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Published on: October 14, 2022
Slit-ventricle syndrome secondary to shunt-induced suture ossification
1Department of Neurosurgery, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA. albrigl@chplink.chp.edu
Insights
Children with slit-ventricle syndrome and shunt issues may develop shunt-induced craniostenosis. This condition, characterized by abnormal cranial sutures, can be treated with cranial expansion surgery.
Area of Science:
- Pediatric Neurosurgery
- Craniofacial Surgery
- Neurology
Background:
- Slit-ventricle syndrome can lead to increased intracranial pressure (ICP) even with functioning cerebrospinal fluid (CSF) shunts.
- This presentation is unusual and warrants further investigation into underlying causes.
Observation:
- Five children with slit-ventricle syndrome presented with elevated ICP despite functional CSF shunts.
- Imaging revealed cranial suture ossification and erosion of the inner table of the cranium.
- Absence of CSF over the cerebral convexities was noted on MRI.
Findings:
- Histological examination of removed sutures showed abnormal fibrous tissue with foci of cartilage and bone.
- Surgical intervention with cranial expansion operations resolved symptoms in all patients.
- The findings suggest a link between chronic CSF overdrainage and suture pathology.
Implications:
- Chronic CSF overdrainage may dampen cerebral pressure waves, leading to understimulation of calvarial growth and shunt-induced craniostenosis.
- Cranial expansion surgery may be a more effective treatment than subtemporal decompression for this specific condition.
- This study highlights the importance of considering shunt-induced craniostenosis in children with slit-ventricle syndrome and elevated ICP.
Objective:
To report five children with slit-ventricle syndrome who were found to have increased intracranial pressure despite functioning cerebrospinal fluid shunts.
Methods:
Computed tomographic scans demonstrated erosion of the inner table of the cranium and sclerosis of the cranial sutures, particularly the coronal suture. Magnetic resonance imaging scans demonstrated no cerebrospinal fluid over the convexities. The patients were treated with cranial expansion operations that included removal of the sclerotic sutures, which were examined histologically.
Results:
Postoperatively, symptoms resolved for all children. Sutures were abnormal and contained foci of cartilage and bone within abnormally arranged fibrous tissue.
Conclusion:
We postulate that chronic overdrainage of cerebrospinal fluid via shunts dampens the normal cerebral pressure waves; growth of the calvarium is thus understimulated, and this leads to ossification of the sutures, which become unable to expand to allow normal brain growth. Shunt-induced craniostenosis should be considered for children with symptoms of slit-ventricle syndrome for whom shunts are functional but intracranial pressure is increased. Cranial expansion operations may be more appropriate treatments than subtemporal decompressions for such children, given the diffuseness of the suture pathological features.
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