A 29-year-old man presented with tonic-clonic seizures. Initial MRI showed a lesion
centered on the white matter of the left frontal lobe, with restricted diffusion and
contrast enhancement on its margins and low rCBV and hypometabolismon PET-CT, suggestive
of a tumefactive demyelination lesion ([Figure 1]). Patient underwent surgical biopsy, with no signs of malignancy ([Figure 2]). Two months later, control MRI showed a new lesion on the brainstem, with solid
enhancement and hypermetabolism on PET-CT, compatible with lymphoma ([Figures 3] and [4]).
Demyelinating sentinel lesions preceding CNS lymphomas are a rare entity and its pathophysiology
is not fully understood[1],[2].
Figure 1 A: Axial diffusion weighted imaging (DWI), showing a left frontal lesion with restricted
diffusion on the lesion’s free margin, oriented towards the white matter, suggestive
of demyelinating nature. B: Axial post-gadolinium T1, showing contrast enhancement
on the lesions free margin. C: Coronal post-gadolinium T1 shows the left frontal lesion,
insinuating towards the corpus callosum, but with no frank signs of invasion. Notice
the spared brainstem.
Figure 2 Histopathological findings from surgical biopsy. A: Hematoxicilin-eosin 100x, amplified
on B, shows a diffuse inflammatory infiltrate composed by T-lymphocytes, confirmed
by immunohistochemistry for CD3 marker on C, plasmacytes (CD138 on D) and foamy macrophages
(CD68 on E). The sample was negative for malignancy and markers for B cells were negative
(not shown).
Figure 3 Control MRI two months later, demonstrates persistent restricted diffusion (A), but
less enhancement of the left frontal lesion (B). C (coronal post-gadolinium T1): Its
caudal aspect extends and invades the corpus callosum. Notice the development of a
new and solid-enhancing lesion on the brainstem, extending along the cerebral peduncles
and the postoperative changes on the left frontal lobe.
Figure 4 PET-CT and MRI fusion, showing the hypometabolic behavior of the original left frontal
lesion (A), in contrast with hypermetabolism on the corpus callosum (B) and brainstem
(C) lesions, inferring different etiologies.
