Expected Examination Finding: Dyskinetic (Choreoathetotic) Cerebral Palsy
The expected finding in an infant with a history of jaundice and neurological sequelae is dyskinetic (choreoathetotic) cerebral palsy, not spastic or hypotonic findings. 1, 2
Neurological Sequelae of Chronic Bilirubin Encephalopathy (Kernicterus)
The chronic form of bilirubin encephalopathy, termed kernicterus, presents with a characteristic pattern of neurological findings:
Primary Motor Manifestations
- Severe athetoid (choreoathetotic) cerebral palsy is the hallmark motor finding 1, 2
- This dyskinetic movement disorder distinguishes kernicterus from other forms of cerebral palsy that typically present with spasticity 1, 2
Associated Neurological Features
- Auditory dysfunction including sensorineural hearing loss 1, 2
- Paralysis of upward gaze (vertical gaze palsy) 1, 2
- Dental-enamel dysplasia 1, 2
- Intellectual deficits and other cognitive handicaps (less common) 1
Clinical Context and Pathophysiology
Acute Phase Progression
During the acute phase of bilirubin encephalopathy, infants may initially present with hypotonia and lethargy in the early stage 1, 2. However, this progresses to hypertonia with backward arching (retrocollis and opisthotonus) in the intermediate phase 1, 2. The chronic sequelae that develop after survival represent permanent neurological damage, characterized by the dyskinetic movement pattern rather than persistent hypotonia 1, 2.
Important Clinical Distinction
- The question asks about an infant who previously had jaundice with neurological sequelae, indicating chronic findings 1, 2
- Hypotonia may be seen acutely during the early phase of bilirubin toxicity, but is not the chronic sequela 1, 2
- Spastic cerebral palsy is not characteristic of kernicterus and suggests alternative etiologies 1, 2
Key Clinical Pitfall
Do not confuse the acute presentation with chronic sequelae. While hypotonia may appear during the early acute phase of bilirubin encephalopathy, the established chronic neurological damage manifests as dyskinetic/choreoathetotic movements, not persistent hypotonia or spasticity 1, 2. The specific pattern of basal ganglia injury from bilirubin toxicity produces the characteristic extrapyramidal movement disorder 1, 2.