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1.
J Alzheimers Dis ; 97(1): 193-204, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38108349

RESUMO

BACKGROUND: Subjective cognitive decline (SCD) refers to the self-reported persistent cognitive decline despite normal objective testing, increasing the risk of dementia compared to cognitively normal individuals. OBJECTIVE: This study aims to investigate the attributes of SCD patients who demonstrated memory function improvement. METHODS: In this prospective study of SCD, a total of 120 subjects were enrolled as part of a multicenter cohort study aimed at identifying predictors for the clinical progression to mild cognitive impairment or dementia (CoSCo study). All subjects underwent 18F-florbetaben PET and brain MRI scans at baseline and annual neuropsychological tests. At the 24-month follow-up, we classified SCD patients based on changes in memory function, the z-score of the Seoul verbal learning test delayed recall. RESULTS: Of the 120 enrolled patients, 107 successfully completed the 24-month follow-up assessment. Among these, 80 patients (74.8%) with SCD exhibited memory function improvements. SCD patients with improved memory function had a lower prevalence of coronary artery disease at baseline and performed better in the trail-making test part B compared to those without improvement. Anatomical and biomarker analysis showed a lower frequency of amyloid PET positivity and larger volumes in the left and right superior parietal lobes in subjects with improved memory function. CONCLUSIONS: Our prospective study indicates that SCD patients experiencing memory improvement over a 24-month period had a lower amyloid burden, fewer cardiovascular risk factors, and superior executive cognitive function. Identifying these key factors associated with cognitive improvement may assist clinicians in predicting future memory function improvements in SCD patients.


Assuntos
Doença de Alzheimer , Disfunção Cognitiva , Demência , Humanos , Estudos Longitudinais , Estudos de Coortes , Estudos Prospectivos , Disfunção Cognitiva/epidemiologia , Neuroimagem , Testes Neuropsicológicos , Doença de Alzheimer/psicologia
2.
J Korean Med Sci ; 37(10): e50, 2022 Mar 14.
Artigo em Inglês | MEDLINE | ID: mdl-35289135

RESUMO

As coronavirus disease 2019 (COVID-19) has spread worldwide, the rate of COVID-19 vaccination uptake is encouraging. Neurological complications associated with COVID-19 vaccines such as stroke, Guillain-Barré syndrome, and Bell's palsy have been reported. Recently, late-onset myasthenia gravis (MG) following COVID-19 vaccination has been reported. To date, however, there has been no evidence of increased risk of early-onset MG following COVID-19. Here, we report a case of a patient with new-onset MG that arose after receiving a COVID-19 vaccine. A 33-year-old woman suddenly experienced generalized weakness and diplopia on the evening she had received the second dose of the Pfizer-BioNTech COVID-19 vaccine. The temporal relationship suggests that this new-onset MG is related to the vaccination. It also implies that COVID-19 vaccination could trigger early-onset MG symptoms in patients at risk of MG.


Assuntos
Vacina BNT162/efeitos adversos , Miastenia Gravis/etiologia , Adulto , Eletromiografia , Feminino , Humanos , Miastenia Gravis/diagnóstico , Miastenia Gravis/fisiopatologia , Neostigmina/farmacologia , República da Coreia , Fatores de Tempo
3.
J Stroke Cerebrovasc Dis ; 30(4): 105623, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33486342

RESUMO

In the present report, we discussed the case of a 57-year-old man with unilateral masticatory muscle weakness, nystagmus, skew deviation and facial hypesthesia due to pontine tegmental infarction. Trigeminal motor neuropathy attributed to brain infarction is very rare. Brain magnetic resonance imaging revealed a small dot-like infarction lesion in the pontine tegmentum. Masticatory muscle weakness was confirmed by an electrophysiological study performed on the day after admission in which there was an incomplete interference pattern without spontaneous denervation activity, suggesting that the patient's masseter muscle weakness was caused by an infarction of the trigeminal motor nucleus proper or trigeminal motor nerve fascicles rather than Wallerian degeneration of the trigeminal nerve or the progression of masseter muscle degeneration.


Assuntos
Infartos do Tronco Encefálico/complicações , Paralisia Facial/etiologia , Músculo Masseter/inervação , Debilidade Muscular/etiologia , Núcleo Motor do Nervo Trigêmeo/irrigação sanguínea , Doenças do Nervo Trigêmeo/etiologia , Doença Aguda , Infartos do Tronco Encefálico/diagnóstico por imagem , Infartos do Tronco Encefálico/fisiopatologia , Paralisia Facial/diagnóstico , Paralisia Facial/fisiopatologia , Humanos , Masculino , Mastigação , Pessoa de Meia-Idade , Debilidade Muscular/diagnóstico , Debilidade Muscular/fisiopatologia , Doenças do Nervo Trigêmeo/diagnóstico , Doenças do Nervo Trigêmeo/fisiopatologia
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