2025 Poster Presentations
P129: CYSTIC MASS IN THE CEREBELLOPONTINE ANGLE AFTER PRIOR VESTIBULAR SCHWANNOMA RESECTION IN SETTING OF NEWLY DIAGNOSED HIV
Krish Suresh, MD; Erika Woodson, MD; Southern California Permanente Medical Group
We present the case of a 67-year-old gentleman who presented with a new mass of the cerebellopontine angle after prior definitive treatment of vestibular schwannoma (VS). The patient originally underwent Cyberknife radiosurgery for a right-sided 3.2 cm VS in 2011. He had local control with tumor shrinkage until MRI in 2016 demonstrated abrupt cystic enlargement of the tumor to 3.7 cm. The patient underwent gross total resection via translabyrinthine craniotomy in 2016, with no atypical cells on pathology. Subsequent MRIs demonstrated no residual or recurrent tumor for six years.
In July of 2024, the patient developed acute-onset right facial numbness, facial palsy, and ataxia. MRI revealed a complex cystic mass in the cerebellopontine angle (CPA), characterized by peripheral enhancement, central diffusion restriction, vasogenic edema and invasion of the adjacent fat graft, pons and middle cerebellar peduncle (Figure 1). These findings were concerning for malignant degeneration of the patient’s prior VS, with differential diagnosis including other malignancy, inflammatory process, and infectious process. Concurrent medical conditions delayed immediate plans for biopsy, including Shigella and Clostridium difficile infections. Throughout this course, he received a few one-time doses of IV antibiotics in the preliminary phases of his hospitalizations; the Shigella was not treated and the only long-term antibiotics he took were oral vancomycin and fidaxomicin for the C. diff. He was started on glucocorticoids for the facial weakness. Despite this, the patient’s facial paralysis progressed to include the contralateral side. Interval imaging demonstrated improved appearance of the cystic component in the extracranial fat graft, but progressive leptomeningeal involvement along the pons (Figure 2). Further medical workup revealed a new diagnosis of HIV with a high viral load and depleted T cell count, and the patient was rapidly initiated on antiretroviral therapy in addition to the steroids. Subsequent imaging revealed near-total resolution of the mass with disappearance of the cystic component and return of fat signal in the mastoid cavity, and only a small residual focus of enhancement in the medial aspect of the surgical bed (Fig 3).
This patient’s presentation presents a diagnostic dilemma. Initially, radiation-induced malignant degeneration of the patient’s prior VS was felt most likely due to the invasive imaging characteristics and diagnosis of HIV, which is pathogenetically linked to development of malignancy. Complete response to steroid treatment, however, would not be anticipated from a sarcomatous lesion. An infectious process such as a brain abscess was also considered. However, this similarly would not be expected to resolve in an immunocompromised patient without targeted prolonged antibiotic therapy. We believe the most likely diagnosis in this case is central nervous system lymphoma (CNSL). CNSL has been described to present with “sentinel lesions”, transient symptomatic contrast enhancing lesions that may recede spontaneously, with glucocorticoid treatment, or possibly due to host immunity in setting of antiretroviral therapy. Furthermore, CNSL is considered to be an AIDS-defining illness. Further work-up is underway with consideration of biopsy vs. CSF analysis pending clinical progress and stabilization.
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