Global or multidomain developmental delay is a clinical descriptor rather than a single etiologic diagnosis. A structured history, neurological examination, hearing and vision assessment, and appropriately selected genetic, metabolic and neuroimaging investigations are therefore central to evaluation.^1–3

MRI provides superior delineation of cortical malformations, white-matter injury, commissural abnormalities and sequelae of perinatal insults. Its yield is higher in clinically selected children with abnormal head circumference, focal neurological signs, seizures or an abnormal neurological examination than in unselected populations.^1,4–6

The present study evaluated the spectrum of structural brain MRI findings in young children with neurodevelopmental delay and examined whether abnormal MRI was associated with neonatal antecedents and clinically observable neurological features. Developmental-quotient analyses are intentionally reserved for a separate manuscript to prevent duplicate publication of tables and outcomes.

METHODS

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

Participants: Seventy-eight children aged 6 months to 5 years were enrolled from the outpatient department, pediatric neurology clinic and child development clinic. Eligible children had developmental delay as the primary complaint with onset in the first year of life. Children with clinically apparent or strongly suspected neurodegenerative disease, and delay secondary to non-cerebral chronic or acquired conditions, were excluded.

Clinical and imaging assessment: Each child underwent structured antenatal, intranatal, neonatal, developmental and family history-taking and detailed physical and neurological examination. All children underwent 1.5-T brain MRI using T1-weighted, T2-weighted and FLAIR sequences. More than one MRI category could be assigned to a child; therefore category percentages are not mutually exclusive and may total more than 100%.

Statistical analysis: Categorical data are presented as frequency and percentage. Patient-level 2×2 tables were constructed from the master data collected. Fisher exact tests were used because several expected cell counts were below five. All tests were two-sided and p<0.05 was considered statistically significant.

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

RESULTS

The cohort comprised 58 boys (74.4%) and 20 girls (25.6%); 48 children (61.5%) were aged 13–36 months. Seventy children had at least one abnormal MRI finding, giving an imaging abnormality rate of 89.7%. Specific abnormalities included diffuse cerebral cortical atrophy (n=33), encephalomalacia/gliosis (n=13), periventricular leukomalacia (n=18), prominent white-matter hyperintensity (n=37), and less frequent migrational disorders, leukodystrophy patterns, kernicterus, tuberous sclerosis, Leigh-pattern changes and hydrocephalus.

Table 1. Spectrum of structural brain MRI findings (n=78)

Categories are non-mutually exclusive.

Table 2. Neonatal complications in relation to MRI status

Rows are not mutually exclusive because a child could have more than one neonatal complication.

Table 3. Motor examination pattern in relation to MRI status (n=78)

Table 4. Patient-level associations with abnormal MRI

Two-sided Fisher exact tests applied.

DISCUSSION

The principal finding was a high prevalence of MRI abnormality (89.7%) in a tertiary, clinically selected cohort. This proportion should not be interpreted as the yield of routine screening in all children with developmental delay: referral enrichment, the requirement for delay beginning in infancy and the high frequency of motor abnormalities increase the pre-test probability of structural disease. Systematic review evidence similarly shows marked heterogeneity in MRI yield according to case selection and imaging technique.^3,6

White-matter abnormalities, corpus-callosal thinning and cortical abnormalities were the dominant patterns. Such findings are biologically compatible with perinatal white-matter injury, hypoxic–ischemic injury and developmental malformation, but an imaging pattern alone does not establish causation. MRI interpretation should be integrated with timing of exposure, neonatal course, examination and—where indicated—genetic or metabolic testing.^2,5,7

The concentration of abnormal MRI among children with quadriparesis, diplegia and hemiparesis supports targeted imaging when focal or pyramidal motor signs are present. Practice parameters for cerebral palsy and developmental delay likewise support neuroimaging when an etiology has not been established, with MRI preferred to CT because of its superior anatomical resolution and absence of ionizing radiation.^1,8

Birth asphyxia and neonatal complications were associated with abnormal MRI. These associations require cautious interpretation: histories may be subject to recall error, exposures overlapped, the cohort had no typically developing comparison group, and the cross-sectional design cannot establish causality. Furthermore, the source terminology “birth asphyxia” was based on recorded history rather than a contemporary composite definition incorporating cord gases, Apgar scores and encephalopathy staging.

LIMITATIONS

This was a single-centre study with a modest, referral-enriched sample. MRI reporting was category based. Several imaging categories overlapped.

CONCLUSION

Structural brain MRI abnormalities were common in young children with neurodevelopmental delay selected from specialist clinics. White-matter abnormalities, corpus-callosal thinning and cortical abnormalities predominated. Adverse neonatal histories and focal motor deficits identified children with particularly high proportions of abnormal imaging. These data support clinically targeted MRI as part of a broader etiologic assessment, while underscoring that imaging patterns must be interpreted alongside the clinical phenotype and verified perinatal history.

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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