachers' version of the Vanderbilt Assessment Scale, a rating scale grounded in Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnostic criteria, was employed to diagnose ADHD. Results: The prevalence of ADHD in this study was 9.57% (67 out of 700), with a mean age of 8.9 years. ADHD was more prevalent in boys than in girls, with a sex ratio of 3:1. The combined type of ADHD was the most common (52.3%), followed by the attention deficit type (29.8%) and the hyperactive-impulsive type (17.9%). Conclusion: The prevalence of ADHD among schoolchildren in middle-income countries, such as India, is sufficiently high to impose a significant societal burden. Therefore, it is imperative that all elementary school teachers receive training on how to screen for indicators of ADHD.