Causes of Vocal Fold Paralysis.

BACKGROUND: Vocal fold paralysis (VFP) can result from a variety of diseases or surgeries and has various causes. This study determined concurrent etiologies in patients who were treated in a teaching hospital (tertiary medical center). METHODS: A retrospective review of medical records of patients with VFP from September 2010 to December 2019 was performed to determine the etiology. Patients with laryngeal/hypopharyngeal malignancies, those with incomplete examination and follow-up data were excluded from the study. During the follow-ups, cases involving recovery were also excluded. RESULTS: One hundred and ninety-four patients with a determined etiology were included: 113 males and 81 females. Unilateral VFP was present in 178 patients, and 16 presented with bilateral VFP. The causes of unilateral VFP were surgical for 61.3%, neoplastic for 17.5%, idiopathic for 10.3%, traumatic for 1.5%, central for 4.7%, cardiovascular for 2%, radiation-induced for 1.5%, and inflammatory for 1%. Thyroidectomy was the most common surgery for unilateral VFP and was the cause for 54 patients. Lung cancer was responsible for 15 cases and was the most common neoplastic etiology of unilateral VFP. For those who presented with bilateral VFP, surgery was the most common cause and accounted for 56.3% of the incidences. In terms of gender, surgery was the most common cause for both sexes, accounting for 62 of 113 male patients and 57 of 81 female patients. Four cases recovered during the follow-ups and these were excluded. CONCLUSION: Surgery and in particular, thyroidectomy, was the most common cause of VFP for these series. Central nervous system disorders were the cause of VFP (4.5%). Central nervous system disorders, especially cerebrovascular accidents that induced VFP, could not be neglected. Radiation-induced cranial nerve paralysis in the head and neck cancer was possible causes. The percentage for the causes of unilateral VFP, surgery increased and the percentage for neoplasm decreased for Taiwan.

Expression of Crip2, a LIM-domain-only protein, in the mouse cardiovascular system under physiological and pathological conditions.

LIM domain-containing proteins mediate protein-protein interactions and play regulatory roles in various physiopathological processes. The mRNA of Crip2, a LIM-only gene, has been detected abundantly in developing and adult hearts but its cell-type specific expression profile has not been well characterized. In this study, we showed that Crip2 is highly expressed in the myocardium, moderately expressed in the endocardium and absent from the epicardium of the developing mouse heart. Interestingly, Crip2 expression is present in the endocardial cells that line both endocardial cushions, whereas it is markedly reduced in the cushion mesenchymes during valve leaflet formation. In the developing vascular system, Crip2 is detected in the endothelial cells of both blood and lymphatic vessels. Consistent with the expression pattern observed in embryos, Crip2 is also highly expressed in the myocardium, endocardium and coronary vascular endothelial cells of the adult heart. In the cardiomyocytes, Crip2 is colocalized with cardiac troponin T in the thin-filaments of sarcomeres. Nonetheless, experimental studies revealed that the expression level of Crip2 is not altered in the isoproterenol (ISO) induced hypertrophic heart. Moreover, Crip2 is detected in endothelial cells of the neovasculature during wound healing and tumor growth. The persistence of Crip2 expression in cardiovascular tissues implies that Crip2 might exert an important impact on the cardiovascular development, maintenance and homeostasis.