Jordi A Matías-Guiu1, María Nieves Cabrera-Martín2, Ana Cortés-Martínez3, Vanesa Pytel4, Teresa Moreno-Ramos5, Celia Oreja-Guevara6, José Luis Carreras7, Jorge Matías-Guiu8. 1. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: jordimatiasguiu@hotmail.com. 2. Department of Nuclear Medicine, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: mncabreram@hotmail.com. 3. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: anncortesm@gmail.com. 4. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: Vanesa.pytel@gmail.com. 5. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: tmorenoramos@yahoo.es. 6. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: orejacbn@gmail.com. 7. Department of Nuclear Medicine, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: joseluis.carreras@salud.madrid.org. 8. Department of Neurology, Hospital Clínico San Carlos, San Carlos Institute for Health Research (IdISSC), Complutense University of Madrid, Calle Profesor Martín Lagos, s/n, 28040 Madrid, Spain. Electronic address: matiasguiu@gmail.com.
Abstract
BACKGROUND: Pseudotumoral multiple sclerosis is a rare form of demyelinating disease of the central nervous system. Positron emission tomography (PET) using amyloid-tracers has also been suggested as a marker of damage in white matter lesions in multiple sclerosis due to the nonspecific uptake of these tracers in white matter. METHOD: We present the case of a 59 year-old woman with a pathological-confirmed pseudotumoral multiple sclerosis, who was studied with the amyloid tracer 18F-florbetaben. The patient had developed word-finding difficulties and right hemianopia twelve years ago. In that time, MRI showed a lesion on the left hemisphere with an infiltrating aspect in frontotemporal lobes. Brain biopsy showed demyelinating areas and inflammation. During the following years, two new clinical relapses occurred. RESULTS: 18F-florbetaben PET showed lower uptake in the white matter lesion visualized in the CT and MRI images. Decreased tracer uptake was also observed in a larger area of the left hemisphere beyond the lesions observed on MRI or CT. White matter lesion volume on FLAIR was 44.2mL, and tracer uptake change between damaged white matter and normal appearing white matter was - 40.5%. Standardized uptake value was inferior in the pseudotumoral lesion than in the other white matter lesions. CONCLUSION: We report the findings of amyloid PET in a patient with pseudotumoral multiple sclerosis. This case provides further evidence on the role of amyloid PET in the assessment of white matter and demyelinating diseases.
BACKGROUND:Pseudotumoral multiple sclerosis is a rare form of demyelinating disease of the central nervous system. Positron emission tomography (PET) using amyloid-tracers has also been suggested as a marker of damage in white matter lesions in multiple sclerosis due to the nonspecific uptake of these tracers in white matter. METHOD: We present the case of a 59 year-old woman with a pathological-confirmed pseudotumoral multiple sclerosis, who was studied with the amyloid tracer 18F-florbetaben. The patient had developed word-finding difficulties and right hemianopia twelve years ago. In that time, MRI showed a lesion on the left hemisphere with an infiltrating aspect in frontotemporal lobes. Brain biopsy showed demyelinating areas and inflammation. During the following years, two new clinical relapses occurred. RESULTS: 18F-florbetaben PET showed lower uptake in the white matter lesion visualized in the CT and MRI images. Decreased tracer uptake was also observed in a larger area of the left hemisphere beyond the lesions observed on MRI or CT. White matter lesion volume on FLAIR was 44.2mL, and tracer uptake change between damaged white matter and normal appearing white matter was - 40.5%. Standardized uptake value was inferior in the pseudotumoral lesion than in the other white matter lesions. CONCLUSION: We report the findings of amyloid PET in a patient with pseudotumoral multiple sclerosis. This case provides further evidence on the role of amyloid PET in the assessment of white matter and demyelinating diseases.
Authors: Chris W J van der Weijden; Jan F Meilof; Anouk van der Hoorn; Junqing Zhu; Chunying Wu; Yanming Wang; Antoon T M Willemsen; Rudi A J O Dierckx; Adriaan A Lammertsma; Erik F J de Vries Journal: Eur J Nucl Med Mol Imaging Date: 2022-04-02 Impact factor: 10.057
Authors: Jorge Matías-Guiu; Jordi A Matías-Guiu; Paloma Montero-Escribano; Juan A Barcia; Alejandro A Canales-Aguirre; Juan C Mateos-Diaz; Ulises Gómez-Pinedo Journal: Front Neurol Date: 2020-07-07 Impact factor: 4.003