Abstract / Summary
Abstract Background Space-occupying cerebellar infarction is a potentially fatal neurological condition because progressive edema within the restricted posterior fossa may cause fourth ventricular obstruction, acute hydrocephalus, brainstem compression, and herniation. Suboccipital decompressive craniectomy is recommended when neurological deterioration or radiological evidence of mass effect develops. However, the potential benefit of surgery after severe deterioration remains an important clinical consideration. Case presentation: A 49-year-old woman with systemic arterial hypertension and obesity developed an acute reduction in consciousness and progressive neurological deterioration approximately 48 hours before admission to a specialized center. She required orotracheal intubation for airway protection, and her Glasgow Coma Scale score was below 9. Cranial computed tomography demonstrated an extensive left cerebellar infarction with marked edema, compression of the fourth ventricle, obstructive hydrocephalus, and brainstem compression. She underwent urgent suboccipital decompressive craniectomy combined with external ventricular drainage. Neurological improvement was observed during the early postoperative period. On the second postoperative day, her Glasgow Coma Scale score increased to 13, spontaneous movement of all four limbs was present, and she was successfully extubated. The external ventricular drain was removed on the sixth postoperative day. She was discharged with a Glasgow Coma Scale score of 15 and no focal neurological deficits. Conclusions Suboccipital decompressive craniectomy may provide substantial neurological benefit in selected patients with space-occupying cerebellar infarction, even after severe impairment of consciousness, provided that irreversible brainstem injury has not occurred. Surgical decisions should integrate the neurological examination, radiological evidence of posterior fossa mass effect and hydrocephalus, clinical progression, and the presumed viability of the brainstem rather than relying exclusively on the time elapsed since symptom onset.