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Homolateral hemiparesis as an early sign of cerebellar mass effect
K B Kanis1, A H Ropper, L S Adelman
1Neurology Service, St. Elizabeth's Medical Center, Boston, MA 02135.
Abstract:
A patient with Wallenberg's syndrome and an inferior cerebellar infarction developed progressive hemiplegia ipsilateral to the infarction as cerebellar edema emerged. An MRI showed diagonal displacement of the medulla with impaction of the pyramids against the clivus; the hemiplegia resolved after posterior fossa decompression. In the pathologic specimen, the pyramids were flattened and showed small subpial ischemic lesions. Progressive ipsilateral hemiparesis in the setting of cerebellar infarction is an early sign of posterior fossa mass effect similar to the Kernohan's notch phenomenon.
Insights
Progressive hemiplegia following cerebellar infarction can indicate posterior fossa mass effect. Surgical decompression resolved symptoms, highlighting the importance of early recognition in Wallenberg's syndrome cases.
Area of Science:
- Neurology
- Neuroscience
- Neurosurgery
Background:
- Wallenberg's syndrome, characterized by brainstem and cerebellar signs, can arise from cerebellar infarction.
- Cerebellar edema following infarction can lead to significant mass effect within the posterior fossa.
Observation:
- A patient with Wallenberg's syndrome and inferior cerebellar infarction presented with progressive ipsilateral hemiplegia.
- Cerebellar edema was observed to cause diagonal displacement of the medulla and pyramidal impaction against the clivus on MRI.
Findings:
- Pathologic examination revealed flattened pyramids with subpial ischemic lesions.
- The patient's hemiplegia resolved completely after undergoing posterior fossa decompression surgery.
Implications:
- Progressive ipsilateral hemiparesis in cerebellar infarction may be an early indicator of posterior fossa mass effect.
- This presentation is analogous to Kernohan's notch phenomenon, emphasizing the need for prompt neurosurgical evaluation.
- Posterior fossa decompression is an effective treatment for resolving mass effect-induced neurological deficits in cerebellar infarction.