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Background: Oculomotor nerve palsy is often associated with diabetes mellitus or caused by compression by a cerebral aneurysm. Here, we report a rare case of oculomotor nerve palsy caused by compression by the posterior cerebral artery (PCA). Case Description: A 66-year-old woman suddenly developed diplopia and right blepharoptosis. Her symptoms suggested incomplete right oculomotor nerve palsy. Magnetic resonance imaging showed that a sharp curve in the right PCA had compressed the right oculomotor nerve. Microvascular decompression surgery was performed. Intraoperative findings showed that the P2 portion of the PCA had caused an indentation in the oculomotor nerve in the prepontine cistern. The transposition of the PCA with a prosthesis released the pressure. After the operation, her right blepharoptosis gradually improved. She had fully recovered by 48 days after the operation. Conclusion: Neurovascular compression (NVC) is recognized as the cause of hemifacial spasms, trigeminal neuralgia, and glossopharyngeal neuralgia. This case report demonstrated that NVC can also cause oculomotor nerve palsy. A high index of clinical suspicion can detect vascular compression of the oculomotor nerve. Prompt diagnosis and appropriate surgical management can achieve clinical improvement. [ABSTRACT FROM AUTHOR]

Background: Cryptococcal meningoencephalitis (CM) causes cerebral infarction, typically, lacunar infarction in the basal ganglia. However, massive cerebral infarction leading to death is rare and its pathophysiology is unclear. We report a case of CM causing massive cerebellar infarction, which led to cerebral herniation and death.Case Presentation: A 56-year-old man who suffered from dizziness and gait disturbance for one month was admitted to our hospital and subsequently diagnosed with a cerebellar infarction. He had a past medical history of hepatitis type B virus infection and hepatic failure. Although the findings on magnetic resonance imaging (MRI) imitated an arterial infarction of the posterior inferior cerebellar artery, an accompanying irregular peripheral edema was observed. The ischemic lesion progressed, subsequently exerting a mass effect and leading to impaired consciousness. External and internal decompression surgeries were performed. Cryptococcus neoformans was confirmed in the surgical specimen, and the patient was diagnosed with CM. In addition, venule congestion in the parenchyma was observed with extensive fibrosis and compressed veins in the subarachnoid space. The patient died 26 days after admission. Autopsy revealed that pathological changes were localized in the cerebellum.Conclusion: C. neoformans can induce extensive fibrosis of the subarachnoid space, which may compress small veins mechanically inducing venule congestion and massive cerebral infarction. In such cases, the clinical course can be severe and even rapidly fatal. An atypical pattern of infarction on MRI should alert clinicians to the possibility of C. neoformans infection. [ABSTRACT FROM AUTHOR]