This report was written by the Japanese Society of Dysphagia Rehabilitation, the Japanese Association of Rehabilitation Nutrition, the Japanese Association on Sarcopenia and Frailty, and the Society of Swallowing and Dysphagia of Japan to consolidate the currently available evidence on the topics of sarcopenia and dysphagia. Histologically, the swallowing muscles are of different embryological origin from somatic muscles, and receive constant input stimulation from the respiratory center. Although the swallowing muscles are striated, their characteristics are different from those of skeletal muscles. The swallowing muscles are inevitably affected by malnutrition and disuse; accumulating evidence is available regarding the influence of malnutrition on the swallowing muscles. Sarcopenic dysphagia is defined as dysphagia caused by sarcopenia of the whole body and swallowing‐related muscles. When sarcopenia does not exist in the entire body, the term “sarcopenic dysphagia” should not be used. Additionally, sarcopenia due to neuromuscular diseases should be excluded; however, aging and secondary sarcopenia after inactivity, malnutrition and disease (wasting disorder and cachexia) are included in sarcopenic dysphagia. The treatment of dysphagia due to sarcopenia requires both dysphagia rehabilitation, such as resistance training of the swallowing muscles and nutritional intervention. However, the fundamental issue of how dysphagia caused by sarcopenia of the swallowing muscles should be diagnosed remains unresolved. Furthermore, whether dysphagia can be caused by primary sarcopenia should be clarified. Additionally, more discussion is required on issues such as the relationship between dysphagia and secondary sarcopenia, as well as the diagnostic criteria and means for diagnosing dysphagia caused by sarcopenia. Geriatr Gerontol Int 2019; 19: 91–97.

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Fifteen patients suffering from visual disturbance of varying degrees caused by a mucocele of the posterior ethmoid and/or sphenoid sinuses underwent marsupialization of a mucocele into the nasal cavity. Five of the eight patients with severe visual loss worse than 20/200 showed recovery of measurable vision. Two of these five were operated on within 24 hours after the onset of visual loss and showed marked recovery to 20/25 and 20/15. The other seven patients who had relatively mild visual disturbance experienced improvement of visual acuity or remission of subjective complaints such as blurred vision post-operatively. During operation partial bony defect was found in the optic canal in 12 patients and in the skull base in 12 patients. A good understanding of this disease by ophthalmologists and otolaryngologists is essential for early diagnosis and prompt surgical treatment to avoid permanent visual dysfunction and operative sequelae.

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