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MR Imaging in Toxoplasmosis Encephalitis after Bone Marrow Transplantation: Paucity of Enhancement despite Fulminant Disease

Catalina Ionitaa, Mohammed Wasayd, Lucia Balosa and Rohit Bakshia,b,c

a Department of Neurology and Pathology, University at Buffalo, SUNY, Buffalo, New York
b Department of Kaleida Health, Imaging Services, New York
c Department of Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, Buffalo, New York
d Department of Neurology, the Aga Khan University , Karachi, Pakistan



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FIG 1. Three serial MR imaging studies obtained during a period of 18 days. Images were obtained by the fluid-attenuated inversion recovery (FLAIR) sequences, with the exception of columns 4 and 6, which were obtained by the postgadolinium T1-weighted sequence. The initial study (top row) revealed a few nonspecific white matter lesions that were thought to be related to cyclosporine toxicity.

The lesions were not seen on noncontrast T1-weighted images or diffusion-weighted images (not shown). After gadolinium administration, lesions were nonenhancing, except for the left parietal-occipital lesion, which shows faint, questionable enhancement. Because of neurologic deterioration, brain MR imaging was repeated (middle row) 6 days after the initial study, revealing worsening lesions in the subcortical white matter, cerebellum, bilateral thalamus, and basal ganglia, with no mass effect or abnormal parenchymal enhancement; there was possibly some increased leptomeningeal enhancement. During the following week, the patient became progressively obtunded and comatose. A third MR imaging study obtained 18 days after the initial study (bottom row) showed continuous progression of lesions in size and distribution, which at this time involved much of the brain. There was a remarkable lack of mass effect and lack of parenchymal enhancement of most lesions; irregular meningeal enhancement with secondary involvement (perhaps by meningeal spread) of the cortex and subcortical areas was suggested. A few lesions were hyperintense on diffusion-weighted images. Apparent diffusion coefficient maps were not obtained to distinguish restricted diffusion versus T2 shine-through (not shown). MR imaging was performed at 1.5 T with the following parameters on each day. Fast spin-echo FLAIR: 5-mm axial sequences with 1-mm section gaps, TR/TE/TI of 10,002/145/2200, matrix of 192 x 256, one signal averaged, and 22-cm field of view. T1-weighted images: 5-mm axial sequences with 1-mm section gaps, TR/TE of 500/20, matrix of 192 x 256, one signal averaged, 22-cm field of view.



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FIG 2. Single- voxel MR spectroscopy (right panel) by using a stimulated-echo acquisition mode with a TR of 1500 ms and TE of 30 ms. The spectral pattern is technically limited and suboptimal (note the poor baseline).

A 2.5 x 2.5 cm voxel of the right putamen lesion was localized based on the FLAIR axial image on day 18 (left panel) at the level of the frontal horns of the lateral ventricle. The spectral pattern shows, from left to right, a moderate increase in choline (solid arrow), a moderate reduction in N-acetyl-aspartate (solid arrow), and a marked lactate peak (solid arrow). There is also a mild prominence of (amino acid) peak (dashed arrow).



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FIG 3. Autopsy findings. Photomicrograph (magnification x600, hematoxylin and eosin stain) of a histologic section of the cerebrum reveals multiple toxoplasma cysts (open arrow), probable neuronal cells with round, dark nuclei (arrowhead), and additional trophozoites in the extracellular space after the cysts rupture (straight arrow). The findings are consistent with those of toxoplasmosis encephalitis.