The use of clonidine for severe and intractable sleep problems in children with neurodevelpmental disorders. A case series
This paper reports on the use of clonidine for the treatment of severe sleep problems associated with behavioural difficulties in children with neurodevelopmental disabilities. Data were obtained from reviewing the case notes of a series of six children with neurodevelopmental disorders of different nature and severity, presenting with problematic sleep. All children in this group showed maintained improvements in their sleep pattern following the use of clonidine with only mild side-effects reported.
Available from: Duke Chen
- ", 2009 ) . Clonidine has also been used to treat sleep disturbances , which in some cases have been reported in up to one - third of patients with FXS ( Ingrassia and Turk , 2005 ; Kronk et al . , 2010 ) . "
[Show abstract] [Hide abstract]
ABSTRACT: Fragile X syndrome is the most common heritable form of mental retardation. It is caused by silencing of the Fmr1 gene and the absence of the encoded protein. The purpose of this study was to examine global protein expression levels of GABA(A) and GABA(B) receptors, and GABAergic enzymes and trafficking proteins in fragile X knockout mice during brain maturation. Quantitative western blotting of homogenates of forebrain revealed that the levels of GABA(A) beta1 and beta3, GABA(B)-R1, NKCC1, KCC2, gephyrin and ubiquilin were not significantly different from wild-type mice at any of the postnatal time points examined. In contrast, the GABA(A) receptor alpha1, beta2, and delta subunits, and the GABA enzymes GABA transaminase and succinic semialdehyde dehydrogenase were down-regulated during postnatal development, while GAD65 was up-regulated in the adult knockout mouse brain. The GABA(A) receptor alpha1 and beta2 subunits displayed a divergent pattern of developmental expression whereby alpha1 was reduced in the immature brain but regained a level of expression similar to wild-type mice by adulthood, while the expression of beta2 was similar to wild-types at postnatal day 5 but reduced at day 12 and in the adult brain. The GABA(A) receptor delta subunit and the GABA catabolic enzymes GABA transaminase and succinic semialdehyde dehydrogenase were simultaneously but transiently decreased only at postnatal day 12. Our results demonstrate that GABA(A) receptor subunits and GABA enzymes display complex patterns of changes during brain development suggesting that dynamic interactions may occur between GABA transmitter levels and GABA receptors in fragile X syndrome.
Available from: Xue Ming
- "Schnoes et al.  reported that clonidine was ranked second by pediatricians for treatment of sleep disorders, including sleep onset, sleep schedule, nighttime awakening, early morning awakening, and parasomnias. Ingrassia and Turk  found clonidine to be effective in treating severe and intractable sleep problems in children with neurodevelopmental disorders . Clonidine was reported to improve nocturnal hypoxemia and obstructive sleep apnea, possibly due to suppression of REM sleep. "
[Show abstract] [Hide abstract]
ABSTRACT: Children with autism spectrum disorders (ASD) often exhibit sleep and behavioral disorders. Treatment of sleep disorders can be difficult in these children. Clonidine, an alpha2-adrenergic receptor agonist, has been shown to be effective in reducing impulsivity, inattention, and hyperactivity, as well as in serving as a sedative for medial procedures. An open labeled retrospective study of clonidine in treatment of insomnia, and/or hyperactivity, inattention, mood disorder, and aggressive behaviors was conducted using parent reports of sleep initiation and maintenance, as well as behaviors prior and during clonidine treatment. Clonidine was effective in reducing sleep initiation latency and night awakening, to a less degree in improving attention deficits hyperactivity, mood instability and aggressiveness in this cohort of 19 children with ASD. The side effects were largely tolerable. Further evaluation with placebo-controlled double-blind clinical trial of clonidine use in ASD will provide more insight into the clinical efficacy and safety of the medicine in ASD.
Available from: education.ed.ac.uk
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.