The sleep/wake rhythm in children with autism

Abstract

The sleep patterns of two groups of children with autism, one with moderate to severe intellectual handicap, and one with mild handicap to normal IQ level, were compared with those of children without autism. Parents completed 14 day sleep diaries and questionnaires. Results suggested that at some stage during childhood, particularly under 8 years of age, the majority of children with autism will experience sleep problems. These problems are likely to be severe in many cases and will generally include one or more of: extreme sleep latencies; lengthy periods of night waking, shortened night sleep; and early morning waking. Such problems may have some specificity for autism as they appear to be rare in non-handicapped children and in children with mild degrees of intellectual handicap. It is likely that sleep problems in early childhood are related to the severe social difficulties present in autism and the consequent inability of these children to use social cues to synchronize their sleep/wake cycle. Continued sleep difficulties at older ages and with higher IQ may also be related to arousal and anxiety factors.

Reduced axonal localization of a Caps2 splice variant impairs axonal release of BDNF and causes autistic-like behavior in mice

“…Impaired circadian rhythm. Autism is frequently accompanied by an abnormal sleep-wake rhythm (39,40). Regarding the circadian rhythm of locomotor activity under a 12-h light/dark cycle, we detected no differences in the sleep-wake rhythm among wildtype, Caps2 +/Δex3 , and Caps2 Δex3/Δex3 mice.…”

Association of Per1 and Npas2 with autistic disorder: support for the clock genes/social timing hypothesis

“…6 The role of per1 in modulating high-frequency oscillators concerned with communicative timing, [69][70][71] together with our findings of association of per1 with autistic disorder, strengthens the notion that temporal deficits are quintessential to autistic disorder. [21][22][23][24][25][26]28,29,39 Purkinje neurons are important for learning appropriate timing 120,121 and their abnormally low number in the cerebella of autistic subjects 115,122 is considered a keystone biological observation implicating cerebellar dysfunction. 123,124 In this context, reports of a per1 interacting protein (PIPS) in rat that co-translocates with per1 into the nucleus 125 and which is further shown to be required for neuronal growth factor-mediated neuronal survival in P12 cells, 126 tentatively suggests a role for per1 in the lack of Purkinje neurons of the cerebellum in autism.…”

“…Newson 22 ), with hypotheses encompassing circadian, communicative and/or neurological aspects of timing. 21,[23][24][25][26][27][28][29] For example, Boucher 25 suggests a core timing deficit presenting different manifestations by its effect on the elements of an integrated system of neural and physiological oscillators. Wimpory et al 21 hypothesize a causative, concurrent and developmental role 30 for timing deficit in autistic disorder and that this deficit is derived from pathological variations in the structure/ function of clock/clock-related genes.…”

The Possible Interplay of Synaptic and Clock Genes in Autism Spectrum Disorders

“…This problem persists through childhood because 50-80% of children with ASD show highly significant increased sleep latency and nocturnal awakenings (Richdale and Prior 1995;Taira et al 1998;Takase et al 1998;Hering et al 1999;Elia et al 2000;Hayashi 2000;Schreck and Mulick 2000;Gail Williams et al 2004;Wiggs and Stores 2004;Limoges et al 2005;Oyane and Bjorvatn 2005;Polimeni et al 2005;Allik et al 2006;Hare et al 2006;Liu et al 2006;Malow et al 2006). An extensive survey of the sleep problems observed in ASD was recently reported by Liu et al (2006).…”