Recently, it has been suggested that sleep problems in autism spectrum disorder (ASD) not only are associated symptoms, but may be deeply related to ASD pathogenesis. Common clinical practice relating to developmental disorders, has shown that parents of children with ASD have often stated that it is more difficult to raise children in the neonatal period because these children exhibit sleep problems. This study investigated the possibility that abnormal neonatal sleep-wake rhythms are related to future ASD development. We administered questionnaires to assess parent(s) of children with ASD and controls. A retrospective analysis was conducted among 121 children with ASD (94 male and 27 female children) recruited from the K-Development Support Center for Children (K-ASD), 56 children with ASD (40 male and 16 female children) recruited from the H-Children's Sleep and Development Medical Research Center (H-ASD) and 203 children (104 male and 99 female children) recruited from four nursery schools in T-city (control). Irritable/over-reactive types of sleep-wake rhythms that cause difficulty in raising children, such as 1) frequently waking up, 2) difficulty falling asleep, 3) short sleep hours, and 4) continuous crying and grumpiness, were observed more often in ASD groups than in the control group. Additionally, the number of the mothers who went to bed after midnight during pregnancy was higher in the ASD groups than in the control group. Sleep-wake rhythm abnormalities in neonates may be considerable precursors to future development of ASD. Formation of ultradian and postnatal circadian rhythms should be given more attention when considering ASD development. Although this is a retrospective study, the results suggest that a prospective study regarding this issue may be important in understanding and discovering intervention areas that may contribute to preventing and/or properly treating ASD.

We report a 13-year-old male patient with Charcot-Marie-Tooth disease (CMT) type 2 who developed severe neuropathy because of vincristine (VCR) for his acute lymphoblastic leukemia. A clumsy gait, muscle weakness in his fingers, and inverted champagne bottlelike muscle in the lower limbs were noticed after remission induction treatment for acute lymphoblastic leukemia, which included VCR at a total dose of 8 mg/m. An electrophysiologic study showed an almost normal median motor nerve conduction velocity (approximately 50 m/s), markedly reduced M-wave amplitude and sensory disturbance. He was diagnosed as CMT type 2 based on his symptoms and electrophysiologic findings. His symptoms gradually worsened, and even after VCR was discontinued, he could not walk alone for 7 months. VCR has previously been considered to be relatively safe in CMT type 2, however, some patients with CMT type 2 might show severe neurologic toxicities, as seen in patients with CMT type 1.