|
 |
| INTERESTING IMAGE |
|
|
|
| Year : 2021 | Volume
: 36
| Issue : 1 | Page : 88-89 |
|
|
F-18 fluorodeoxyglucose positron emission tomography metabolic phenotype in myelin oligodendrocyte glycoprotein antibody–positive autoimmune epilepsy
Madhavi Tripathi1, Arun Raj Sreedharan Thankarajan1, Manjari Tripathi2, Ajay Garg3, Bhargavi Ramanujam2, Snigdha1, Chandrasekhar Bal1
1 Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurology, Cardiothoracic and Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India
3 Department of Neuroradiology, Cardiothoracic and Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India
| Date of Submission | 23-Jul-2020 |
| Date of Decision | 20-Aug-2020 |
| Date of Acceptance | 11-Sep-2020 |
| Date of Web Publication | 04-Mar-2021 |
Correspondence Address:
Dr. Madhavi Tripathi
Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi - 110 029
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijnm.IJNM_167_20
 Abstract | | |
We describe the metabolic phenotype on F-18 fluorodeoxyglucose positron emission tomography (PET) in a 13-year-old female with myelin oligodendrocyte glycoprotein (MOG) antibody–positive encephalitis. Unilateral hemispheric hypometabolism on PET may be the metabolic phenotype of autoimmune epilepsy associated with MOG antibody.
Keywords: Autoimmune encephalitis, fluorodeoxyglucose positron emission tomography, myelin oligodendrocyte glycoprotein, myelin oligodendrocyte glycoprotein
How to cite this article:
Tripathi M, Sreedharan Thankarajan AR, Tripathi M, Garg A, Ramanujam B, Snigdha, Bal C. F-18 fluorodeoxyglucose positron emission tomography metabolic phenotype in myelin oligodendrocyte glycoprotein antibody–positive autoimmune epilepsy. Indian J Nucl Med 2021;36:88-9 |
How to cite this URL:
Tripathi M, Sreedharan Thankarajan AR, Tripathi M, Garg A, Ramanujam B, Snigdha, Bal C. F-18 fluorodeoxyglucose positron emission tomography metabolic phenotype in myelin oligodendrocyte glycoprotein antibody–positive autoimmune epilepsy. Indian J Nucl Med [serial online] 2021 [cited 2021 Jun 23];36:88-9. Available from: https://www.ijnm.in/text.asp?2021/36/1/88/310788 |
A 13-year-old female presented with recent-onset left focal seizures and painful vision reduction in both eyes. Contrast-enhanced magnetic resonance imaging (MRI) was performed. Axial T1 [Figure 1]a, T2 [Figure 1]b, and fluid attenuated inversion recovery (FLAIR) [Figure 1]c images at the level of upper midbrain showed multifocal subcortical white matter lesions, iso-hypointense on T1, hyperintense in T2 and FLAIR, in the right perisylvian region [arrows in [Figure 1]b and [Figure 1]c. Coronal T2-weighted image (WI) [Figure 1]d showed focal hyperintense lesions in the right inferior frontal (long arrow in d) and superior temporal [short arrow in [Figure 1]d subcortical white matter; these lesions [long arrow and short arrows in [Figure 1]f enhanced in postgadolinium coronal T1-WI [Figure 1]f. Postgadolinium axial T1-WIs [Figure 1]e showed patchy subcortical enhancement (arrow in e) in the right cerebral hemisphere. She was referred for 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) to rule out paraneoplastic etiology. Brain axial and coronal PET-MR fusion images revealed hypometabolism in the right cerebral hemisphere including both visual cortices [Figure 1]g and [Figure 1]h. No metabolically active lesion to suggest a primary was identified on whole body PET. Cerebrospinal fluid did not reveal any significant abnormality, and screening for AQP4, NMDAR, AMPA, LGI1, CASPR2, and TPO antibodies was negative, while myelin oligodendrocyte glycoprotein (MOG)–IgG was strongly positive. She was started on methylprednisolone pulse therapy following which there was improvement in vision. | Figure 1: Contrast-enhanced magnetic resonance axial T1 (a), T2 (b), and fluid attenuated inversion recovery (c) images showing multifocal subcortical white matter lesions, iso-hypointense on T1, hyperintense in T2 and fluid attenuated inversion recovery (arrows). Coronal T1-weighted image (d) showing focal hyperintense lesions in the right inferior frontal (long arrow) and superior temporal (short arrow) subcortical white matter, which (long and short arrows) enhanced in postgadolinium coronal T1-weighted image (f). Postgadolinium axial T1-weighted (e) images showing patchy subcortical enhancement (arrow) in the right cerebral hemisphere. Axial and coronal positron emission tomography/magnetic resonance fusion images revealed hypometabolism in the right cerebral hemisphere (g and h)
Click here to view |
MOG antibodies are directed against a myelin protein MOG expressed at the outermost lamellae of the myelin sheath in the central nervous system (CNS).[1],[2] The phenotypic presentation of inflammatory diseases with MOG antibodies can be similar to that of neuromyelitis optica spectrum disease with unilateral or bilateral optic neuritis.[3],[4] The other presentation that has been described in adults is a unilateral hemispheric cortical encephalitis, wherein hyperperfusion was noted on single photon emission computed tomography.[5] The MRI and PET findings in this 13-year-old girl supported a unilateral hemispheric involvement. Different metabolic patterns have been reported on 18F-FDG PET in autoimmune encephalitis with hypometabolism and hypermetabolism; however, so far, hemispheric involvement has not been reported.[6],[7],[8],[9] Inflammatory demyelinating diseases with overlapping clinical features, as well as similarities in MRI, often make diagnosis at onset difficult,[10] and 18F-FDG PET/CT metabolic phenotyopes could be useful in specific antibody subtypes such as anti-MOG.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Bakhti M, Aggarwal S, Simons M. Myelin architecture: Zippering membranes tightly together. Cell Mol Life Sci 2014;71:1265-77.  |
| 2. | Paz Soldán MM, Pirko I. Biogenesis and significance of central nervous system myelin. Semin Neurol 2012;32:9-14. |
| 3. | Kim SM, Woodhall MR, Kim JS, Kim SJ, Park KS, Vincent A, et al. Antibodies to MOG in adults with inflammatory demyelinating disease of the CNS. Neurol Neuroimmunol Neuroinflamm 2015;2:e163. |
| 4. | Sato DK, Callegaro D, Lana-Peixoto MA, Waters PJ, de Haidar Jorge FM, Takahashi T, et al. Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders. Neurology 2014;82:474-81. |
| 5. | Ogawa R, Nakashima I, Takahashi T, Kaneko K, Akaishi T, Takai Y, et al. MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy. Neurol Neuroimmunol Neuroinflamm 2017;4:e322. |
| 6. | Solnes LB, Jones KM, Rowe SP, Pattanayak P, Nalluri A, Venkatesan A, et al. Diagnostic Value of 18F-FDG PET/CT Versus MRI in the Setting of Antibody-Specific Autoimmune Encephalitis. J Nucl Med 2017;58:1307-13. |
| 7. | Probasco JC, Solnes L, Nalluri A, Cohen J, Jones KM, Zan E, et al. Abnormal brain metabolism on FDG-PET/CT is a common early finding in autoimmune encephalitis. Neurol Neuroimmunol Neuroinflamm 2017;4:e352. |
| 8. | Tripathi M, Tripathi M, Roy SG, Parida GK, Ihtisham K, Dash D, et al. Metabolic topography of autoimmune non-paraneoplastic encephalitis. Neuroradiology 2018;60:189-98. |
| 9. | Newey CR, Sarwal A, Hantus S. [(18) F]-Fluoro-deoxy-glucose positron emission tomography scan should be obtained early in cases of autoimmune encephalitis. Autoimmune Dis 2016;2016:9450452. |
| 10. | Reindl M, Waters P. Myelin oligodendrocyte glycoprotein antibodies in neurological disease. Nat Rev Neurol 2019;15:89-102. |
[Figure 1]
|
