Lloyd, Robin M.

Abstract Introduction Obstructive Sleep Apnea (OSA) in children and adolescents is commonly discussed amongst dental specialists. Physical attributes such as a high and narrow palate, dolichofacial appearance, and retrognathic mandible are reported to increase pediatric risk for OSA. Previous research states rapid maxillary expansion decreases AHI in children with OSA and may be an effective treatment option. Current literature does not report a consistent method of measuring a maxillary transverse deficiency nor does it report a numerical maxillary threshold deficiency that requires expansion in pediatric patients with OSA. Our aims are to compare two different orthodontic diagnostic methods for measuring the maxillary transverse dimension and to assess whether patients diagnosed with mild, moderate, or severe OSA have a numerical threshold for maxillary deficiency. Methods Participants were ages 7-17 years old (average 11.7 years) with no history of orthodontic treatment, craniofacial syndromes, craniosynostosis forms, or nasal abnormalities. Those with and without adenoids and tonsils were included. Participants presented to the Mayo Clinic Sleep Center for their polysomnogram. Their dentition was scanned, and a digital model was rendered. The maxillary transverse dimension was measured via two different methods: McNamara’s Analysis and Andrew’s Six Elements of Orofacial Harmony. Results There were 65 participants: 31 diagnosed with OSA (13 Mild, 4 Moderate, 5 Severe, and 9 Other) and 34 without (controls). Patients in the Other category were diagnosed based on clinical findings. No statistical difference was found between the maxillary transverse measurements of patients with versus without OSA or between the OSA categories. Patients with OSA were more likely to have permanent teeth (61.3% vs 32.4%, p=0.019), tonsils removed (54.8% vs 26.5%, p=0.020), and to have snored during the PSG (83.9% vs 55.9%, p=0.048). Conclusion Conclusions based on this pilot study should be interpreted carefully due to limited sample sizes. No statistically significant differences of the maxillary transverse dimension were found between those with and without OSA using either diagnostic method. No numerical maxillary deficiency threshold was found. Maxillary expansion should not be recommended based on OSA diagnosis alone. Referral to a dental specialist is recommended based on dental needs. Support (if any) Support was provided by Mayo Clinic CTSA grant UL1TR002377.

Secondary narcolepsy occurs as a consequence of lesions involving the hypothalamic region that subserve wakefulness. Although observations on the characteristics of secondary narcolepsy have been published in adults, information on this topic in children is sparse. This is a retrospective study of characteristics and outcome of secondary narcolepsy in children. The medical records of 10 children with this condition at Mayo Clinic, Rochester, were reviewed. Characteristics of the underlying neurologic disorder, narcolepsy subtype, multiple sleep latency tests, medications used and outcome were extracted. Age at diagnosis of narcolepsy was between 6 and 17 years. Five of 10 patients had onset of excessive sleepiness within 1 year of diagnosis of the primary neurologic disorder. Six of 10 patients had type 1 narcolepsy (with cataplexy) whereas 4/10 had type 2 (without cataplexy). The clinical course was variable, with 8/10 continuing to require treatment for sleepiness at a mean period 6.6±6.2 years after diagnosis. One patient with narcolepsy type 1 due to Niemann Pick type C disease had died. One patient with narcolepsy type 2 due to craniopharyngioma had spontaneous remission of sleepiness. The 5/10 patients surviving with narcolepsy type 1 have continued to require pharmacotherapy for both sleepiness and cataplexy. This study draws attention to an important chronic sequel of childhood brain lesions that has variable, etiology-specific outcome. The rare occurrence of spontaneous resolution of childhood narcolepsy symptoms, not previously described, is also discussed.

Abstract Introduction The ICSD-3 describes NREM-related parasomnias as abnormal sleep related complex movements where motor behavior occurs in the setting of absent or very minimal higher cognitive function. A population-based twin study reported that 3.9% of men and 3.1 % of women sleepwalk (SW) with 30% reported experiencing injury (Hublin 1997). Sleep related eating disorder (SRED) may be a variant of SW with a reported prevalence of 0.5-5 % (Michalska 2016). This study examined SW and SRED in a population-based sample permitting review of associated features, risk factors and outcomes. Methods The records-linkage system of the Rochester Epidemiology Project that includes all adults residing in Olmsted County MN was searched for documentation of patients seeking care for at least two episodes of sleepwalking and/or sleep eating. Records from 2007-2016 were included. Results 56 cases were identified with 50 (89 %) having SW and 16 (29%) SRED. The gender breakdown was 50% male and 50% female with the mean age at diagnosis of 40 (SD 13). Childhood parasomnia events were reported by 23/36 (62%) and a family history in 21/35 (64%). Data were unavailable for the others. The number of parasomnia incidents was ≥ 10 for 21 (37%). A variety of experiences were documented, including leaving the bedroom (39%), injury (25%), and exiting through a window/balcony (5%). Associated factors were sleep deprivation (52%), untreated obstructive sleep apnea (34%), antidepressant use (41%), zolpidem use (18%), circadian disruption (14%) and alcohol use (9%). Polysomnography was conducted for 41 (74%). Documented interventions were medication discontinuation (18%) and starting a benzodiazepine (16%). In 21%, no treatment was given. Conclusion This population-based study of adults with clinician diagnosed recurrent SW and SRED revealed equal rates in men and women. The majority of patients with SRED also had SW. 25% of cases were associated with injuries. Support Rochester Epidemiology Project supported by NIH R01 AG034676 and AG052425 and the Mayo Foundation.