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Year : 2021  |  Volume : 36  |  Issue : 4  |  Page : 451-452  

F-18 fluorodeoxyglucose positron-emission tomography/computed tomography showing mammillary body involvement in a case of autoimmune anti-N-methyl D-aspartate antibody encephalitis


1 Department of Nuclear Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Gastroenterology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission23-Apr-2021
Date of Decision22-Sep-2021
Date of Acceptance27-Sep-2021
Date of Web Publication15-Dec-2021

Correspondence Address:
Prof. Bhagwant Rai Mittal
Department of Nuclear Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.ijnm_54_21

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   Abstract 


Autoimmune encephalitis with antibodies against neuronal cell surface antigens is a group of neuropsychiatric disorders, with anti-N-methyl D-aspartate (NMDAR) encephalitis being one of them. We report a case of a young male patient who presented with complaints of seizures associated with fever, rapidly progressing memory loss, and choreoathetoid movements for 1 month. His serum was strongly positive for anti-NMDAR receptor antibodies. F-18 fluorodeoxyglucose positron-emission tomography/computed tomography for the brain revealed hypermetabolism involving bilateral basal ganglia and bilateral mammillary bodies associated with hypometabolism in bilateral occipital lobes.

Keywords: Anti-N-methyl D-aspartate encephalitis, autoimmune encephalitis, fluorodeoxyglucose, mammillary body


How to cite this article:
Vankadari K, Kumar R, Samanta J, Singh H, Mittal BR. F-18 fluorodeoxyglucose positron-emission tomography/computed tomography showing mammillary body involvement in a case of autoimmune anti-N-methyl D-aspartate antibody encephalitis. Indian J Nucl Med 2021;36:451-2

How to cite this URL:
Vankadari K, Kumar R, Samanta J, Singh H, Mittal BR. F-18 fluorodeoxyglucose positron-emission tomography/computed tomography showing mammillary body involvement in a case of autoimmune anti-N-methyl D-aspartate antibody encephalitis. Indian J Nucl Med [serial online] 2021 [cited 2022 Jan 17];36:451-2. Available from: https://www.ijnm.in/text.asp?2021/36/4/451/332623



A 23-year-old male patient came with chief complaints of seizures (2–3 episodes/day) for 1 month associated with altered behavior and fever for 15 days. Later, his ability to respond to verbal commands slowly deteriorated along with the appearance of choreoathetoid movements for 7 days. EEG done for seizure evaluation revealed diffuse encephalitis. Serum tested strongly positive for anti-N-methyl D-aspartate (NMDAR) receptor antibodies (cell-based assays). Axial F-18 fluorodeoxyglucose (FDG) positron-emission tomography (PET), computed tomography (CT), and fused PET/CT brain images [Figure 1]a, [Figure 1]b, [Figure 1]c revealed hypermetabolism involving the bilateral basal ganglia (solid arrow) along with hypometabolism in the bilateral occipital cortices (filled arrow) with no morphological abnormality in the corresponding CT images. Axial [Figure 1]d, [Figure 1]e, [Figure 1]f and coronal [Figure 1]g, [Figure 1]h, [Figure 1]i F-18 FDG PET, CT, and fused PET/CT brain images revealed hypermetabolism involving bilateral mammillary bodies (dotted arrows) relative to cerebral cortex with no morphological abnormality in the corresponding CT images.
Figure 1: Axial F-18 FDG PET, CT, and fused PET/CT brain images (a-c) revealed hypermetabolism involving the bilateral basal ganglia (solid arrow) along with hypometabolism in the bilateral occipital cortices (filled arrow) with no morphological abnormality in the corresponding CT images. Axial (d-f) and coronal (g-i) F-18 FDG PET, CT, and fused PET/CT brain images revealed hypermetabolism in red nucleus. FDG: Fluorodeoxyglucose, PET: Positron-emission tomography, CT: Computed tomography

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Anti-NMDAR receptor encephalitis is a most frequently reported autoimmune limbic encephalitis characterized predominantly by IgG antibodies against the GluN1 subunit of MMDA receptor in the cerebrospinal fluid (CSF) and serum.[1] This disorder most frequently affects younger women and children, accounting for 80% of patients, but can also be seen in younger men and older individuals.[2] Most of the patients with this disorder show hypermetabolism involving the hippocampus, amygdala, and parahippocampal gyrus in isolation or bilateral occipital lobe hypometabolism on F-18 FDG PET.[3] In the case of severe neurological disability with choreoathetoid movements, bilateral basal ganglia are involved by these antibodies, as seen in our case.[4] This index case shows rare bilateral mammillary body involvement, representing a pair of paramedian small round bodies located in the undersurface of the brain. These play an important role in recollective memory formation by relaying impulses from the hippocampal region to the anterior thalamus (Papez circuit). Memory loss seen in this case may be attributed to the involvement of bilateral mammillary bodies.

In most cases, the exact trigger mechanism for these antibodies remains unknown, but few studies reported association with herpes viral infections, ovarian and testicular teratomas.[5],[6] Diagnosis is often confirmed by the presence of rapidly progressing clinical symptoms and elevated anti-NMDAR antibodies in the CSF and serum. F-18 FDG PET can support the diagnosis by showing hypermetabolism in the involved structures during the acute phase and also helps to rule out rare yet possible underlying malignancy in the body. Establishing the diagnosis with clinical features, serum investigations, and F-18 FDG PET is important because symptoms associated with this syndrome improve with immunotherapy in more than 60% of the cases.[7] Autoimmune encephalitis with antibodies against neuronal surface antigens confers better prognosis with lesser risk of cancer than those with antibodies against neurocytoplasmic antigen.[8],[9] The findings, in this case, emphasize the potential role of F-18 FDG PET as an imaging biomarker for confirmation of autoimmune encephalitis.

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 Top

1.
Granerod J, Ambrose HE, Davies NW, Clewley JP, Walsh AL, Morgan D, et al. Causes of encephalitis and differences in their clinical presentations in England: A multicentre, population-based prospective study. Lancet Infect Dis 2010;10:835-44.  Back to cited text no. 1
    
2.
Titulaer MJ, McCracken L, Gabilondo I, Armangué T, Glaser C, Iizuka T, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: An observational cohort study. Lancet Neurol 2013;12:157-65.  Back to cited text no. 2
    
3.
Probasco JC, Solnes L, Nalluri A, Cohen J, Jones KM, Zan E, et al. Decreased occipital lobe metabolism by FDG-PET/CT: An anti-NMDA receptor encephalitis biomarker. Neurol Neuroimmunol Neuroinflamm 2018;5:e413.  Back to cited text no. 3
    
4.
Maeder-Ingvar M, Prior JO, Irani SR, Rey V, Vincent A, Rossetti AO. FDG-PET hyperactivity in basal ganglia correlating with clinical course in anti-NDMA-R antibodies encephalitis. J Neurol Neurosurg Psychiatry 2011;82:235-6.  Back to cited text no. 4
    
5.
Hacohen Y, Deiva K, Pettingill P, Waters P, Siddiqui A, Chretien P, et al. N-methyl-D-aspartate receptor antibodies in post-herpes simplex virus encephalitis neurological relapse. Mov Disord 2014;29:90-6.  Back to cited text no. 5
    
6.
Dai Y, Zhang J, Ren H, Zhou X, Chen J, Cui L, et al. Surgical outcomes in patients with anti-N-methyl D-aspartate receptor encephalitis with ovarian teratoma. Am J Obstet Gynecol 2019;221:485.e1-485.e10.  Back to cited text no. 6
    
7.
Dalmau J, Gleichman AJ, Hughes EG, Rossi JE, Peng X, Lai M, et al. Anti-NMDA-receptor encephalitis: Case series and analysis of the effects of antibodies. Lancet Neurol 2008;7:1091-8.  Back to cited text no. 7
    
8.
Honnorat J, Cartalat-Carel S, Ricard D, Camdessanche JP, Carpentier AF, Rogemond V, et al. Onco-neural antibodies and tumour type determine survival and neurological symptoms in paraneoplastic neurological syndromes with Hu or CV2/CRMP5 antibodies. J Neurol Neurosurg Psychiatry 2009;80:412-6.  Back to cited text no. 8
    
9.
Dalmau J, Graus F, Villarejo A, Posner JB, Blumenthal D, Thiessen B, et al. Clinical analysis of anti-Ma2-associated encephalitis. Brain 2004;127:1831-44.  Back to cited text no. 9
    


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