Neurolymphomatosis (NL), or lymphomatous infiltration of peripheral nerves, is a rare neurologic manifestation that usually develops in patients with widespread systemic non-Hodgkin’s lymphoma (NHL) but may be the sole relapse site of NHL [1]. Cranial neuropathy is an unusual syndrome of NL that is sometimes difficult to diagnose using conventional imaging modalities. We report a patient with NL of cranial neuropathy in whom fusion F-fluoro-2-deoxyD-glucose (FDG) PET-CT aided in establishing the diagnosis of NL. A previously healthy, 66-year-old man presented with gastric lymphoma of CD20-positive, diffuse large B-cell phenotype. A thorough systemic evaluation revealed Ann Arbor stage IV NHL with multiple metastases in the neck and lung lymph nodes. Eight cycles of R-CHOP chemotherapy lead to complete remission. Three months later, he acutely developed left facial numbness, followed by rightsided peripheral facial palsy and diplopia. Over the next 2 weeks, he continued to deteriorate to the point of complete bilateral ptosis, bilateral facial hypesthesia, and severe dysarthria. On admission, he was alert and fully oriented. Neurologic examination was significant for 5-mm pupils unreactive to light, bilateral complete ptosis, remarkable extraocular movement limitations, bilateral facial anesthesia, and facial diplegia, consistent with bilateral third, fifth, and seventh nerve palsies. Brain MRI showed enlargement and enhancement of the cisternal segments of bilateral trigeminal nerves that was extending to the Meckel’s caves and cavernous sinuses, more pronounced in the left (Fig. 1a). Whole body fusion PET-CT was performed to assess the extent of relapse, showing increased FDG uptake along the bilateral trigeminal nerves and Meckel’s caves, stronger in the left (Fig. 1b). CSF analysis revealed 8 white cells/mm, markedly increased protein (340 mg/dl), and positive cytology for malignant lymphocytes. CSF tests for tuberculosis, virus, parasite, syphilis, and fungus were all negative. Finally, a diagnosis of NL involving multiple cranial nerves was made. Intense chemotherapy was scheduled but delayed due to bouts of serious infections. He could not recover from septicemia and multiple organ failure despite aggressive treatments, and finally he died two weeks later. Our patient’s MRI revealed enlargement and enhancement of trigeminal nerves, suggesting direct lymphomatous infiltration. However, these MRI findings are not specific for perineural spread of neoplastic diseases but can also be seen in various infectious and inflammatory processes. PET revealed increased FDG uptake in the trigeminal nerves and Meckel’s caves, probably representing lymphomatous infiltration of cranial nerves, subsequently confirmed with positive CSF cytology. J. H. Kim (&) AE J. H. Jang AE S.-B. Koh Department of Neurology, Guro Hospital, Korea University School of Medicine, 80 Guro-Dong, Guro-Ku, Seoul 152-703, Republic of Korea e-mail: jhkim.merrf@gmail.com J Neurooncol (2006) 80:209–210 DOI 10.1007/s11060-006-9164-7