Background: The head impulse test is a valuable clinical test that can help identify peripheral vestibular dysfunction by observing corrective saccades that return the eyes to the target of interest. Corrective saccades have been classified as covert if the onset occurs before the end of the head impulse and as overt if they occur afterwards. However, the mechanism that trigger these saccades remain unclear.Objective: The objective of this study was to examine the role of neck input in generating overt as well as covert saccades.Methods: Sixteen patients (9 males and 7 females: age 35-80 years, average 62.7 years old) who showed corrective saccades during the head impulse test were included. Twelve patients had unilateral vestibular dysfunction, and 4 patients had bilateral vestibular dysfunction. Patients underwent both the head impulse test (HIT) and the body impulse test (BIT) in a randomized order. While the head is rotated horizontally in HIT, the body is rotated horizontally in BIT. During BIT, the neck is fixed by a cervical collar (neck lock extrication collar) to reduce somatosensory input from the neck. The head movements and eye movements were recorded and analyzed by the video HIT recording system.Results: In all 16 patients, corrective saccades were observed in HIT as well as in BIT. While there were no significant differences in peak head velocities between HIT and BIT (p = 0.33, paired t-test), the VOR gain in BIT was significantly smaller than that in HIT (p = 0.011, paired t-test). The number of overt saccades per trial in BIT was significantly decreased compared to that in HIT (p < 0.001, paired t-test) whereas there were no significant differences in the number of covert saccades between the two tests. The proportion of overt saccades among all corrective saccades in BIT was significantly lower than the proportion in HIT (p < 0.001, paired t-test).Conclusions: Somatosensory input from the neck contributes to the generation of overt saccades and reinforces the vestibulo-ocular reflex complementing the retinal slip during high frequency head movements.

Patients with m.3243A>G mutation of mitochondrial DNA develop bilaterally symmetric sensorineural hearing loss. However, it is unclear how fast their hearing loss progresses over time, and whether they experience rapid progression of hearing loss. In the present study, we conducted a long-term hearing evaluation in patients with MELAS or MIDD who harbored the m.3243A>G mutation of mitochondrial DNA. A retrospective chart review was performed on 15 patients with this mutation who underwent pure-tone audiometry at least once a year for more than two years. The mean follow-up period was 12.8 years. The mean progression rate of hearing loss was 5.5 dB per year. Hearing loss progressed rapidly to be profoundly deaf in seven patients during the observation period. Heteroplasmy and age-corrected heteroplasmy levels correlated with the age of onset of hearing loss. These results indicate that patients with m.3243A>G mutation have a gradual progression of hearing loss in the early stages and rapid decline in hearing to be profoundly deaf in approximately half of the patients. Although it is possible to predict the age of onset of hearing loss from heteroplasmy and age-corrected heteroplasmy levels, it is difficult to predict whether and when the rapid hearing loss will occur.

Clinical evidence of the effectiveness of cochlear implantation for hearing loss with mitochondrial DNA mutation is limited. Most reports have only described short-term postoperative speech perception, which may not reflect the limitations of cochlear implantation caused by progressive retrocochlear dysfunction. The present study aimed to investigate long-term speech perception after cochlear implantation in patients with severe to profound hearing loss associated with mitochondrial DNA mutation. A retrospective chart review was performed on patients with mitochondrial DNA mutation who had undergone cochlear implantation at the Department of Otolaryngology and Head and Neck Surgery at the University of Tokyo Hospital. We extracted data on causative mutations, clinical types, clinical course, perioperative complications, and short-term and long-term postoperative speech perception. Nine patients with mitochondrial DNA mutation underwent cochlear implantation. The mean observation period was 5.5 ± 4.2 years (range, 1–13 years), and seven patients were followed for more than 3 years. Two of the seven patients who initially showed good speech perception exhibited deterioration during long-term follow-up. The absence of an acute progression of cognitive decline in patients, showing a gradual decrease in speech perception, suggests that the deterioration of speech perception was caused by progressive retrocochlear degeneration. Although most patients with mitochondrial DNA mutation maintained good speech perception for more than 3 years after cochlear implantation, retrocochlear degeneration could cause the deterioration of speech perception during long-term follow-up.

Objectives: This study investigates the association of pretreatment underweight, sarcopenia, and cancer cachexia with survival outcome in hypopharyngeal cancer (HPC) radiotherapy. Methods: This retrospective observational study analyzed 167 patients with newly diagnosed HPC treated with definitive radiotherapy. The definitions of underweight, sarcopenia, and cancer cachexia are based on the international consensus of the European Palliative Care Research Collaborative. Underweight and sarcopenia were analyzed in all 167 patients, while cachexia analyses were restricted to the 117 patients for whom pretreatment weight-loss data were available. Survival outcomes were estimated using the Kaplan–Meier method and compared using the log-rank test, and subsequently analyzed using multivariate Cox proportional hazards models. Results: The median follow-up period was 28 months. Cachexia analyses were restricted to the 117 patients for whom pretreatment weight-loss data were available; of these, 45 (38%) met criteria for cancer cachexia. Patients with underweight (n = 76, 46%) or cancer cachexia had significantly lower locoregional control, disease-free survival, and overall survival compared to those not underweight and without cachexia, respectively, whereas there was no difference in any outcome between patients with sarcopenia (n = 54, 32%) and those without. Given the definitional overlap among underweight, sarcopenia, and cachexia, these three variables were entered into the multivariate analysis separately—which included age, sex, performance status, double cancer, T-classification, N-classification, chemotherapy administration, treatment era, and radiation dose—confirming that underweight and cancer cachexia remained independently associated with worse LRC, DFS, and OS. In the fully adjusted multivariate Cox proportional hazards models, the hazard ratios for mortality risk were 1.9 (95% confidence interval [CI], 1.1–3.4; p = 0.030) and 2.0 (95% CI, 1.1–3.8; p = 0.032) for patients with underweight or cancer cachexia, respectively. Conclusions: Pretreatment underweight and cancer cachexia negatively impact survival outcomes, including locoregional control, in HPC radiotherapy. Prospective studies with standardized nutritional assessment protocols, pre-specified intervention arms, and sufficient sample sizes are essential to validate these findings and to establish the clinical benefit of pre-treatment nutritional optimization in this patient population.