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Published on: June 11, 2020
Anatomic localization of dyskinesia in children with "profound" perinatal hypoxic-ischemic injury
P D Griffiths1, M R Radon, A R Crossman
1Academic Unit of Radiology, University of Sheffield, Sheffield, UK.
Insights
Injury to the subthalamic nucleus (STN) in newborns with hypoxic-ischemic brain damage (HIBD) is linked to later development of dyskinetic cerebral palsy (CP). This finding helps explain movement disorder variations in infants with HIBD.
Area of Science:
- Neurology
- Pediatrics
- Radiology
Background:
- Cerebral palsy (CP) is a common consequence of perinatal hypoxic-ischemic brain damage (HIBD).
- Understanding the specific brain injury patterns that lead to different types of CP, such as dyskinetic and spastic CP, is crucial for targeted interventions.
- The subthalamic nucleus (STN) is implicated in movement disorders, making it a key area of interest in HIBD research.
Purpose of the Study:
- To investigate the anatomical substrates of dyskinesia in children with CP resulting from acute profound hypoxic-ischemic injury.
- To identify specific brain injury sites that differentiate between dyskinetic and spastic CP.
- To specifically examine the role of the subthalamic nucleus (STN) in the development of movement disorders.
Main Methods:
- Retrospective review of MRI scans from 40 children diagnosed with CP due to acute profound hypoxic-ischemic injury.
- Standardized high-resolution MRI protocol using a 1.5T scanner.
- Analysis by two pediatric neuroradiologists, with logistic regression used to identify predictors of CP type.
Main Results:
- Children with dyskinetic CP showed more frequent injury to the STN, indicated by increased T2 signal intensity.
- Children with spastic CP exhibited more severe white matter damage near the paracentral lobule.
- Injuries to the putamen, caudate, and globus pallidus were not significant predictors of dyskinesia.
Conclusions:
- A significant association exists between hypoxic-ischemic injury to the STN at birth and the subsequent development of dyskinetic CP.
- This finding provides insight into the neurological basis for movement disorder variations in infants with HIBD.
Background And Purpose:
CP is a common feature of perinatal HIBD in the context of "acute profound" injury, and in this article, we have studied the possible anatomic substrates of dyskinesia. We have reviewed the extent of brain injury in children with dyskinetic and spastic CP due to acute profound hypoxia to identify sites of injury that explain why only some children develop movement disorders. It is known that the STN has a role in the development of movement disorders; therefore, we have specifically studied it.
Materials And Methods:
We retrospectively reviewed MR imaging of 40 consecutive children referred to our center with CP confirmed to be due to acute profound hypoxic-ischemic injury. All children received the same high-resolution MR imaging protocol with the same 1.5T scanner. Two pediatric neuroradiologists reviewed the imaging. Logistic regression was applied to identify multivariable predictors that differentiate dyskinetic and spastic CP.
Results:
Twenty children had dyskinetic CP and 20 had spastic CP. Children with dyskinetic CP had more frequent injury to the STN, as manifest by increased T2 signal intensity. Children with spastic CP had more severe damage to white matter in the vicinity of the paracentral lobule. Injuries to the putamen, caudate, and globus pallidus were not significant predictors of dyskinesia.
Conclusions:
We have shown an association between hypoxic-ischemic injury to the STN at birth and the emergence of dyskinesia later in life.
