Leptomeningeal Carcinomatosis of Metastatic Primary Prostate
Leptomeningeal carcinomatosis continues to be a diagnostic challenge due to limited and varying sensitivities of diagnostic modalities used. However, the advances in MRI gadolinium imaging should place its findings equivalent or superior to lumbar puncture in terms of consistency, sensitivity, and risk to the patient.

Prognosis remains poor despite advances in therapies due to limited evidence from studies and variable/limited response to treatment that is limited by toxicity.

Understanding the molecular mechanisms of metastasis to the brain may help detect and evaluate better, focused therapies targeting tumor-specific molecular markers across different tumor types.

Early and prompt diagnosis will prolong life. Patients with hematologic or solid tumors who have clinical symptoms of leptomeningeal carcinomatosis warrant screening with routine cranial imaging.

A 65-year-old male with a past medical history of hypothyroidism, restless leg syndrome, and established stage 4 prostate cancer with metastasis to the liver and bone completed radiation and chemotherapy. He presented with gradually worsening, a generalized weakness for 2 weeks, associated with multiple episodes of non-bilious, non-bloody vomiting for 1 week before admission. He had no sick contacts, fever, cough, abdominal pain, dysuria, or recent travel history. The remaining review of systems was unremarkable. The patient's prostate cancer diagnosis was confirmed by biopsy (Gleason score of 9), and he started his medical management with leuprolide. Over the next 2 years after diagnosis, he was effectively treated with the following medications: abiraterone, cabazitaxel, radium-223, and enzalutamide.

Vital signs were unremarkable during admission and throughout his hospitalization. Physical examination, including a complete central nervous system exam, was unremarkable, with intact cranial nerves and without neurologic deficits. He did not appear cachectic. Laboratory workup on admission showed: white blood cell count of 2.5, hemoglobin of 9.7, corrected calcium of 6.6, potassium of 3.1, alkaline phosphatase of 221, the prostate-specific antigen of 182, and ferritin level of 1,336.

MRI of the brain with contrast showed bilateral temporal lobe edema with middle cranial fossa dural thickening/enhancement. An abnormal enhancement extended to the margins of both orbital apices and the right cavernous sinus. Leptomeningeal enhancement in the posterior fossa was also noted. CT head with contrast showed irregular, nodular dural thickening and enhancement related to the right temporal region with adjacent temporal and frontal lobe edema. CT of the chest/abdomen/pelvis showed multiple sclerotic lesions throughout the pelvis, lumbar spine, thoracic spine, and ribs consistent with metastatic disease. Multiple 1–2 cm masses in the liver were noted. Diagnostic LP was performed to evaluate for leptomeningeal spread of prostate cancer. Cerebrospinal fluid (CSF) analysis showed normal RBC, WBC, and glucose; however, elevated total protein levels and atypical cells consistent with adenocarcinoma were seen. Upon discharge, the patient was seen as an outpatient and started on olaparib. He continued olaparib, but did not remain in the area and hence was not offered intrathecal chemotherapy (ITC).