Background Newborns sleep about 80% of the time. Gastroesophageal reflux (GER) disease is prevalent in about 10% of NICU infants. Concurrent polysomnography and pH-impedance studies clarify relationship of GER with sleep. Aims To characterize spatio-temporal and chemical characteristics of impedance-positive GER and define symptom associations in sleep and wake states in symptomatic neonates. We hypothesized that frequency of impedance-positive GER events and their association with cardiorespiratory symptoms is greater during sleep. Methods Eighteen neonates underwent concurrent polysomnography with pH-impedance study. Impedance-positive GER events (weakly acidic or acidic) were categorized between sleep vs. wake states: Symptom Index = # of symptoms with GER/total symptoms*100, Symptom Sensitivity Index = # of GER with symptoms/Total GER*100 and Symptom Association Probability = [(1-Probability of observed association between reflux and symptoms)*100]). Results We analyzed 317 GER events during 116 hours of polysomnography. During wake vs. sleep respectively, the median (interquartile range) frequency of impedance-positive GER was 4.9(3.1–5.8) vs. 1.4(0.7–1.7)events/hour (P<0.001), proximal migration was 2.6(0.8–3.3) vs. 0.2(0.0–0.9)events/hour (P<0.001); Symptom Index for cardiorespiratory symptoms for impedance-positive events was 22.5 (0–55.3) vs. 6.1(0–13), P=0.04 while Symptom Sensitivity Index was 9.1(0–23.1) vs. 18.4 (0–50), P=0.04 though Symptom Association Probability was similar, (P=0.68). Conclusions Contrary to our hypothesis, frequency of GER in sleep is lesser; however, spatio-temporal and chemical characteristics of GER and symptom generation mechanisms are distinct. For cardiorespiratory symptoms during sleep, lower Symptom Index entails evaluation for etiologies other than GER disease, higher Symptom Sensitivity Index implies heightened esophageal sensitivity and similar Symptom Association Probability indicates other mechanistic possibilities.

Homozygosity for the methylenetetrahydrofolate reductase (MTHFR) 677C>T mutation (MTHFR TT) has been linked to an increased risk for stroke, coronary artery disease, and migraine headaches. The authors analyzed the potential link between MTHFR 677C>T homozygosity and childhood stroke. A true association might facilitate screening, recurrence risk stratification, and treatment in patients with cerebrovascular disease. They performed a retrospective chart review of children tested for the MTHFR 677C>/T mutation; 533 patients underwent MTHFR testing, and 8% were homozygous for the MTHFR 677C>T mutation. There was no difference in the cohort compared with the prevalence in the general population. This suggests that the MTHFR 677 C>T polymorphism played a minimal role or no role in stroke risk. However, the data suggest that the MTHFR TT genotype may influence migraine susceptibility in children because there was a higher proportion of migraine patients (28.6%) with the MTHFR TT homozygous genotype.

A 9-year-old boy with primary myoclonus dystonia with comorbid severe attention deficit hyperactive disorder (ADHD) also had sleep onset and maintenance insomnia. Polysomnography showed features of non-rapid eye movement parasomnia. Daily bedtime clonidine helped sleep and hyperactivity. ADHD symptoms improved with 40 mg daily lisdexamphetamine mesylate. As the myoclonus and dystonia symptoms progressed, clonazepam was initiated at a dose of 0.5 mg daily at bedtime. It was anticipated that clonazepam would also improve parasomnia. Concomitant with the initiation of clonazepam, he developed a sleep-related eating disorder (SRED) continuing almost throughout the night. The symptoms went away upon stopping clonazepam. This is the first description of clonazepam producing SRED though it is the treatment of choice for this disorder.