Jong Kuk Kim1, Byung-Jo Kim2, Ha Young Shin3, Kyong Jin Shin4, Tai-Seung Nam5, Jung Im Seok6, Bum Chun Suh7, Jeeyoung Oh8, Yeo Jung Kim4, Jong Seok Bae9. 1. Department of Neurology, College of Medicine, Dong-A University, Busan, Republic of Korea. 2. Department of Neurology, College of Medicine, Korea University, Seoul, Republic of Korea. 3. Department of Neurology, College of Medicine, Yonsei University, Seoul, Republic of Korea. 4. Department of Neurology, College of Medicine, Inje University, Busan, Republic of Korea. 5. Department of Neurology, College of Medicine, Chonnam National University, Gwangju, Republic of Korea. 6. Department of Neurology, College of Medicine, Catholic University of Daegu, Daegu, Republic of Korea. 7. Department of Neurology, College of Medicine, Sungkyunkwan University, Seoul, Republic of Korea. 8. Department of Neurology, School of Medicine, Kunkuk University, Seoul, Republic of Korea. 9. Department of Neurology, College of Medicine, Hallym University, Seoul, Republic of Korea. Electronic address: lwsbae@naver.com.
Abstract
OBJECTIVE: Delayed facial palsy (DFP) has often been described during the recovery stage of Fisher syndrome (FS), but the implications of DFP in FS pathophysiology have not been reported previously. The aim of this study was to identify the incidence and clinical course of DFP in FS, and to determine its clinical/pathophysiological implications in FS. METHODS: About 71 FS patients were enrolled from seven university-based hospitals in Korea. DFP was defined with respect to new development of unilateral or bilateral facial palsies with delayed onset after either the nadir or improvement of initial neurological signs of FS. RESULTS: Eleven of the 71 patients (16%) satisfied the definition of DFP. No other cranial palsies developed as a delayed pattern. With the exception of two patients with bulbar involvement, DFP developed after a latent period of upper-cranial neuropathies. Comparison of FS patients without and with DFP revealed no significant clinical, serological, or electrophysiological differences. All except one patient with DFP exhibited a good outcome within 1 month of follow-up. CONCLUSION: DFP was identified as a common and specific phenomenon in FS. Nearly all cases of DFP were developed in a descending manner and were associated with a good outcome, while other cranial neuropathies developed or followed as a sequential pattern. These findings suggest the involvement of so-called "descending reversible paralysis" in the pathophysiology of FS.
OBJECTIVE:Delayed facial palsy (DFP) has often been described during the recovery stage of Fisher syndrome (FS), but the implications of DFP in FS pathophysiology have not been reported previously. The aim of this study was to identify the incidence and clinical course of DFP in FS, and to determine its clinical/pathophysiological implications in FS. METHODS: About 71 FS patients were enrolled from seven university-based hospitals in Korea. DFP was defined with respect to new development of unilateral or bilateral facial palsies with delayed onset after either the nadir or improvement of initial neurological signs of FS. RESULTS: Eleven of the 71 patients (16%) satisfied the definition of DFP. No other cranial palsies developed as a delayed pattern. With the exception of two patients with bulbar involvement, DFP developed after a latent period of upper-cranial neuropathies. Comparison of FS patients without and with DFP revealed no significant clinical, serological, or electrophysiological differences. All except one patient with DFP exhibited a good outcome within 1 month of follow-up. CONCLUSION: DFP was identified as a common and specific phenomenon in FS. Nearly all cases of DFP were developed in a descending manner and were associated with a good outcome, while other cranial neuropathies developed or followed as a sequential pattern. These findings suggest the involvement of so-called "descending reversible paralysis" in the pathophysiology of FS.