Diagnostic criteria for autoimmune encephalitis: utility and pitfalls for antibody-negative disease

Dalmau, Josep; Graus, Francesc

doi:10.1016/s1474-4422(23)00083-2

Cited by 52 publications

(21 citation statements)

References 95 publications

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“…Importantly, these were not intended to be used as standalone criteria, but rather as the minimum requirements to suspect AIE. 127 In patients who only meet criteria for possible AIE but in whom alternative diagnoses have reasonably been excluded, a controlled immunotherapy trial with predefined distinct and objective treatment measures of efficacy can be considered with involvement of a specialist in autoimmune neurology.…”

Section: Use Of Corticosteroids After Initial Treatmentmentioning

confidence: 99%

Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults

Hahn,

Budhram,

Alikhani

et al. 2024

Can. J. Neurol. Sci.

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Autoimmune encephalitis is increasingly recognized as a neurologic cause of acute mental status changes with similar prevalence to infectious encephalitis. Despite rising awareness, approaches to diagnosis remain inconsistent and evidence for optimal treatment is limited. The following Canadian guidelines represent a consensus and evidence (where available) based approach to both the diagnosis and treatment of adult patients with autoimmune encephalitis. The guidelines were developed using a modified RAND process and included input from specialists in autoimmune neurology, neuropsychiatry and infectious diseases. These guidelines are targeted at front line clinicians and were created to provide a pragmatic and practical approach to managing such patients in the acute setting.

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Section: Use Of Corticosteroids After Initial Treatmentmentioning

confidence: 99%

Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults

Hahn,

Budhram,

Alikhani

et al. 2024

Can. J. Neurol. Sci.

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“…These cases may be challenging to classify, but clues from diligent clinical observation as well as clinical criteria are available to guide proper diagnosis. 15 Attention is needed to avoid misdiagnosis of autoimmune encephalitis based on positive results from autoantibody panels requested in the absence of clear indication to test, or with poorly significant results (such as low-titer anti-GAD) or using older assays with limited validity (such as anti-VGKC). Indeed, proper interpretation of the available biomarkers is of paramount importance in the era of precision medicine.…”

Section: Redefining Disease Classificationmentioning

confidence: 99%

Reshaping neuroimmunology: diagnosis and treatment in the era of precision medicine

dos Passos,

Adoni,

Mendes

et al. 2023

Arq Neuropsiquiatr

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Precision medicine has revolutionized the field of neuroimmunology, with innovative approaches that characterize diseases based on their biology, deeper understanding of the factors leading to heterogeneity within the same disease, development of targeted therapies, and strategies to tailor therapies to each patient. This review explores the impact of precision medicine on various neuroimmunological conditions, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), optic neuritis, autoimmune encephalitis, and immune-mediated neuropathies. We discuss advances in disease subtyping, recognition of novel entities, promising biomarkers, and the development of more selective monoclonal antibodies and cutting-edge synthetic cell-based immunotherapies in neuroimmunological disorders. In addition, we analyze the challenges related to affordability and equity in the implementation of these emerging technologies, especially in situations with limited resources.

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“…Therefore, it is necessary to develop new drugs to address this issue. Anti-NMDAR encephalitis is generally regarded as a form of neuroinflammation, though the current understanding of its pathogenesis remains unclear [ 5 ]. Despite comprising only 2% of human body weight, the adult brain is responsible for 20% of the body's resting metabolic rate, with a high demand for metabolic energy [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Exploring the neuroprotective role of artesunate in mouse models of anti-NMDAR encephalitis: insights from molecular mechanisms and transmission electron microscopy

Liu,

Huang,

Qian

et al. 2024

Cell Commun Signal

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Background The pathway involving PTEN-induced putative kinase 1 (PINK1) and PARKIN plays a crucial role in mitophagy, a process activated by artesunate (ART). We propose that patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis exhibit insufficient mitophagy, and ART enhances mitophagy via the PINK1/PARKIN pathway, thereby providing neuroprotection. Methods Adult female mice aged 8–10 weeks were selected to create a passive transfer model of anti-NMDAR encephalitis. We conducted behavioral tests on these mice within a set timeframe. Techniques such as immunohistochemistry, immunofluorescence, and western blotting were employed to assess markers including PINK1, PARKIN, LC3B, p62, caspase3, and cleaved caspase3. The TUNEL assay was utilized to detect neuronal apoptosis, while transmission electron microscopy (TEM) was used to examine mitochondrial autophagosomes. Primary hippocampal neurons were cultured, treated, and then analyzed through immunofluorescence for mtDNA, mtROS, TMRM. Results In comparison to the control group, mitophagy levels in the experimental group were not significantly altered, yet there was a notable increase in apoptotic neurons. Furthermore, markers indicative of mitochondrial leakage and damage were found to be elevated in the experimental group compared to the control group, but these markers showed improvement following ART treatment. ART was effective in activating the PINK1/PARKIN pathway, enhancing mitophagy, and diminishing neuronal apoptosis. Behavioral assessments revealed that ART ameliorated symptoms in mice with anti-NMDAR encephalitis in the passive transfer model (PTM). The knockdown of PINK1 led to a reduction in mitophagy levels, and subsequent ART intervention did not alleviate symptoms in the anti-NMDAR encephalitis PTM mice, indicating that ART’s therapeutic efficacy is mediated through the activation of the PINK1/PARKIN pathway. Conclusions At the onset of anti-NMDAR encephalitis, mitochondrial damage is observed; however, this damage is mitigated by the activation of mitophagy via the PINK1/PARKIN pathway. This regulatory feedback mechanism facilitates the removal of damaged mitochondria, prevents neuronal apoptosis, and consequently safeguards neural tissue. ART activates the PINK1/PARKIN pathway to enhance mitophagy, thereby exerting neuroprotective effects and may achieve therapeutic goals in treating anti-NMDAR encephalitis.

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Diagnostic criteria for autoimmune encephalitis: utility and pitfalls for antibody-negative disease

Cited by 52 publications

References 95 publications

Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults

Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults

Reshaping neuroimmunology: diagnosis and treatment in the era of precision medicine

Exploring the neuroprotective role of artesunate in mouse models of anti-NMDAR encephalitis: insights from molecular mechanisms and transmission electron microscopy

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