Abstract:
Background: Early neurological assessment in infancy aims to identify infants at risk for Cerebral Palsy (CP) through the evaluation of tone, posture, and early motor patterns. Among these assessments, the Hammersmith Infant Neurological Examination (HINE) is widely used as a standardized tool, providing defined cut-offs to determine CP risk. However, during the first months of life, neurological examination may be influenced by conditions transiently altering the expression of postural control, in the absence of consistent structural brain damage. Gastroesophageal Reflux (GER) is a common clinical finding in infants with central hypotonia and is well documented in the literature, especially among children with genetic syndromes characterized by early neuromotor vulnerability, including Down syndrome and Prader-Willi syndrome. Its role in transiently modifying the clinical expression of early neurological signs and potentially complicating their interpretation during infancy remains undefined.
Objective: To investigate the relationship between HINE findings—particularly tone- and posture-related items—and the presence of GER, and to explore whether GER-related symptomatology may mimic early signs of cortical motor impairment, potentially suggesting an increased risk for CP.
Methods: We conducted a retrospective observational study including infants evaluated within the first year of corrected age, classified as low risk for CP, and presenting clinical symptoms of GER during infantile follow-up. Neurological examinations were analyzed with particular focus on HINE tone- and posture-related items. The internal coherence of neurological findings, the presence of axial–appendicular tone discrepancies, and longitudinal evolution were examined. Clinical features of GER and therapeutic interventions were documented.
Results: Preliminary data from 55 infants revealed a recurring neurological profile characterized by central hypotonia associated with incongruent postural and motor responses. Although baseline tone was reduced, several infants displayed abnormal postural reactions, extensor patterns, asymmetric responses, and altered axial control, particularly during pull-to-sit, ventral suspension, spontaneous posture, and selected passive tone items. These findings generated HINE scores and clinical patterns phenotypically compatible with early cortical or focal motor involvement, potentially simulating early indicators of cerebral palsy. Notably, these abnormalities lacked consistency across the neurological examination and demonstrated progressive improvement over time, particularly following the management of reflux-related symptoms.
Conclusions: Our findings are consistent with the hypothesis that, in infants with underlying hypotonia, gastroesophageal reflux may act as a neurological mimic, transiently interfering with postural control and tone expression. This interaction may generate neurological signs phenotypically resembling early cortical motor impairment and result in falsely pathological HINE scores suggestive of increased CP risk. Recognition of this mechanism may help clinicians interpret early neurological examinations more accurately and reduce the risk of false-positive prognostic assessments during infancy.
