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Published on: January 17, 2013
Basilar Artery Vasospasm as a Cause of Post-Operative Cerebellar Mutism Syndrome
Marwa Deghedy1, Barry Pizer1, Ram Kumar2
1Department of Oncology, Alder Hey Children's NHS Foundation Trust, Eaton Road, Liverpool L12 2AP, UK.
Insights
Post-operative cerebellar mutism syndrome (CMS) in children can be caused by basilar artery vasospasm, a rare finding. Early vascular imaging and treatment led to rapid recovery in a pediatric patient.
Area of Science:
- Pediatric Neurosurgery
- Neurocritical Care
- Neuroradiology
Background:
- Post-operative cerebellar mutism syndrome (CMS), or posterior fossa syndrome (PFS), is a common complication following posterior fossa tumor resection in children, with unclear pathophysiology.
- Existing research suggests potential mechanisms like axonal damage, edema, or perfusion defects, but MRI has not identified a consistent anatomical cause.
Observation:
- A 16-year-old boy developed CMS three days after medulloblastoma resection, with initial imaging revealing a posterior fossa hematoma requiring evacuation.
- Subsequent CT angiography and MRI angiography demonstrated basilar artery vasospasm linked to a cerebellopontine angle hematoma.
Findings:
- The patient received nimodipine and hypervolemia, leading to the reversal of radiological lesions and the return of vocalization without speech within five days.
- Neurological deficits gradually improved over several months, indicating a favorable prognosis after targeted treatment.
Implications:
- This case highlights basilar artery vasospasm as a rare but treatable cause of pediatric CMS, emphasizing the importance of early vascular imaging in select cases.
- The findings suggest that prompt diagnosis and intervention for vasospasm can significantly improve outcomes for children experiencing post-operative cerebellar mutism.
Abstract:
Post-operative cerebellar mutism syndrome (CMS), also known as posterior fossa syndrome (PFS), is a well-recognized and frequent complication of surgery for posterior fossa tumours in children and young people. Its incidence varies between 8 and 31%, and the pathophysiological mechanisms of delayed onset and resolution of cerebellar mutism are not clear, but axonal damage, oedema, and perfusion defects may be involved. Magnetic resonance imaging has failed to reveal a universal anatomical substrate or a single definite mechanism of injury. We present a case of 16-year-old boy who developed CMS three days after resection of a medulloblastoma, a primary fourth ventricular tumour. Early post-operative imaging showed bleeding in the posterior fossa which required evacuation. CT angiography seven days after surgery demonstrated basilar artery vasospasm. Magnetic resonance brain angiography confirmed persistent narrowing of a segment of the basilar artery closely related to a left cerebellopontine (CP) angle peri-operative haematoma. The patient was treated with nimodipine and hypervolemia. The patient started vocalisation without speech five days later with reversal of radiological lesions. Further recovery of post-operative neurological deficits occurred over a protracted period of several months. This case represents a rare cause of post-operative CMS, with rapid initial recovery that occurred after specific treatment directed at the cause. To our knowledge, this is the first reported case showing mutism associated with basilar artery vasospasm with imaging evidence. This case may suggest the need to undertake urgent vascular imaging in selected cases of post-operative CMS.
