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Peer-reviewedCC BY-NC-SASurgical neurology international

Severe early postoperative brainstem infarction after vestibular schwannoma resection: A case report and literature review.

  1. 1Department of Neurosurgery, Hospital Ángeles Querétaro, Querétaro, Mexico.
  2. 2Centro Neurológico ABC, Hospital ABC Santa Fe, Santa Fe, Mexico City, Mexico.
  3. 3Department of General Surgery, Mexican Social Security Institute, Querétaro, Mexico.

Abstract

Background

Postoperative brainstem infarction is a rare and potentially devastating complication of vestibular schwannoma resection. While symptomatic arterial narrowing is recognized in other contexts, its role in posterior fossa tumor surgery remains poorly defined. We report a case of severe brainstem infarction and analyze the diagnostic challenges in instances where definitive vascular injury could not be confirmed.Case description

We report the case of a 36-year-old woman who developed severe neurological deterioration immediately after resection of a right cerebellopontine angle vestibular schwannoma. The procedure was uneventful, with no major intraoperative hemorrhage or vascular injury and minor subarachnoid blood contamination during tumor resection. Initial postoperative magnetic resonance imaging (MRI), including diffusion-weighted imaging, showed no hemorrhagic or ischemic lesions; however, repeat MRI with magnetic resonance angiography (MRA) on postoperative day 1 demonstrated right midbrain and upper pontine infarction associated with mild narrowing of the right posterior cerebral and superior cerebellar arteries. Because the vascular narrowing was modest and digital subtraction angiography, serial vascular imaging, and direct assessment of perforator involvement were unavailable, vasospasm was considered a possible but unconfirmed contributing mechanism. Alternative etiologies, including perforator injury, traction-related ischemia, microembolic phenomena, thrombosis, transient hypoperfusion, or early radiologically occult ischemia, could not be excluded. Despite intensive care management, including intravenous nimodipine, the patient developed severe persistent neurological deficits, with a Karnofsky Performance Status of 40 at 3-month follow-up.Conclusion

This case highlights the diagnostic complexity of severe early postoperative brainstem infarction. Mild posterior circulation narrowing on MRA may raise suspicion for a vascular-related process, but it should not be interpreted as definitive evidence of causality in the absence of digital subtraction angiography, serial vascular imaging, or direct assessment of perforator involvement. In patients with unexplained neurological deterioration after posterior fossa surgery, early vascular imaging and broad consideration of vascular and ischemic mechanisms are essential to guide management and avoid overattribution to a single pathophysiological process.

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BibTeX
@article{galeazzi2026severe,
  title = {{Severe early postoperative brainstem infarction after vestibular schwannoma resection: A case report and literature review.}},
  author = {Domingo Stefanoni Galeazzi and Gerardo Guinto and Gianfranco Stefanoni Pérez},
  journal = {Surgical neurology international},
  year = {2026},
  month = oct,
  doi = {10.25259/sni_168_2026},
  url = {https://europepmc.org/article/MED/42974569},
  note = {CC BY-NC-SA},
}
RIS
TY  - JOUR
TI  - Severe early postoperative brainstem infarction after vestibular schwannoma resection: A case report and literature review.
AU  - Domingo Stefanoni Galeazzi
AU  - Gerardo Guinto
AU  - Gianfranco Stefanoni Pérez
PY  - 2026
DA  - 2026/10/02
JO  - Surgical neurology international
DO  - 10.25259/sni_168_2026
UR  - https://europepmc.org/article/MED/42974569
AB  - Background  Postoperative brainstem infarction is a rare and potentially devastating complication of vestibular schwannoma resection. While symptomatic arterial narrowing is recognized in other contexts, its role in posterior fossa tumor surgery remains poorly defined. We report a case of severe brainstem infarction and analyze the diagnostic challenges in instances where definitive vascular injury could not be confirmed.Case description  We report the case of a 36-year-old woman who developed severe neurological deterioration immediately after resection of a right cerebellopontine angle vestibular schwannoma. The procedure was uneventful, with no major intraoperative hemorrhage or vascular injury and minor subarachnoid blood contamination during tumor resection. Initial postoperative magnetic resonance imaging (MRI), including diffusion-weighted imaging, showed no hemorrhagic or ischemic lesions; however, repeat MRI with magnetic resonance angiography (MRA) on postoperative day 1 demonstrated right midbrain and upper pontine infarction associated with mild narrowing of the right posterior cerebral and superior cerebellar arteries. Because the vascular narrowing was modest and digital subtraction angiography, serial vascular imaging, and direct assessment of perforator involvement were unavailable, vasospasm was considered a possible but unconfirmed contributing mechanism. Alternative etiologies, including perforator injury, traction-related ischemia, microembolic phenomena, thrombosis, transient hypoperfusion, or early radiologically occult ischemia, could not be excluded. Despite intensive care management, including intravenous nimodipine, the patient developed severe persistent neurological deficits, with a Karnofsky Performance Status of 40 at 3-month follow-up.Conclusion  This case highlights the diagnostic complexity of severe early postoperative brainstem infarction. Mild posterior circulation narrowing on MRA may raise suspicion for a vascular-related process, but it should not be interpreted as definitive evidence of causality in the absence of digital subtraction angiography, serial vascular imaging, or direct assessment of perforator involvement. In patients with unexplained neurological deterioration after posterior fossa surgery, early vascular imaging and broad consideration of vascular and ischemic mechanisms are essential to guide management and avoid overattribution to a single pathophysiological process.
SN  - 2229-5097
SN  - 2152-7806
ER  -