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PubMedDate not supplied

MRI study of the pituitary gland in adolescent depression.

Abnormalities in pituitary function have been described in major depressive disorder (MDD) and may reflect neurodevelopmental abnormalities. We hypothesized alterations in the pituitary in early onset MDD. We measured the volume of the pituitary gland in 17 MDD (mean+/-S.D.=16.67+/-1.83 years; 8M, 9F) patients and 17 age and sex matched healthy controls (mean+/-S.D.=16.23+/-1.61 years; 8M, 9F) using 1.45 mm thick T(1)-weighted coronal MRI images. A trained rater blind to diagnosis did all measurements. ANCOVA covarying for age, sex and intracranial volume (ICV) revealed a significant difference between the two groups (F=6.43, df=1, 29, P=0.02; MDD subjects demonstrated a 25% increase in pituitary gland volume). Age was significantly correlated with pituitary volume in the healthy controls (r=0.62, P=0.008) but not the MDD group. No significant relationships between pituitary size and clinical severity were found in the MDD patients. To our knowledge, this is the first study that reports larger pituitary volumes in early onset major depression. These findings provide new evidence of abnormalities of the pituitary in early onset MDD, possibly related to neuroendocrine dysfunction.

Adolescent↗

PubMed1997

Corpus callosal morphology in treatment-naive pediatric obsessive compulsive disorder.

1. Abnormalities in association circuits have been described in Obsessive Compulsive Disorder (OCD) and may reflect neurodevelopmental abnormalities. Primary and association cortices are topographically mapped in the corpus callosum (CC). The authors hypothesized alterations in CC subdivisions that connect association, but not primary cortices in pediatric OCD. The authors predicted that normal age-related increases in CC area would be absent in OCD. 2. The authors compared the midsagittal magnetic resonance images of 21 psychotropic-naive, nondepressed OCD patients, 7.2-17.7 years, and 21 case-matched healthy controls. Total CC area as well as that of the anterior, middle and posterior genu, anterior and posterior bodies, isthmus, and the anterior, middle and the posterior splenii were measured. 3. All of the CC regions except the isthmus were significantly larger in OCD patients than in controls. CC area correlated significantly with OCD symptom severity but not illness duration. The age-related increase in CC size seen in normal subjects was absent in OCD patients. 4. These findings support theories of abnormal association cortex development in OCD but also suggest possible abnormalities of other primary cortical regions as well.

Adolescent↗

PubMed2002

Biochemical markers predicting survival in peroxisome biogenesis disorders.

OBJECTIVE: To identify prognostic markers reflecting the extent of peroxisome dysfunction in primary skin fibroblasts from patients with peroxisome biogenesis disorders (PBD). BACKGROUND: PBD are a genetically heterogeneous group of disorders due to defects in at least 11 distinct genes. Zellweger syndrome is the prototype of this group of disorders, with neonatal adrenoleukodystrophy and infantile Refsum disease as milder variants. Common to these three disorders are liver disease, variable neurodevelopmental delay, retinopathy, and perceptive deafness. Because genotype-phenotype studies are complicated by the genetic heterogeneity among patients with PBD, the authors evaluated a series of biochemical markers as a measure of peroxisome dysfunction in skin fibroblasts. METHODS: Multiple peroxisomal functions including de novo plasmalogen synthesis, dihydroxyacetonephosphate acyltransferase (DHAPAT) activity, C26:0/C22:0 ratio, C26:0 and pristanic acid beta-oxidation, and phytanic acid alpha-oxidation were analyzed in fibroblasts from a series of patients with defined clinical phenotypes. RESULTS: A poor correlation with age at death was found for de novo plasmalogen synthesis, C26:0/C22:0 ratio, and phytanic acid alpha-oxidation. A fairly good correlation was found for pristanic acid beta-oxidation, but the best correlation was found for DHAPAT activity and C26:0 beta-oxidation. A mathematic combination of DHAPAT activity and C26:0 beta-oxidation showed an even better correlation. CONCLUSIONS: DHAPAT activity and C26:0 beta-oxidation are the best markers in predicting life expectancy of patients with PBD. Combination of both markers gives an even better prediction. These results contribute to the management of patients with PBD.

Acyltransferases↗

PubMed2026

Efficacy of pharmacological and microbiota-based therapies in preclinical models of autism spectrum disorder: a systematic review.

BACKGROUND: Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental condition in which pharmacological and microbiota-targeted interventions are emerging as promising therapeutic avenues. Animal models are the main tool to investigate etiology, molecular mechanisms and screening for pharmacological therapies. Methodological differences, outcome measure variability, incomplete reporting, biological confounders, and overgeneralization of the results made evaluating innovative pharmacological agents challenging. These limitations in the field highlight a need for systematic and standardized research to reliably assess and translate pharmacological interventions from ASD animal models to human clinical relevance. SUBJECTS: This systematic review synthesized efficacy evidence for pharmacological and microbiota-based therapies across established ASD animal models. RESULTS: We identified 52 recent (2010-2025) studies that reported key ASD behavioral outcomes after pharmacological or microbiota-focused treatments. Interventions were grouped into therapeutic classes - including oxytocinergic agents, E/I balance therapeutic targets, metabolic drugs, cannabinoids, purine-based interventions and emerging targets - alongside microbiota-directed strategies such as probiotics, prebiotics, and fecal microbiota transplantation. By integrating effect directions and robustness across models, we identified most potential drug candidates, evaluated the efficacy of novel strategies, and recognized critical translational gaps. The reviewed studies demonstrate that ASD-like behavioral deficits in preclinical models can be modulated through interventions targeting diverse biological systems, including neurotransmission, neuroinflammation, metabolism, and the gut-brain axis. CONCLUSIONS: These findings support the multifactorial nature of ASD pathophysiology which arises from a network of interacting systemic processes rather than a single molecular defect. It could explain the limited success of traditionally narrowly targeted interventions and suggest a paradigm shift into a more systemic approach.

Animals↗

PubMedDate not supplied

[Phenotypic variability of deletion 22q11.2. An analysis of 16 observations with special emphasis on the neurological manifestations].

INTRODUCTION: The microdeletion 22q11.2 affects 1/4000 live births and constitutes the most frequent interstitial chromosomal alteration in humans. It is involved in a heterogeneous series of phenotypic expressions. AIMS: To determine the most important clinical characteristics in a series of patients with this genetic molecular disorder. PATIENTS AND METHODS: We conducted a retrospective study of 16 patients who had been diagnosed, by means of FISH or PCR, as having microdeletion 22q11.2, and the following data were evaluated in a protocolised manner: sex, age, family background, characteristics of the pregnancy, birth, neonatal and post-neonatal periods, clinical and semiological data, as well as the results from the complementary explorations carried out according to the predominant pathology. RESULTS: The age at which the diagnosis was made oscillated between newly born and 8 years, with a predominance of males over females in a ratio of 3.2/1. In all, 81% of patients presented neurological disorders. Brain malformations were seen in six, hypoplasia of the anguli oris muscle in five, congenital facial palsy in three which was associated with brain malformations in one patient, retarded neurodevelopment in six cases and neurogenic arthrogryposis in one. Other findings such as congenital heart disease (75%), skeletal disorders (37%), peculiar phenotypes (31%), nephrourological disorders (19%) and hypoacusis (19%) constitute significant manifestations of the process. Some of the most noteworthy occasional events include retarded height and weight development, hypocalcemia and cleft palate. In one case involving a child whose mother suffered from chronic alcoholism, there were both phenotypic traits of this entity and of foetal alcohol syndrome at the same time. In four of the patients the FISH technique did not detect the deletion, which was confirmed by a technique involving DNA amplification with PCR. CONCLUSIONS: The presence of central and peripheral neurological alterations, together with cardiac, skeletal, renal and auditory disorders was confirmed, as was the existence of neurodevelopmental retardation and a peculiar phenotype. Both the frequency and the kind of disorder coincided with what has been described earlier. A number of facts stand out owing to their novelty. These include the high incidence of asymmetric crying facies, the existence of data compatible with foetal alcohol syndrome in one of the patients with this clinical entity, and the association with neurogenic arthrogryposis in another, which are circumstances that suggest the possibility of a causal relation with the deletion 22q11.2. Using DNA amplification with PCR is seen to be of greater diagnostic efficacy than the FISH technique.

Abnormalities, Multiple↗

PubMed2002

Increased gyrification in Williams syndrome: evidence using 3D MRI methods.

Understanding patterns of gyrification in neurogenetic disorders helps to uncover the neurodevelopmental etiology underlying behavioral phenotypes. This is particularly true in Williams syndrome (WS), a condition caused by de novo deletion of approximately 1 to 2 Mb in the 7q11.23 region. Individuals with WS characteristically possess an unusual dissociation between deficits in visual-spatial ability and relative preservations in language, music, and social drive. A preliminary postmortem study reported anomalous gyri and sulci in individuals with WS. The present study examined gyrification patterns in 17 participants with WS (10 females, 7 males; mean age 28 years 11 months, SD 8 years 6 months) and 17 age- and sex-matched typically developing control participants (mean age 29 years 1 month, SD 8 years 1 month) using new automated techniques in MRI. Significantly increased cortical gyrification was found globally with abnormalities being more marked in the right parietal (p=0.0227), right occipital (p=0.0249), and left frontal (p=0.0086) regions. These results suggest that one or more genes in the 7q11.23 region are involved during the critical period when cortical folding occurs, and may be related to the hypothesized dorsal/ventral dissociation in this condition.

Adult↗

PubMedDate not supplied

Subjective cognitive dysfunction in first-episode and chronic schizophrenic patients.

Previous studies indicate that first-episode and chronic schizophrenic patients do not differ regarding neuropsychological performance as assessed with standard cognitive tasks. For the present study, it was investigated whether first-episode and chronic schizophrenics report similar subjective cognitive deficits. The Frankfurt Complaint Questionnaire (FCQ), a scale devised for assessing subjective cognitive disturbances in schizophrenia, was administered to 20 first-episode and 36 chronic schizophrenic patients, as well as 20 healthy controls. The schizophrenic subsamples did not differ on any of the FCQ subscales or on a "lie scale," measuring illness denial. Psychopathological ratings were comparable for both groups. As expected, healthy subjects reported significantly less cognitive and perceptual problems than schizophrenic patients. In marked contrast to a Kraepelinian view of schizophrenia, the present data confirm previous studies conducted with objective neuropsychological tests that schizophrenia is a neurodevelopmental rather than a neurodegenerative disorder.

Adult↗

PubMed2006

Guidelines for the management of spontaneous preterm labor.

Preterm birth is defined as delivery at <37 completed weeks of pregnancy (World Health Organization). Spontaneous preterm birth (SPB) includes preterm labor, preterm spontaneous rupture of membranes, preterm premature rupture of membranes (PPROM) and cervical weakness; it does not include indicated preterm delivery for maternal or fetal conditions. Early SPB (<32 weeks' gestation) is associated with an increased higher perinatal mortality rate, inversely proportional to gestational age. The pathophysiologic events that trigger SPB are largely unknown but include decidual hemorrhage (abruption), mechanical factors (uterine overdistention or cervical incompetence), and hormonal changes (perhaps mediated by fetal or maternal stress). In addition, several cervicovaginal infections have been associated with preterm labor. SPB is also the leading cause of long-term morbidity, including neurodevelopmental handicap, cerebral palsy, seizure disorders, blindness, deafness and non-neurological disorders, such as bronchopulmonary dysplasia and retinopathy of prematurity. Delaying delivery may reduce the rate of long-term morbidity by facilitating the maturation of developing organs and systems. The benefits of administration of antepartum glucocorticosteroids to reduce the incidence and severity of respiratory distress syndrome may be exploited by delay. Delay may also permit transfer of the fetus in utero to a center with neonatal intensive care unit facilities. There is considerable variation in the way that spontaneous preterm labor (SPTL) is diagnosed, managed and treated internationally. The development of clinical guidelines requires an evidence-based approach to improve outcome and allow more efficient use of resources. With recent advances in our understanding of the etiology and mechanisms of SPTL and the availability of safer, more specific tocolytics, it was felt that guidelines should be developed to achieve, if possible, an European consensus in patient diagnosis, management and treatment.

Anti-Bacterial Agents↗

PubMed1999

Pituitary dysfunction, morbidity and mortality with congenital midline malformation of the cerebrum.

UNLABELLED: The purpose of this study was to review systematically a series of patients with congenital midline brain defects and pituitary dysfunction in early childhood and to quantitate the degree of dysfunction and clinical outcome. This study was a retrospective analysis of case notes of patients with pituitary dysfunction associated with either a midline cerebral anomaly and/or optic nerve hypoplasia. Forty patients were studied: 2 with semilobar holoprosencephaly, 2 with lobar holoprosencephaly, 18 with septo-optic dysplasia with an intact septum pellucidum, 7 with septo-optic dysplasia with an absent septum pellucidum, 7 with agenesis of the corpus callosum and 4 patients with isolated pituitary hypoplasia. An early age of diagnosis, feeding difficulties, neurodevelopmental disability, visual impairment and seizures were common occurrences. Despite disordered neuro-anatomy, most seizure disorders were caused by hypoglycaemia or hypernatraemia. Hypotensive/hypoglycaemic crises accounted for two out of three deaths within the study population. Most of patients had multiple pituitary hormone deficiency with growth hormone and adrenocorticotrophic hormone deficiency occurring most commonly. Unequivocal isolated hypothalamic dysfunction was an uncommon finding. In congenital midline brain malformation there is a spectrum of disordered neuro-anatomy associated with variable pituitary dysfunction. Clinical manifestations such as convulsions and developmental delay may be due to disordered metabolism and/or neuro-anatomy. CONCLUSION: Children with congenital midline brain defects frequently manifest convulsions, neurodevelopmental disability and poor growth due to disordered metabolism and/or neuro-anatomy. Treating clinicians must be aware of the complex, dynamic neurological and metabolic nature of these patients and their potential for early demise.

Abnormalities, Multiple↗

PubMed1998

MRI study of cavum septi pellucidi in schizophrenia, affective disorder, and schizotypal personality disorder.

OBJECTIVE: A cavum between the septi pellucidi may reflect neurodevelopmental anomalies in midline structures of the brain. The authors examined cavum septi pellucidi in subjects with schizophrenia, affective disorder, and schizotypal personality disorder and in normal subjects. METHOD: Thirty schizophrenic patients (15 chronic, 15 first-episode), 16 patients with affective disorder (first-episode), 21 patients with schizotypal personality disorder, and 46 normal subjects were evaluated with magnetic resonance imaging. Cavum septi pellucidi was assessed by counting the number of 1.5-mm slices containing cavum septi pellucidi. RESULTS: The presence or absence of cavum septi pellucidi did not differentiate among groups. However, the prevalence of abnormal cavum septi pellucidi (i.e., cavum septi pellucidi contained on four or more slices) was 30.4% for schizophrenic patients (36.4% for chronic, 25.0% for first-episode), 20.0% for patients with affective disorder, 18.8% for patients with schizotypal personality disorder, and 10.3% for normal subjects. When the authors used the Nopoulos et al. criteria for rating cavum septi pellucidi, which omitted borderline cases with cavum septi pellucidi on three slices, the prevalence of abnormal cavum septi pellucidi increased to 35.0% for schizophrenia (40.0% for chronic, 30.0% for first-episode), 25.0% for affective disorder, 27.3% for schizotypal personality disorder, and 13.0% for normal subjects. There was a statistically significant difference in ratings between schizophrenic and normal subjects. CONCLUSIONS: The results suggest that alterations in midline structures during the course of neurodevelopment may play a role in the pathogenesis of schizophrenia.

Adult↗

PubMed1984

Familial neonatal and infantile seizures: an autosomal-dominant disorder.

Familial neonatal seizures are an important and probably underrecognized disorder. A family with six affected individuals in three generations was evaluated and their clinical characteristics were compared with those of 15 families previously reported in the literature. An analysis of the 116 affected individuals uncovered a typical clinical picture of onset of seizures by 2 to 8 days of life in an otherwise healthy appearing infant, and cessation of seizures by 1 to 6 months. Results of diagnostic evaluations were normal, and the pathogenesis of the disorder is still unclear. Long-term neurodevelopmental outcome was normal except for an increased rate (11%) of subsequent seizures in childhood or as an adult. The disorder was inherited as an autosomal-dominant trait with a high degree of penetrance.

Adult↗

PubMed2003

The impact of intrauterine exposure versus postnatal environment in neurodevelopmental toxicity: long-term neurobehavioral studies in children at risk for developmental disorders.

Various investigators have shown that enriched environment may positively affect the early brain development of experimental animals. Environment was also shown to positively affect the development of young children born to mothers of low socio-economic class (low SES). It is unknown, however, to what extent can an enriched environment improve the developmental outcome of children born with slight brain damage. We studied the development of preschool and early school age children born to heroin dependent parents raised at home or adopted in comparison to children suffering only from environmental deprivation (low parental SES) and to controls. They were examined by several professionals, using standard, age appropriate, neurological and psychological tests. Similar evaluations were performed on a group of early school age children born to mothers with pregestational or with gestational diabetes and on a group of children born prematurely, with a birth weight of less than 1500 g using various developmental tests. Young children born to heroin dependent mothers and fathers raised at home and children of low SES had, in comparison to controls, lower intellectual skills and a higher rate of inattention. This persisted at school age, too. Children born to heroin dependent mothers adopted at a young age and hence being raised in a good environment had normal intellectual function but a high rate of inattention and behavioral problems. We also examined the school age children for possible presence of ADHD and found a high rate of ADHD among all children born to heroin dependent parents including those adopted, as well as in the children with low parental SES. Similar findings regarding the strong positive influence of an enriched environment were observed in children born to diabetic mothers, where the intellectual abilities of the children were directly related with parental education. The cognitive abilities of the children born prematurely were also strongly associated with parental education and not with the degree of perinatal complications. In conclusion, in all groups of children at high risk for developmental problems was found that the environment has a strong influence on their intellectual abilities but not on motor skills or attention span. A good environment (high parental SES) may significantly improve the outcome.

Child↗

PubMed1992

Neural development is regulated by classical neurotransmitters: dopamine D2 receptor stimulation enhances neurite outgrowth.

The classical neurotransmitters serotonin and dopamine are thought to be involved in the etiology or treatment of a variety of psychiatric disorders. Recent studies suggest that these neurotransmitters may also have roles as neural morphogens during brain development. Previously, we have demonstrated that stimulation of serotonin 5-HT1A receptors selectively inhibited neurite branching in an in vitro system (Sikich et al 1990). In the present study, the developmental role of dopamine D2 receptors in the control of neurite outgrowth has been investigated by quantitating the morphological response of cortical neurons to agonist stimulation in vitro. Cultures of fetal rat frontal, cortical neurons were shown to express both alternatively spliced forms of D2 receptor messenger RNA (mRNA). The larger mRNA form predominated (D2A444:D2A415 ratio of about 6:1). In a small but significant percentage of these neurons, culture in the presence of the D2 receptor selective agonist, quinpirole, resulted in a three-to ten-fold increase in the length of neurites and in the number of branch points per neurite. These effects were blocked by the D2 receptor antagonists eticlopride and spiperone. Early abnormalities in the stimulation of dopamine or serotonin receptor subtypes could lead to the types of neuroanatomical changes observed in studies of schizophrenia, bipolar affective disorder, and autism. These morphogenic effects of classical transmitters could unite neurodevelopmental and neurotransmitter theories of the etiology of severe psychiatric disorders.

Animals↗

PubMed1992

Effects of age and alcoholism on the prevalence of panic disorder.

Findings are reported evaluating the effects of aging and alcoholism histories on the 6-month prevalence rates of panic disorder. The data were collected in 5 communities as part of the Epidemiologic Catchment Area (ECA) study: New Haven, CT; Baltimore, MD; St. Louis, MO; Durham, NC; and Los Angeles, CA. Reanalysis of ECA data provided additional support for a decline in the prevalence of panic disorder among elderly people. In addition, the presence of a history of alcohol abuse or dependence was associated with significantly elevated panic disorder rates in younger individuals, but an earlier decline in panic disorder prevalence with age, regardless of gender. These findings offer preliminary support for neurodevelopmental hypotheses for the onset and outgrowing of panic disorder. They also highlight the impact of alcoholism on the course of panic disorder.

Adolescent↗

PubMed2006

Metallothioneins and zinc dysregulation contribute to neurodevelopmental damage in a model of perinatal viral infection.

Neonatal Borna disease (NBD) virus infection in the Lewis rat results in life-long viral persistence and causes behavioral and neurodevelopmental abnormalities. A hallmark of the disorder is progressive loss of cerebellar Purkinje and dentate gyrus granule cells. Findings of increased brain metallothionein-I and -II (MT-I/-II) mRNA expression in cDNA microarray experiments led us to investigate MT isoforms and their relationship to brain zinc metabolism, cellular toxicity, and neurodevelopmental abnormalities in this model. Real-time PCR confirmed marked induction of MT-I/-II mRNA expression in the brains of NBD rats (40.5-fold increase in cerebellum, p<0.0001; 6.8-fold increase in hippocampus, p=0.003; and 9.5-fold increase in striatum, p=0.0012), whereas a trend toward decreased MT-III mRNA was found in hippocampus (1.25-fold decrease, p=0.0841). Double label immunofluorescence revealed prominent MT-I/-II expression in astrocytes throughout the brain; MT-III protein was decreased in granule cell neurons and increased in astrocytes, with differential subcellular distribution from cytoplasmic to nuclear compartments in NBD rat hippocampus. Modified Timm staining of hippocampus revealed reduced zinc in mossy fiber projections to the hilus and CA3, accumulation of zinc in glial cells and degenerating granule cell somata, and robust mossy fiber sprouting into the inner molecular layer of the dentate gyrus. Zinc Transporter 3 (ZnT-3) mRNA expression was decreased in hippocampus (2.3-fold decrease, p= 0.0065); staining for its correlate protein was reduced in hippocampal mossy fibers. Furthermore, 2 molecules implicated in axonal pathfinding and mossy fiber sprouting, the extracellular matrix glycoprotein, tenascin-R (TN-R), and the hyaluronan receptor CD44, were increased in NBD hippocampal neuropil. Abnormal zinc metabolism and mechanisms of neuroplasticity may contribute to the pathogenesis of disease in this model, raising more general implications for neurodevelopmental damage following viral infections in early life.

Animals↗

PubMedDate not supplied

[Current issues on schizoaffective disorder].

Schizoaffective disorder is relatively common in clinical settings, with studies suggesting that the disorder accounts for 10-30% of admissions to inpatients mental health facilities for functional psychosis. Lifetime prevalence is estimated to be between 0.5 and 0.8%. Since its initial description by Kasanin in 1933, the concept has undergone many changes, moving on from that of acute psychosis toward a position located between affective and schizophrenic disorder. In current classification systems this position seems to be closer to the latter one. However DSM IV and ICD-10 differ according to the nature of symptoms, especially the psychotic ones, and the temporal relationship of the psychotic symptoms to the mood symptoms. Psychotic features may include paranoid, cognitive and negative symptoms but mood-congruent and mood-incongruent psychotic features can also be found during mood episodes. The disorder has an episodic course and a prognosis usually intermediate between that of schizophrenia and affective disorder. It has been commonly subtyped into a bipolar and a depressive type, but more recently a division into a concurrent and a sequential type has been proposed too, based on longitudinal findings. Family studies using current diagnostic criteria show that the pattern of illness in relatives suggests that schizoaffective probands may have as high a familial liability to schizophrenia and affective illness as do those probands with only one of the disorders. In addition to biological and neuroendocrine investigation, schizoaffective disorder has been addressed in some neuroimaging, neuropathological, cognitive and neurodevelopmental studies which tend however to confirm its location between the two disorders, but closer to the schizophrenic pole. Several hypotheses have been proposed to account for the nature of schizoaffective disorder. Current data tend to favor the ranging of the disorder within a unitary spectrum of functional psychosis the diathesis of which could be activated by an episode of mood disorder. In contrast to the extensive research devoted to the development of pharmacologic agents for the treatment of schizophrenia and mood disorders, the optimal pharmacological treatment of schizoaffective disorder has been relatively unstudied which may, for instance, explain the lack of treatment guidelines. Nonetheless, despite the paucity of data in this area, some authors recommend the use of atypical anti-psychotics alone or in combination treatment as first line medi-cations both for the short and long term treatment. Research on schizoaffective disorder has been marred by the variability of its definition. Even if doubts have been expressed about the reliability of current diagnostic criteria, they seem to define a syndrome that differs meaningfully from both schizophrenia and affective disorder. Further studies are however still necessary, especially with regard to the subtyping of the disorder and its pharmacological treatment.

Diagnostic and Statistical Manual of Mental Disord↗

PubMed1999

Motor disorders and attention-deficit/hyperactivity disorder.

Motor and perceptual output problems were associated with hyperactivity before ADHD was described in North America. Many European pediatricians continue to consider these deficits along with inattention and hyperactivity to be part of one disorder. Motor deficits are an associated neurodevelopmental deficit in a substantial number of ADHD patients. In order for the patients' need to be addressed, pediatricians must be able to recognize motor coordination deficits and make appropriate recommendations to the patients' caregivers.

Apraxias↗

PubMed2026

Effectiveness of Caregiver-Mediated Spoken Language Interventions for Children Under Five at Risk of Developmental Language Disorder: A Systematic Review and Meta-Analysis.

BACKGROUND AND AIMS: Caregiver-mediated interventions are commonly used by Speech and Language Therapists to support early language development. Developmental Language Disorder (DLD) is associated with reduced quality of life throughout the lifespan. Understanding factors that predict intervention success is essential for developing appropriate, cost-effective therapy provision for the approximately 12% of preschool children who present with early markers for Developmental Language Disorder (DLD). This systematic review and meta-analysis examined the effectiveness of caregiver-mediated spoken language interventions for under-fives at risk of DLD, and factors influencing intervention effectiveness. METHODS: A systematic review following PRISMA guidelines was conducted. Five electronic databases were searched to identify experimental studies comparing caregiver-mediated spoken language interventions to control conditions in under-fives presenting with risk factors for DLD. Risk factors included prematurity, socioeconomic factors, caregiver language development concerns, and formal or informal language screening or assessment scores. Twenty-six experimental studies with 1407 child participants were included in qualitative synthesis. Meta-analysis was performed on nine Randomised Controlled Trials involving 947 children. RESULTS: Effectiveness was examined for outcomes including child language gains, child wellbeing, inclusion and attainment. Meta-analysis indicated a significant effect of caregiver-mediated spoken language interventions on language outcomes compared to treatment-as-usual, non-language intervention or waitlist control conditions. Non-language outcomes were evaluated via qualitative synthesis. Interventions significantly improved language development trajectories for under-fives presenting with risk factors or early markers for DLD. CONCLUSION AND IMPLICATIONS: This review contributes to the growing evidence base demonstrating that caregiver-mediated interventions can positively impact language development and wellbeing outcomes for children under five at risk of DLD. These findings support the implementation of caregiver-mediated environmental language interventions in clinical practice to maximise accessibility and cost-effectiveness while delivering optimal outcomes for vulnerable populations. WHAT THIS PAPER ADDS: What is already known on this subject Previous research on caregiver-mediated spoken language interventions has highlighted gaps in the evidence regarding the impact of risk factors, demographic characteristics, dosage and intervention components on child language outcomes. Developmental Language Disorder has relatively high population prevalence, estimated at 7%. Prevalence is associated with risk factors including low household socioeconomic status (SES), prematurity and late language emergence. In contrast to its prevalence, there is low public and professional awareness of DLD and a low diagnostic rate. Therefore, a strengthened evidence base and additional insights into the factors affecting success of family-based interventions is important in order to increase the effectiveness of service provision and care planning for this underserved population. Timely and effective intervention with young children presenting with early markers for DLD has the potential to offer lifelong improvement to their wellbeing, inclusion and attainment outcomes. Recent systematic reviews of the effectiveness of caregiver-mediated language interventions had differences in population age range and diagnostic inclusion criteria. What this paper adds to existing knowledge Our review examines the effectiveness of caregiver-mediated early spoken language interventions on child language, attainment and wellbeing, and on caregiver self-efficacy and adherence to language support strategies. Our population was children under five presenting with risk factors for Developmental Language Disorder, in the absence of other neurodevelopmental or genetic conditions such as intellectual disability or autism. This review adds depth and detail to the evidence base supporting the effectiveness of caregiver-mediated spoken language interventions in improving outcomes for this population of young children, and factors that influence their success. What are the potential or actual clinical implications of this work? The high prevalence of Developmental Language Disorder, estimated at around 7% of the population, and the strong association with risk factors including low SES, prematurity and late language emergence, coupled with the low awareness of DLD and low diagnostic rate, mean that a strengthened evidence base and additional insights into the factors affecting success of family-based interventions can increase the effectiveness of service provision and care planning for this population. Timely and effective intervention in this group of young children has the potential to improve wellbeing and attainment outcomes across the lifespan. This review contributes to our understanding of how to implement cost-effective, socially valid and maximally engaging partnership working with families of young children at risk for DLD.

Humans↗