Ting Wan1,2, Xiuming Jin1,2, Lin Lin1,2, Yongfeng Xu3, Yingying Zhao1,2. 1. a Eye Center, Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China . 2. b Zhejiang Provincial Key Lab of Ophthalmology , Hangzhou , China and. 3. c Department of Neurology , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Abstract
PURPOSE: To investigate the relationship between meibomian gland dysfunction (MGD) and incomplete blinking caused by cranial nerve seven (CN VII) palsy. METHODS: A prospective case series of 60 consecutive patients with unilateral CN VII palsy was evaluated for MGD. According to the House-Brackmann scale, patients were divided into complete or incomplete blinking group, with the incomplete group further subdivided to early, middle or late stage according to the paralysis duration. Schirmer's I test, tear break-up time (BUT), superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression were evaluated. Unaffected contralateral eyes were used as control for comparison. RESULTS: A paired sample t-test between affected and unaffected eyes demonstrated a significant difference for BUT, superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the incomplete blinking group. However, only BUT showed significant difference between affected and unaffected eyes in complete blinking group. Furthermore, we showed that paralysis duration was related to the incidence of MGD. Significant difference was demonstrated between the affected and unaffected eyes for superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the middle and late stage, but not early stage. CONCLUSIONS: These findings suggest that the inability to blink completely induced by CN VII palsy for more than one week might contribute to the development of MGD. Clinical optimization of blinking may ameliorate MGD symptom and benefit CN VII palsy patients.
PURPOSE: To investigate the relationship between meibomian gland dysfunction (MGD) and incomplete blinking caused by cranial nerve seven (CN VII) palsy. METHODS: A prospective case series of 60 consecutive patients with unilateral CN VII palsy was evaluated for MGD. According to the House-Brackmann scale, patients were divided into complete or incomplete blinking group, with the incomplete group further subdivided to early, middle or late stage according to the paralysis duration. Schirmer's I test, tear break-up time (BUT), superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression were evaluated. Unaffected contralateral eyes were used as control for comparison. RESULTS: A paired sample t-test between affected and unaffected eyes demonstrated a significant difference for BUT, superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the incomplete blinking group. However, only BUT showed significant difference between affected and unaffected eyes in complete blinking group. Furthermore, we showed that paralysis duration was related to the incidence of MGD. Significant difference was demonstrated between the affected and unaffected eyes for superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the middle and late stage, but not early stage. CONCLUSIONS: These findings suggest that the inability to blink completely induced by CN VII palsy for more than one week might contribute to the development of MGD. Clinical optimization of blinking may ameliorate MGD symptom and benefit CN VII palsypatients.
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