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RISS 인기검색어
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- 저자 : Nortina Shahrizaila (검색결과 2 건)
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Determining the Utility of the Guillain-Barré Syndrome Classification Criteria
Cheng-Yin Tan,Siti Nur Omaira Razali,Khean Jin Goh,Nortina Shahrizaila 대한신경과학회 2021 Journal of Clinical Neurology Vol.17 No.2
Background and Purpose Several variants of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) exist, but their frequencies vary in different populations and do not always meet the inclusion criteria of the existing diagnostic criteria. However, the GBS classification criteria by Wakerley and colleagues recognize and define the clinical characteristics of each variant. We applied these criteria to a GBS and MFS cohort with the aim of determining their utility. Methods Consecutive GBS and MFS patients presenting to our center between 2010 and 2020 were analyzed. The clinical characteristics, electrophysiological data, and antiganglioside antibody profiles of the patients were utilized in determining the clinical classification. Results This study classified 132 patients with GBS and its related disorders according to the new classification criteria as follows: 64 (48.5%) as classic GBS, 2 (1.5%) as pharyngeal-cervical- brachial (PCB) variant, 7 (5.3%) as paraparetic GBS, 29 (22%) as classic MFS, 3 (2.3%) as acute ophthalmoparesis, 2 (1.5%) as acute ataxic neuropathy, 2 (1.5%) as Bickerstaff brainstem encephalitis (BBE), 17 (12.9%) as GBS/MFS overlap, 4 (3%) as GBS/BBE overlap, 1 (0.8%) as MFS/PCB overlap, and 1 (0.8%) as polyneuritis cranialis. The electrodiagnosis was demyelinating in 55% of classic GBS patients but unclassified in 79% of classic MFS patients. Anti-GM1, anti-GD1a, anti-GalNAc-GD1a, and anti-GD1b IgG ganglioside antibodies were more commonly detected in the axonal GBS subtype, whereas the anti-GQ1b and anti-GT1a IgG ganglioside antibodies were more common in classic MFS and its subtypes. Conclusions Most of the patients in the present cohort met the criteria of either classic GBS or MFS, but variants were seen in one-third of patients. These findings support the need to recognize variants of both syndromes in order to achieve a more-complete case ascertainment in GBS.
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Sharifah Azira Taufik,Norlina Ramli,Ai Huey Tan,Shen-Yang Lim,Mohd Taufiq Abdul Ghani,Nortina Shahrizaila 대한신경과학회 2024 Journal of Clinical Neurology Vol.20 No.3
Background and Purpose There is increasing evidence that the anterior visual pathways are involved in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD). This study investigated longitudinal changes in retinal nerve fiber layer (RNFL) thickness in patients with ALS and PD with the aim of better understanding their roles as biomarkers of disease progression. Methods This study recruited 21 ALS patients, 19 age-matched PD patients, and 21 agematched healthy controls. Patient demographics and clinical scores relating to the respective diseases were documented. The RNFL thickness was measured using optical coherence tomography at baseline and after 6 months. Results At baseline, the RNFL in the superior quadrant was significantly thinner in the patients with ALS than in healthy controls (109.90±22.41 μm vs. 127.81±17.05 μm [mean±standard deviation], p=0.008). The RNFL thickness did not differ significantly between the ALS and PD patients or between the PD patients and healthy controls. At 6 months, there was further significant RNFL thinning in patients with ALS, for both the overall thickness (baseline: median=94.5 μm, range=83.0–106.0 μm; follow-up: median=93.5 μm, range=82.5–104.5 μm, p=0.043) and the thickness in the inferior quadrant (median=126 μm, range=109.5–142.5 μm; and median= 117.5 μm, range=98.5–136.5 μm; respectively, p=0.032). However, these changes were not correlated with the ALS functional scores. In contrast, the patients with PD did not demonstrate a significant change in RNFL thickness between the two time points. Conclusions The RNFL thickness is a promising biomarker of disease progression in patients with ALS but not in those with PD, which has a slower disease progression.
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