Developmental delay in early childhood may affect motor, language, cognitive, adaptive and personal-social domains. Developmental assessment describes the child’s current functional level, guides early intervention and supports etiologic evaluation; it does not by itself identify the cause.^1–3

Perinatal and neonatal insults—including hypoxic–ischemic injury, prematurity, infection and severe jaundice—may adversely influence neurodevelopment. Their contribution varies by population and quality of obstetric and neonatal care, and associations in clinic-based studies may be distorted by referral patterns and retrospective recall.^4–7

This manuscript focuses on the developmental phenotype and perinatal correlates in children already identified with developmental delay. Its objective was to describe DQ severity and evaluate associations with recorded antenatal, intranatal and neonatal factors. MRI findings and MRI–clinical correlations are intentionally excluded to prevent overlap with the companion imaging article.

METHODS

Study design and setting: This descriptive cross-sectional study was performed at Chacha Nehru Bal Chikitsalaya, affiliated with Maulana Azad Medical College, Delhi over one year.

Participants: Children aged 6 months to 5 years attending the outpatient, pediatric neurology or child development clinics were eligible when developmental delay was the primary complaint and had begun in the first year of life. Clinically apparent or strongly suspected neurodegenerative disorders and delay secondary to non-cerebral chronic or acquired conditions were excluded. Seventy-eight children were enrolled.

Developmental assessment: Development was assessed using Gesell-based clinical methods across motor, adaptive/fine-motor, language and personal-social domains. Developmental age was estimated and DQ calculated as developmental age divided by chronological age ×100. The DQ was grouped as <20, 20–49, 50–70 and >70.

Perinatal variables: Structured history covered gestation, antenatal problems, delivery, intranatal events, neonatal complications and selected family and past history. Because several events could coexist, antecedent frequencies were not mutually exclusive.

Statistical analysis: Results are summarized as mean, median with interquartile range (IQR), number and percentage. DQ distributions between children with and without each clinical feature were compared using two-sided Mann–Whitney U tests because DQ was non-normally distributed in several subgroups. A p value <0.05 was considered statistically significant. Analyses were reconstructed from all 78 master-chart records.

Ethical considerations: Ethics approval was obtained from the IEC of Maulana Azad Medical College, Delhi.

RESULTS

Table 1. Age and sex distribution of participants (n=78)

Table 2. Chronological age, developmental age and developmental quotient by age group

Table 3. Distribution of developmental quotient (n=78)

Table 4. Recorded possible antecedents of developmental delay

Table 5. Developmental quotient according to clinical and perinatal features

Two-sided Mann–Whitney U tests applied. IQR, interquartile range.

DISCUSSION

The cohort showed substantial developmental impairment: three quarters of children had DQ 20–49 and the overall mean DQ was approximately 40. The lower mean DQ in older age groups may reflect delayed referral, increasing divergence from age expectations, survival or referral selection, or measurement limitations; the cross-sectional design cannot distinguish these explanations.

Birth asphyxia was the most frequently recorded antecedent, followed by prematurity/low birth weight and fetal distress. Prospective work in low- and middle-income settings has demonstrated adverse developmental trajectories after birth asphyxia, while outcomes after prematurity vary with gestational age, neonatal morbidity and access to follow-up and early intervention.^5–7

Although children with birth asphyxia had a numerically lower median DQ, the difference was not statistically significant (p=0.094). The only significant subgroup difference was a lower DQ among children with abnormal motor findings (p=0.037), a clinically coherent association because motor function contributes directly to the developmental phenotype and to Gesell-based performance.

Aetiologic evaluation of developmental delay increasingly prioritizes careful phenotyping, hearing and vision assessment, chromosomal microarray and genomic testing when appropriate, with targeted metabolic testing and neuroimaging based on clinical clues. Regardless of etiology, timely referral for early intervention should proceed in parallel with diagnostic investigation.^1–3

LIMITATIONS

This was a small, single-centre, referral-based cross-sectional study without a typically developing comparison group. Perinatal exposures were largely history based and potentially overlapping. Domain-specific developmental results, assessor reliability and instrument standardization were not reported. Several subgroup comparisons were exploratory and no correction was made for multiple testing. The cross-sectional design precludes causal inference, and multivariable modelling was not justified by the modest sample and event distribution.

CONCLUSION

Most children in this specialist-clinic cohort had marked developmental impairment, with DQ 20–49 forming the largest group. Abnormal motor findings were associated with lower DQ, whereas birth asphyxia, neonatal complications, prematurity and seizures were not significantly associated with DQ in the patient-level reanalysis. The results support structured developmental surveillance and early intervention while cautioning against assigning developmental severity to individual perinatal antecedents from this cross-sectional dataset.

ACKNOWLEDGEMENT

The authors gratefully acknowledge Dr. Bibek Talukdar, Department of Pediatric Neurology, Maulana Azad Medical College, Delhi; the faculty and staff of the Department of Pediatrics, Radiodiagnosis, and Neurology at Chacha Nehru Bal Chikitsalaya, Maulana Azad Medical College, Delhi that supported the clinical and radiological evaluation of the children. The authors sincerely acknowledge Dr Shailendra Vashistha (Assistant Professor, Transplant Immunology HLA Lab, Dept of IHTM, GMC, Kota) for his valuable guidance in scientific manuscript preparation and the VAssist Research Team (www.thevassist.com) for assistance with manuscript formatting and technical support. The authors wholeheartedly thank all participating children and their parents or guardians.

CONFLICT OF INTEREST: None declared.

SOURCE OF FUNDING: Nil.

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