EGFR L858R lung adenocarcinoma with rapid neurologic decline

What happened, in summary

This 45-year-old woman was admitted in June 2024 after a rapid change in thinking and alertness. After a cold in April, she began sleeping 18 to 20 hours a day. Over the next month, her reactions slowed, she had a minor car accident because of delayed responses, and she developed confused speech, difficulty expressing herself, memory problems, reduced calculation ability, and poor orientation to time and place.

Brain MRI showed many small abnormal lesions across both cerebral hemispheres, the basal ganglia, brainstem, and cerebellum, with restricted diffusion, enhancement, and internal bleeding. Cerebrospinal fluid showed elevated protein and IgG, but infection studies, cultures, and cytology did not identify an infection or malignant cells. A chest CT then found a 49.2 x 30.5 mm mass-like lesion in the left upper lobe. A supraclavicular lymph-node biopsy showed reactive hyperplasia, but later ultrasound bronchoscopy with lung biopsy confirmed lung adenocarcinoma. The tumor was CK7-positive, Napsin A-positive, TTF-1-positive, p40-negative, and carried an EGFR L858R mutation.

Her neurologic illness was difficult to classify. She was discharged on prednisone after initially declining further pulmonary biopsy, but symptoms worsened around 80 days after disease onset, with broader cognitive and neurologic decline. After lung cancer was confirmed, she received amivantamab targeted therapy and entecavir for chronic hepatitis B. Her condition continued to decline quickly. The clinical course was considered most consistent with a combination of paraneoplastic autoimmune neurologic disease and metastatic involvement of the brain parenchyma and meninges from lung adenocarcinoma. She died in the fourth month of the disease course.