Fourteen consecutive children who were newly diagnosed with attention‐deficit hyperactivity disorder (ADHD) and who had never been exposed to stimulants and 10 control children without ADHD underwent polysomnographic studies to quantify Periodic Limb Movements in Sleep (PLMS) and arousals. Parents commonly gave both false‐negative and false‐positive reports of PLMS in their children, and a sleep study was necessary to confirm their presence or absence. The prevalence of PLMS on polysomnography was higher in the children with ADHD than in the control subjects. Nine of 14 (64%) children with ADHD had PLMS at a rate of >5 per hour of sleep compared with none of the control children (p <0.0015). Three of 14 children with ADHD (21%) had PLMS at a rate of >20 per hour of sleep. Many of the PLMS in the children with ADHD were associated with arousals. Historical sleep times were less for children with ADHD. The children with ADHD who had PLMS chronically got 43 minutes less sleep at home than the control subjects (p = 0.0091). All nine children with ADHD who had a PLMS index of >5 per hour of sleep had a long‐standing clinical history of sleep onset problems (>30 minutes) and/or maintenance problems (more than two full awakenings nightly) thus meeting the criteria for Periodic Limb Movement Disorder (PLMD). None of the control children had a clinical history of sleep onset or maintenance problems. The parents of the children with ADHD were more likely to have restless legs syndrome (RLS) than the parents of the control children. Twenty‐five of 28 biologic parents of the children with ADHD and all of the biologic parents of the control children were reached for interview. Eight of twenty‐five parents of the children with ADHD (32%) had symptoms of RLS as opposed to none of the control parents (p = 0.011). PLMS may directly lead to symptoms of ADHD through the mechanism of sleep disruption. Alternative explanations for the association between ADHD and RLS/PLMS are that they are genetically linked, they share a common dopaminergic deficit, or both.

Nine of twelve cases of juvenile diabetes mellitus, representing an unusual geographic and temporal cluster, were investigated for evidence that a specific viral infection might be etiologically related to their occurrence. Eight diabetics had experienced recent "viral-like" illnesses, predominantly repiratory, but these illnesses bore no uniform temporal relation to their onsets of diabetes. Diabetics demonstrated no serologic evidence of a recent viral illness common to all. Elevated titers to only one virus, coxsackie B-3, were more prevalent in diabetics than in controls (33% vs. 6%), but geometric mean titers of diabetics to a panel of 26 common viral antigens were similar to those of controls. These data neither support nor negate the hypothesis that infection with a specific virus precipitates juvenile diabetes mellitus. diabetes mellitus, juvenile; respiratory tract infections

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