Male, 80 years old, with rim enhancing lesion in the left thalamus, and additional lesion in the splenium of the corpus callosum. S/p biposy of the thalamic lesion without tissue diagnosis and no growth of organisms. S/p empiric trials of antibiotics without improvement. A masslike enhancing lesion is evident spanning the left thalamus and midbrain measuring up to 32 x 25 x 27 mm (tv x ap x cc). The lesion shows thick irregular peripheral enhancement with a heterogeneously non-enhancing, susceptibility rimmed central cavity. Parts of the solid enhancing portion of the lesion show mild diffusion restriction, while the central component is non-restricted. On review of the patient's prior imaging, this lesion has fluctuated in size becoming larger (6/2/15), then smaller (7/7/15), then larger again (7/23/15). These changes may reflect alterations in the medication and steroid regimen, so correlation with the medication administration record is suggested. On the present exam, the lesion continues to increase in size and is larger now than on any prior exam. The lesion extends further into the left cerebral peduncle and midbrain, with moderate deformation of the brainstem and slight midline shift to the right.Also noted in relation to the above lesion is a subtle leptomeningeal enhancement of the surface of the left cerebral peduncle. Infiltrative enhancement is also seen along the left optic tract. These findings were not clearly appreciated on prior exams and may therefore be new.A heterogeneous but largely solidly enhancing lesion is also present involving the central and left splenium. Mild internal susceptibility is seen, along with mild questionable restricted diffusion. As with the larger thalamic lesion, the splenial lesion has also fluctuated in size over prior exams, but continues to grow on the present study.Single and multivoxel spectroscopy was performed on both the above described lesions. Strong lipid resonances are seen in the central cavity of the thalamic lesion, but also in the solid enhancing portions of both the thalamic and splenial lesions. Multivoxel spectroscopy reveals gradually increasing choline and decreasing NAA resonances with approach to the solid enhancing portion of the thalamic lesion. It is important to note that elevated choline is seen even in the normal appearing tissue surrounding the lesion. At its peak, the choline resonance in the solid portion of the thalamic lesion is elevated 4 times relative to distant normal tissue. No evidence of any amino acid peaks (marker of bacterial abscess) is seen, nor of any prominent peaks between 3.8 and 3.6 ppm which are reported in the literature to reflect trehalose, a marker of fungal infection.Sequelae of left frontal approach biopsy are seen. A few scattered non specific foci of T2 hyperintensity are seen in the cerebral hemispheres. No other lesions are seen. The ventricles are not dilated. Progressive mass effect is seen on the left lateral ventricle.
A thickly rim enhancing lesion with central cavitation in the left thalamus is evident. This lesion has fluctuated in size over prior exams, perhaps related to the medication and steroid regimen, but continues to grow and has reached its largest size on the present study. Subtle leptomeningeal enhancement of the left cerebral peduncle, and infiltrative enhancement along the left optic tract, seem to be new findings as well. A similar but smaller lesion in the splenium also continues to increase in size.Spectroscopic assessment of both lesions shows the presence of lipid in the central cavity of the thalamic lesion (expected for necrotic tissue), but also in the solid portions of both lesions. Furthermore, the solid portions show significantly elevated choline, reaching 4x normal in the thalamic lesion. Choline elevation, in fact, is seen not only within the lesion, but also in the surrounding normal appearing parenchyma, with gradual return to normal choline levels as distance from the lesion increases suggesting a diffusely infiltrative process. The combination of infiltrative increased choline and increased lipid in the solid portions of the tumor is rather suggestive of lymphoma. While it is true that rim enhancing lymphoma is an entity more commonly seen in the immunocompromised patient, this patient's age may imply some degree of baseline immunosuppression which could account for the enhancement pattern. If not lymphoma, the elevated choline would in general suggest a highly proliferative process, and as such, higher grade glioma would also need to be considered. The possibility of infection, while considered somewhat less likely, should not be dismissed. The imaging and spectroscopic features seem to exclude a typical pyogenic infection. However, atypical infections, including tubercular and fungal, would be reasonable considerations. 