Recognition of seizure semiology and semiquantitative FDG‐PET analysis of anti‐LGI1 encephalitis

Li, Taoran; Zhang, Yu-Di; Wang, Qun; Shao, Xiaoqiu; Lv, Ruijuan

doi:10.1111/cns.13707

Cited by 7 publications

(6 citation statements)

References 36 publications

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“…When considering anti-LGI1 encephalitis has many phenotypes, including FBDS, grand mal seizures, focal aware motor seizures (FAMS), focal impaired awareness (FIAS) as well as hyponatremia. Further FAMS have different metabolic pattern from FBDS and FIAS (42) and hyponatremia may contribute to aberrant brain metabolism (43), there is a need for further prospective study to clarify the impacts of different phenotype on the metabolic characteristics of anti-LGI1encephalitis.…”

Section: Discussionmentioning

confidence: 99%

Subcortical Hypermetabolism Associated With Cortical Hypometabolism Is a Common Metabolic Pattern in Patients With Anti-Leucine-Rich Glioma-Inactivated 1 Antibody Encephalitis

Zhao

Chen

et al. 2021

Front. Immunol.

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PurposeBrain 18F-fluorodeoxyglucose positron emission tomography (FDG PET) is a sensitive technique for assisting in the diagnosis of patients with anti-leucine-rich glioma-inactivated 1 (LGI1) antibody encephalitis. However, the common pattern of this disorder assessed by FDG PET remains unknown. The present study aimed to explore the glucose metabolic patterns of this disorder based on PET voxel analysis.MethodsThis retrospective study enrolled 25 patients with anti-LGI1 encephalitis, who were admitted in Beijing Tiantan Hospital between September 2014 and July 2019. The glucose metabolic pattern was compared between the included patients and 44 age- and gender-matched healthy controls using Statistical Parametric Mapping. Then, the correlation between the metabolic pattern and scaled activities of daily living (ADLs) of the patients was assessed.ResultsThe median time from symptom onset to PET scans was 9 w (range:2-53w). The groupwise analysis revealed that patients with anti-LGI1 encephalitis had left hippocampal hypermetabolism and hypometabolism in almost all neocortical regions. The individual-level results showed most patients presented a decreased metabolism in neocortical regions, as well as an increase in metabolism in the hippocampus and basal ganglia. Furthermore, the metabolic gradient between hippocampus and neocortical regions was positively associated with the ADLs (frontal lobe, r=0.529, P=0.008; parietal lobe, r=0.474, P=0.019; occipital lobe, r=0.413, P=0.045; temporal lobe, r=0.490, P=0.015), respectively. In addition, the patients with facio-brachial dystonic seizures (FBDS) presented bilateral putamen hypermetabolism, when compared to patients without FBDS and healthy controls.ConclusionSubcortical hypermetabolism associated with cortical hypometabolism presented with a common metabolic pattern in patients with anti-LGI1 encephalitis in the present study. The resolution of the metabolic gradient of the hippocampal hypermetabolism and neocortical hypometabolism may bring about improved clinical neurologic disability.

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Section: Discussionmentioning

confidence: 99%

Subcortical Hypermetabolism Associated With Cortical Hypometabolism Is a Common Metabolic Pattern in Patients With Anti-Leucine-Rich Glioma-Inactivated 1 Antibody Encephalitis

Zhao

Chen

et al. 2021

Front. Immunol.

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“…While FBDS is thought to be pathognomonic, other kinds of seizures as well as lower limb involvement have been documented in previous studies [ 5 , 16 ]. In neuroimages, temporo-mesial MRI T2 hyperintensity is considered common; however, as for other subtypes of autoimmune encephalitides, involvement of basal nuclei and insula has been reported, in both morphological and metabolic studies [ 6 - 9 ].…”

Section: Discussionmentioning

confidence: 99%

“…Temporal lobe dysfunction might be related to the development of symptoms such as amnesia, confusion, disorientation, anxiety, and temporal lobe seizures. Recent studies have also highlighted that brain metabolic derangement might also involve areas that are not altered in MRI [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

A Case of Anti-Leucine-Rich Glioma-Inactivated Protein 1 (Anti-LGI1) Encephalitis With an Unusual Frontomesial Motor Cortex T2 MRI Hyperintensity

Papiri¹,

Puca²,

Marcucci³

et al. 2022

Cureus

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Anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis is a rare autoimmune disorder, classified within limbic encephalitides, and characterized by seizures and subacute cognitive-behavioral impairment, mainly affecting short-term memory and usually involving temporo-mesial lobe structures.We present a case of anti-LGI1 encephalitis characterized by focal right lower limb motor seizures and pyramidal signs and responsive to high-dose methylprednisolone. The patient developed an atypical left frontal lobe parasagittal T2 hyperintense lesion on MRI within one month of hospital admission, which has not been described previously in this disease to the best of our knowledge.

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“…6,7 Concurrently, a notable subset of atypical PD patients may gradually develop resistance to levodopa over time. 8,9 Carbidopa has been associated with various adverse effects including gastrointestinal disturbances and psychiatric manifestations such as heightened alertness, increased motor activity, and elevated aggressiveness, as observed in animal studies. Additionally, there is a risk of weight loss and potential vitamin B6 deficiency, which can lead to complications like seizures, particularly with high doses.…”

Section: Introductionmentioning

confidence: 99%

Autophagy‐associated non‐coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis

Hussain,

Moglad,

Afzal

et al. 2024

CNS Neurosci Ther

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BackgroundParkinson's disease (PD) is a degenerative neurological condition marked by the gradual loss of dopaminergic neurons in the substantia nigra pars compacta. The precise etiology of PD remains unclear, but emerging evidence suggests a significant role for disrupted autophagy—a crucial cellular process for maintaining protein and organelle integrity.MethodsThis review focuses on the role of non‐coding RNAs (ncRNAs) in modulating autophagy in PD. We conducted a comprehensive review of recent studies to explore how ncRNAs influence autophagy and contribute to PD pathophysiology. Special attention was given to the examination of ncRNAs' regulatory impacts in various PD models and patient samples.ResultsFindings reveal that ncRNAs are pivotal in regulating key processes associated with PD progression, including autophagy, α‐synuclein aggregation, mitochondrial dysfunction, and neuroinflammation. Dysregulation of specific ncRNAs appears to be closely linked to these pathogenic processes.ConclusionncRNAs hold significant therapeutic potential for addressing autophagy‐related mechanisms in PD. The review highlights innovative therapeutic strategies targeting autophagy‐related ncRNAs and discusses the challenges and prospective directions for developing ncRNA‐based therapies in clinical practice. The insights from this study underline the importance of ncRNAs in the molecular landscape of PD and their potential in novel treatment approaches.

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Recognition of seizure semiology and semiquantitative FDG‐PET analysis of anti‐LGI1 encephalitis

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 7 publications

References 36 publications

Subcortical Hypermetabolism Associated With Cortical Hypometabolism Is a Common Metabolic Pattern in Patients With Anti-Leucine-Rich Glioma-Inactivated 1 Antibody Encephalitis

Subcortical Hypermetabolism Associated With Cortical Hypometabolism Is a Common Metabolic Pattern in Patients With Anti-Leucine-Rich Glioma-Inactivated 1 Antibody Encephalitis

A Case of Anti-Leucine-Rich Glioma-Inactivated Protein 1 (Anti-LGI1) Encephalitis With an Unusual Frontomesial Motor Cortex T2 MRI Hyperintensity

Autophagy‐associated non‐coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis

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