PMC4899566_01
45-year-old male with TMS. Initial imaging of patient, performed at first with new-onset seizure, demonstrates a small periventricular hyperintense lesion (A), with marked worsening of periventricular lesions on imaging performed 6 years later (B) on conventional T2-weighted MRI images.
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Following the cardinal seizure, his outpatient neurologist started him on levetiracetam for seizure prophylaxis and had imaging studies obtained (Fig. 1). Magnetic resonance imaging (MRI) on admission revealed diffuse disease, worse within the left cerebral hemisphere, predominantly superiorly in both frontal lobes and in the left temporal lobe, with associated edema with a left-to-right midline shift of approximately 7 mm, all appearing since an MRI scan six years earlier (Figure 1, Figure 2). A right periventricular lesion likely represented a worsening of a similar lesion that was present on prior imaging (Fig. 1).
45-year-old male with TMS. MRI scans performed on this hospital admission of patient demonstrate a large area of periventricular edema and a trapped left lateral ventricle on conventional T2-weighted MRI (A), with periventricular enhancement on gadolinium-enhanced T1-weighted imaging (B).
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Magnetic resonance imaging (MRI) on admission revealed diffuse disease, worse within the left cerebral hemisphere, predominantly superiorly in both frontal lobes and in the left temporal lobe, with associated edema with a left-to-right midline shift of approximately 7 mm, all appearing since an MRI scan six years earlier (Figure 1, Figure 2). There were also multiple intra-axial, heterogeneously enhancing lesions in the bilateral cerebral hemispheres with surrounding vasogenic edema (Fig. 2).
45-year-old male with TMS. Diffusion tensor imaging (DTI) shows affected periventricular pathways and optic radiations in this case of TMS (A) as compared with a normal control (B) with a loss of color due to decreased neuronal integrity in (A). The fractional anisotropy color legend (C) depicts fiber tract directions.
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DTI maps as well as conventional MRI scans demonstrated destruction, displacement, and invasion of adjacent cerebral parenchyma, white-matter tracts, and juxtacortical U-fibers, imaging features suggestive of a demyelinating process (Figure 3, Figure 4).
45-year-old male with TMS. U-fibers are involved by demyelination in this case of TMS (A) but spared in a comparison case of ischemic small vessel disease (B) as seen on conventional T2-weighted MRI images.
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DTI maps as well as conventional MRI scans demonstrated destruction, displacement, and invasion of adjacent cerebral parenchyma, white-matter tracts, and juxtacortical U-fibers, imaging features suggestive of a demyelinating process (Figure 3, Figure 4).
45-year-old male with TMS. Histochemical and immunohistochemical stains of this patient's periventricular lesion (magnified 400x). (A) Romanovsky smear preparation showing predominance of foam cell macrophages; (B) Hematoxylin and eosin (H&E) stain shows a hypercellular macrophage-rich lesion; (C) Neurofilament protein stain shows persistence of axons (brown); (D) Luxol Fast Blue demonstrates myelin loss (LFB stains myelin blue).
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T-lymphocytes with reactive astrocytes, loss of myelin, and preservation of axons: findings consistent with active demyelination (Fig. 5). The differential diagnosis by pathology at this point was acute demyelinating encephalomyelitis (ADEM), post-infectious demyelination, and multiple sclerosis (MS) of the tumefactive subtype.