encefalitis
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Limbic Encephalitis Diagnosed With 18F-FDG PET/CT
Maria Del Puig Cózar Santiago, MD, PhD, Raul Sanchez Jurado, BTech, Rut Sanz Llorens, BTech,Jose Enrique Aguilar Barrios, BTech, and Jose Ferrer Rebolleda, MD
Abstract: Limbic encephalitis is a subacute onset syndrome characterizedby short-term memory impairment, confusion, temporal lobe epilepsy, hy-pothalamic dysfunction, and psychiatric symptoms. Common causes are au-toimmune disorders or idiopathic disease, although it has been associated totumors. We report the case of a woman arrived at the emergency departmenthaving had fluctuating impaired memory for 2 weeks. The first MRI wasnormal. It was decided to perform lumbar puncture and PET/CT to excludeviral origin or paraneoplastic syndrome. Typical abnormalities were foundin the second MRI (1 month after previous); however, FDG PET is a usefultool that contributes to early detection.
Key Words: limbic encephalitis, PET/CT, MRI
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FIGURE 1. PET/CT1,2 (Philips Gemini TOF16; FOV, 600 mm; 5 mFDG in a patient who was asked to fast for at least 6 hours before150 mg/dL. MIP displayed from posterior to anterior view showedtemporal hippocampus, with involvement of the ipsilateral amygcontralateral amygdala.
Received for publication November 18, 2014; revision accepted October 11, 2015.From the Nuclear Medicine Department, Hospital General Universitario-ERESA,
Valencia, Spain.Conflicts of interest and sources of funding: none declared.Correspondence to: María Del Puig Cózar Santiago, MD, PhD, Nuclear
Medicine Department, Hospital General Universitario-ERESA, AvenidaTres Cruces, S/N 46014 Valencia, Spain. E-mail: [email protected].
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.ISSN: 0363-9762/15/0000–0000DOI: 10.1097/RLU.0000000000001076
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m/slice) 60 minutes after IV injection of 6 mCi (222 MBq) ofthe examination to ensure blood glucose levels belowpathological glucose uptake, increased in the bilateral mesial
dala and glycidic hypermetabolism increased in
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FIGURE 2. PET/CT fusion with MRI (sagittal temporal right lobe, slices displayed from right to left, with a FLAIR sequence).PET/CT shows the extent of inflammation in the hippocampus.3
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FIGURE 3. Brain MRI4 was performed (1.5-T Siemens Sonata system; FOV, 24 cm), which revealed an alteration in the signalintensity of both hippocampus andmesial temporal lobes hyperintense in T2 high resolution (coronal slice in the left side). Bluearrow shows the increasing intensity in the right hippocampus. It was associated with alterations in T1 enhancement (coronalslice in the right side) but not with mass. Gray arrow shows an area of abnormal uptake of paramagnetic contrast in the righthead hippocampus compatible with nonnecrotizing encephalitis seated on the right temporal lobe.5
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FIGURE 4. Diagnostic PET/CT scan (coronal PET slices reconstructed with CT-based attenuation correction using an iterativealgorithm6) where we can visualize initial lesion with high metabolic uptake.7 In addition, whole-body PET/CT8 study showedno lesions consistent with paraneoplastic syndrome.
FIGURE 5. During the follow-up (after 3 months with immunosuppressive therapy and steroids), a new PET/CT was performed,which revealed a marked uptake decrease in the right limbic system with complete resolution in the contralateral lesionshowed in the amygdala.
Clinical Nuclear Medicine • Volume 00, Number 00, Month 2015 Limbic Encephalitis Diagnosed With 18F-FDG PET/CT
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Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. This paper can be cited using the date of access and the unique DOI number which can be found in the footnotes.