Brain perfusion SPECT in limbic encephalitis associated with autoantibody against the glutamate receptor epsilon 2

Kimura, Noriyuki; Kumamoto, Toshihide; Takahashi, Yukitoshi

doi:10.1016/j.clineuro.2013.12.006

Cited by 9 publications

(7 citation statements)

References 14 publications

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“…However, normalizing to the whole brain presents with the pattern visually described in multiple cases thus far, and these quantitative results are beneficial when the interpreter is not familiar with anti-NMDAR encephalitis qualitative presentation. We have quantitatively determined significant parietal hypoperfusion, statistically significant perfusion asymmetry in the temporal lobe and thalamus together with the bilateral hyperperfusion of the frontal lobes, comparable with part of visually detected perfusion abnormalities in earlier described studies [ 27 , 33 , 34 , 35 , 36 ]. In contrast, we have not detected abnormal perfusion in the cerebellum or hyperperfusion of temporal and occipital lobes [ 34 , 36 , 37 ].…”

Section: Discussionsupporting

confidence: 71%

“…We have quantitatively determined significant parietal hypoperfusion, statistically significant perfusion asymmetry in the temporal lobe and thalamus together with the bilateral hyperperfusion of the frontal lobes, comparable with part of visually detected perfusion abnormalities in earlier described studies [ 27 , 33 , 34 , 35 , 36 ]. In contrast, we have not detected abnormal perfusion in the cerebellum or hyperperfusion of temporal and occipital lobes [ 34 , 36 , 37 ]. As an advantage of quantitative analysis, we noticed that visual analysis can recognize an asymmetry between the left and right lobe, or any subsegmental part, but cannot visually presume whether this is the better-perfused side normal or hyperperfunded, which can be the major dilemma in different psychiatric or encephalitis related states.…”

Section: Discussionsupporting

confidence: 71%

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Psychiatric Illness or Immune Dysfunction—Brain Perfusion Imaging Providing the Answer in a Case of Anti-NMDAR Encephalitis

et al. 2022

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Background: We investigated the potential use of SPECT quantification in addition to qualitative brain perfusion analysis for the detection of anti-NMDAR encephalitis. The question is how to normalize brain activity to be able to quantitatively detect perfusion patterns. Usually, brain activity is normalized to a structure considered unaffected by the disease. Methods: Brain [99mTc]-HMPAO SPECT was performed as a method to detect brain perfusion patterns. The patterns of abnormal brain perfusion cannot always be reliably and qualitatively assessed when dealing with rare diseases. Recent advances in SPECT quantification using commercial software have enabled more objective and detailed analysis of brain perfusion. The cerebellum and whole brain were used as the normalization structures and were compared with visual analysis. Results: The quantification analysis performed with whole brain normalization confirmed right parietal lobe hypoperfusion while also detecting statistically significant left-to-right perfusion differences between the temporal lobe and thalamus. Whole brain normalization further described bilateral frontal lobe hyperperfusion, predominantly of the left lobe, and was in accordance with visual analysis. Conclusion: SPECT quantitative brain perfusion analysis, using the whole brain as the normalization structure rather than the cerebellum, in this case, improved confidence in the visual detection of anti-NMDAR encephalitis and provided unexpected solutions to atypical psychiatric dilemmas.

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Section: Discussionsupporting

confidence: 71%

Section: Discussionsupporting

confidence: 71%

Psychiatric Illness or Immune Dysfunction—Brain Perfusion Imaging Providing the Answer in a Case of Anti-NMDAR Encephalitis

et al. 2022

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“…Several papers have reported SPECT findings for similar cases of anti-NMDA receptor encephalitis and autoimmune encephalitis associated with anti-GluR antibodies. Hyperperfusion on SPECT has been observed in the frontal lobe [ 3 , 11 , 12 , 14 , 15 ], temporal lobe [ 3 , 12 , 13 , 14 , 15 ], occipital lobe [ 13 , 15 ], insula [ 13 , 15 ], and basal ganglia [ 11 , 14 , 15 ]. Hypoperfusion, in contrast, has been observed in the frontal lobe [ 3 , 15 ], temporal lobe [ 15 ], parietal lobe [ 15 ], insula [ 15 ], brainstem [ 15 ], and cerebellum [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Dystonic Seizures and Intense Hyperperfusion of the Basal Ganglia in a Patient with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

2017

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This report describes a rare case presenting with dystonic seizures due to anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. The patient was an 18-year-old woman with repeated right-dominant dystonic seizures even under sedation. Single-photon emission computed tomography (SPECT) showed intense hyperperfusion of the caudate nuclei, putamen, globus pallidus, thalamus, and insula on the left side, suggesting encephalitis. Antibodies against NMDA receptors were detected in the sera and cerebrospinal fluids. Immune-mediated treatments were administered. Three months later, the dystonic seizures disappeared. We diagnosed her with anti-NMDA receptor encephalitis. SPECT suggested that the main region of encephalitis was the basal ganglia. Therefore, we propose that the patient’s dystonic seizures may originate from the insula and be generated by intense hyperactivity of the basal ganglia.

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“…Four additional patients, a 13-year-old girl with severe truncal ataxia [ 51 ] and three women aged 36, 45 and 59 years with ‘non-herpetic acute limbic encephalitis’ [ 52 – 55 ] were in addition positive for antibodies to the glutamate receptors epsilon2 (GluRε2), i.e. the N -methyl- d -aspartate receptor subtype 2B (NMDAR2B or NR2B), which have been described in patients with acute limbic encephalitis [ 52 , 56 – 59 ]. In a young boy who had acute encephalitis with refractory, repetitive partial seizures, anti-GluRδ2 antibodies were reportedly present in addition to antibodies to GluRε2/NR2B and antibodies to the glutamate receptor zeta2 (GluRζ1) [ 60 ], i.e.…”

Section: Anti-glurδ2mentioning

confidence: 99%

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

Jarius

Wildemann

2015

J Neuroinflammation

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Serological testing for anti-neural autoantibodies is important in patients presenting with idiopathic cerebellar ataxia, since these autoantibodies may indicate cancer, determine treatment and predict prognosis. While some of them target nuclear antigens present in all or most CNS neurons (e.g. anti-Hu, anti-Ri), others more specifically target antigens present in the cytoplasm or plasma membrane of Purkinje cells (PC). In this series of articles, we provide a detailed review of the clinical and paraclinical features, oncological, therapeutic and prognostic implications, pathogenetic relevance, and differential laboratory diagnosis of the 12 most common PC autoantibodies (often referred to as ‘Medusa head antibodies’ due their characteristic somatodendritic binding pattern when tested by immunohistochemistry). To assist immunologists and neurologists in diagnosing these disorders, typical high-resolution immunohistochemical images of all 12 reactivities are presented, diagnostic pitfalls discussed and all currently available assays reviewed. Of note, most of these antibodies target antigens involved in the mGluR1/calcium pathway essential for PC function and survival. Many of the antigens also play a role in spinocerebellar ataxia. Part 1 focuses on anti-metabotropic glutamate receptor 1-, anti-Homer protein homolog 3-, anti-Sj/inositol 1,4,5-trisphosphate receptor- and anti-carbonic anhydrase-related protein VIII-associated autoimmune cerebellar ataxia (ACA); part 2 covers anti-protein kinase C gamma-, anti-glutamate receptor delta-2-, anti-Ca/RhoGTPase-activating protein 26- and anti-voltage-gated calcium channel-associated ACA; and part 3 reviews the current knowledge on anti-Tr/delta notch-like epidermal growth factor-related receptor-, anti-Nb/AP3B2-, anti-Yo/cerebellar degeneration-related protein 2- and Purkinje cell antibody 2-associated ACA, discusses differential diagnostic aspects, and provides a summary and outlook.

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Brain perfusion SPECT in limbic encephalitis associated with autoantibody against the glutamate receptor epsilon 2

Cited by 9 publications

References 14 publications

Psychiatric Illness or Immune Dysfunction—Brain Perfusion Imaging Providing the Answer in a Case of Anti-NMDAR Encephalitis

Psychiatric Illness or Immune Dysfunction—Brain Perfusion Imaging Providing the Answer in a Case of Anti-NMDAR Encephalitis

Dystonic Seizures and Intense Hyperperfusion of the Basal Ganglia in a Patient with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC

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