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Basal ganglia echogenicity in preterm infants: A case series

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BACKGROUND: Damage to the basal ganglia and thalamus (BGT) can be caused by multiple perinatal factors and may be associated with movement disorders, cognitive delay and visual difficulties. Changes in BGT structure, seen as echogenicity on ultrasound, are difficult to objectively quantify. The aetiology, clinical relevance and developmental outcomes of BGT echogenicity are poorly understood. We aimed to gain a better understanding of the natural history of BGT echogenicity in a preterm population. METHODS: Retrospective review of clinical course, neuroimaging and development in infants born <32weeks gestation over 5 years with evidence of BGT echogenicity. RESULTS: BGT echogenicity was reported in 18/650 infants (2.7%). Echogenicity appeared at a median of 8 days (2–45 days) and resolved on pre-discharge ultrasound in 50%. Thirteen infants had a term corrected MRI brain with abnormal BGT signal seen in 3 infants (23%). All 3 infants had persisting echogenicity on discharge ultrasound. No infant with echogenicity resolution on ultrasound had changes on term MRI. 14 infants had developmental progress available at 1 year corrected. Abnormal development was reported in four children of whom one had BGT changes on term MRI. Two children with persistent BGT changes but an otherwise normal MRI had reported normal neurodevelopment. CONCLUSION: BGT echogenicity is relatively common on routine ultrasound and resolves in the majority of infants by term corrected. This review suggests that at term corrected, normal cranial ultrasound may obviate the need for MRI where no other concerns exist. BGT echogenicity did not appear to independently influence neurodevelopment.
Title: Basal ganglia echogenicity in preterm infants: A case series
Description:
BACKGROUND: Damage to the basal ganglia and thalamus (BGT) can be caused by multiple perinatal factors and may be associated with movement disorders, cognitive delay and visual difficulties.
Changes in BGT structure, seen as echogenicity on ultrasound, are difficult to objectively quantify.
The aetiology, clinical relevance and developmental outcomes of BGT echogenicity are poorly understood.
We aimed to gain a better understanding of the natural history of BGT echogenicity in a preterm population.
METHODS: Retrospective review of clinical course, neuroimaging and development in infants born <32weeks gestation over 5 years with evidence of BGT echogenicity.
RESULTS: BGT echogenicity was reported in 18/650 infants (2.
7%).
Echogenicity appeared at a median of 8 days (2–45 days) and resolved on pre-discharge ultrasound in 50%.
Thirteen infants had a term corrected MRI brain with abnormal BGT signal seen in 3 infants (23%).
All 3 infants had persisting echogenicity on discharge ultrasound.
No infant with echogenicity resolution on ultrasound had changes on term MRI.
14 infants had developmental progress available at 1 year corrected.
Abnormal development was reported in four children of whom one had BGT changes on term MRI.
Two children with persistent BGT changes but an otherwise normal MRI had reported normal neurodevelopment.
CONCLUSION: BGT echogenicity is relatively common on routine ultrasound and resolves in the majority of infants by term corrected.
This review suggests that at term corrected, normal cranial ultrasound may obviate the need for MRI where no other concerns exist.
BGT echogenicity did not appear to independently influence neurodevelopment.

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