Chronotype is associated with the timing of the circadian clock and sleep in toddlers.

Chronotype is a construct reflecting individual differences in diurnal preference. Although chronotype has been studied extensively in school-age children, adolescents and adults, data on young children are scarce. This study describes chronotype and its relationship to the timing of the circadian clock and sleep in 48 healthy children aged 30-36 months (33.4 ± 2.1 months; 24 males). Parents completed the Children's Chronotype Questionnaire (CCTQ) ~2 weeks before the start of the study. The CCTQ provides three measures of chronotype: midsleep time on free days, a multi-item morningness/eveningness score and a single item chronotype score. After 5 days of sleeping on their habitual schedule (assessed with actigraphy and sleep diaries), children participated in an in-home salivary dim light melatonin onset assessment. Average midsleep time on free days was 1:47 ± 0:35, and the average morningness/eveningness score was 26.8 ± 4.3. Most toddlers (58.4%) were rated as 'definitely a morning type' or 'rather morning than evening type', while none (0%) were rated as 'definitely evening type'. More morning types (midsleep time on free days and morningness/eveningness score, respectively) had earlier melatonin onset times (r = 0.45, r = 0.26), earlier habitual bedtimes (r = 0.78, r = 0.54), sleep onset times (r = 0.80, r = 0.52), sleep midpoint times (r = 0.90, r = 0.53) and wake times (r = 0.74, r = 0.34). Parent ratings using the single-item chronotype score were associated with melatonin onset (r = 0.32) and habitual bedtimes (r = 0.27), sleep onset times (r = 0.33) and sleep midpoint times (r = 0.27). Morningness may best characterize circadian preference in early childhood. Associations between chronotype and circadian physiology and sleep timing suggest adequate validity for the CCTQ in this age group. These findings have important implications for understanding the marked variability in sleep timing during the early years of life.

Bow hunter's syndrome in a patient with vertebral artery atresia, an arcuate foramen, and unilateral deafness: a case report.

Bow hunter's syndrome (BHS) is a rare cause of vertebrobasilar insufficiency that occurs when the vertebral artery (VA) is occluded on rotation of the head and neck. This dynamic occlusion of the VA can occur anywhere along its course after it arises from the subclavian artery. Although most cases are associated with compression by osteophytes, cervical spondylosis, or lateral disc herniation, BHS has a highly variable clinical course that depends on the patient's specific anatomy. Therefore, it may be important for clinicians to be aware of anatomical variants that predispose individuals to BHS. Here, we report on a patient with BHS who was found to have two uncommon anatomical anomalies: an atretic right VA and a left-sided arcuate foramen.

The Timing of the Circadian Clock and Sleep Differ between Napping and Non-Napping Toddlers.

The timing of the internal circadian clock shows large inter-individual variability across the lifespan. Although the sleep-wakefulness pattern of most toddlers includes an afternoon nap, the association between napping and circadian phase in early childhood remains unexplored. This study examined differences in circadian phase and sleep between napping and non-napping toddlers. Data were collected on 20 toddlers (34.2±2.0 months; 12 females; 15 nappers). Children followed their habitual napping and non-napping sleep schedules (monitored with actigraphy) for 5 days before an in-home salivary dim light melatonin onset (DLMO) assessment. On average, napping children fell asleep during their nap opportunities on 3.6±1.2 of the 5 days before the DLMO assessment. For these napping children, melatonin onset time was 38 min later (p = 0.044; d = 0.93), actigraphically-estimated bedtime was 43 min later (p = 0.014; d = 1.24), sleep onset time was 59 min later (p = 0.006; d = 1.46), and sleep onset latency was 16 min longer (p = 0.030; d = 1.03) than those not napping. Midsleep and wake time did not differ by napping status. No difference was observed in the bedtime, sleep onset, or midsleep phase relationships with DLMO; however, the wake time phase difference was 47 min smaller for napping toddlers (p = 0.029; d = 1.23). On average, nappers had 69 min shorter nighttime sleep durations (p = 0.006; d = 1.47) and spent 49 min less time in bed (p = 0.019; d = 1.16) than non-nappers. Number of days napping was correlated with melatonin onset time (r = 0.49; p = 0.014). Our findings indicate that napping influences individual variability in melatonin onset time in early childhood. The delayed bedtimes of napping toddlers likely permits light exposure later in the evening, thereby delaying the timing of the clock and sleep. Whether the early developmental trajectory of circadian phase involves an advance associated with the decline in napping is a question necessitating longitudinal data as children transition from a biphasic to monophasic sleep-wakefulness pattern.

Circadian phase and its relationship to nighttime sleep in toddlers.

Circadian phase and its relation to sleep are increasingly recognized as fundamental factors influencing human physiology and behavior. Dim light melatonin onset (DLMO) is a reliable marker of the timing of the circadian clock, which has been used in experimental, clinical, and descriptive studies in the past few decades. Although DLMO and its relationship to sleep have been well documented in school-aged children, adolescents, and adults, very little is known about these processes in early childhood. The purpose of this study was 1) to describe circadian phase and phase angles of entrainment in toddlers and 2) to examine associations between DLMO and actigraphic measures of children's nighttime sleep. Participants were 45 healthy toddlers aged 30 to 36 months (33.5 ± 2.2 months; 21 females). After sleeping on a parent-selected schedule for 5 days (assessed with actigraphy and diaries), children participated in an in-home DLMO assessment involving the collection of saliva samples every 30 minutes for 6 hours. Average bedtime was 2015 ± 0036 h, average sleep onset time was 2043 ± 0043 h, average midsleep time was 0143 ± 0038 h, and average wake time was 0644 ± 0042 h. Average DLMO was 1929 ± 0051 h, with a 3.5-hour range. DLMO was normally distributed; however, the distribution of the bedtime, sleep onset time, and midsleep phase angles of entrainment were skewed. On average, DLMO occurred 47.8 ± 47.6 minutes (median = 39.4 minutes) before bedtime, 74.6 ± 48.0 minutes (median = 65.4 minutes) before sleep onset time, 6.2 ± 0.7 hours (median = 6.1 hours) before midsleep time, and 11.3 ± 0.7 hours before wake time. Toddlers with later DLMOs had later bedtimes (r = 0.46), sleep onset times (r = 0.51), midsleep times (r = 0.66), and wake times (r = 0.65) (all p < 0.001). Interindividual differences in toddlers' circadian phase are large and associated with their sleep timing. The early DLMOs of toddlers indicate a maturational delay in the circadian timing system between early childhood and adolescence. These findings are a first step in describing the fundamental properties of the circadian system in toddlers and have important implications for understanding the emergence of sleep problems and the consequences of circadian misalignment in early childhood.