Sunday, June 21, 2015
Friday, June 19, 2015
Epilepsy Behav. 2013 Dec;29(3):574-7. doi: 10.1016/j.yebeh.2013.08.037.
Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy.
Cannabidiol; Dravet syndrome; Epilepsy; Intractable; Medically refractory seizures; Pediatric; Side effects; Treatment-resistant
Plant-derived cannabinoids (phytocannabinoids) are compounds with emerging therapeutic potential. Early studies suggested that cannabidiol (CBD) has anticonvulsant properties in animal models and reduced seizure frequency in limited human trials. Here, we examine the antiepileptiform and antiseizure potential of CBD using in vitro electrophysiology and an in vivo animal seizure model, respectively. CBD (0.01–100 μM) effects were assessed in vitro using the Mg2+-free and 4-aminopyridine (4-AP) models of epileptiform activity in hippocampal brain slices via multielectrode array recordings. In the Mg2+-free model, CBD decreased epileptiform local field potential (LFP) burst amplitude [in CA1 and dentate gyrus (DG) regions] and burst duration (in all regions) and increased burst frequency (in all regions). In the 4-AP model, CBD decreased LFP burst amplitude (in CA1 only at 100 μM CBD), burst duration (in CA3 and DG), and burst frequency (in all regions). CBD (1, 10, and 100 mg/kg) effects were also examined in vivo using the pentylenetetrazole model of generalized seizures. CBD (100 mg/kg) exerted clear anticonvulsant effects with significant decreases in incidence of severe seizures and mortality compared with vehicle-treated animals. Finally, CBD acted with only low affinity at cannabinoid CB1 receptors and displayed no agonist activity in [35S]guanosine 5′-O-(3-thio)triphosphate assays in cortical membranes. These findings suggest that CBD acts, potentially in a CB1
Cannabidiol Displays Antiepileptiform and Antiseizure Properties In Vitro and In VivoS⃞
What is the evidence? Orthodontic Treatment of PEDIATRIC Sleep Apnea with Rapid Maxillary Expansion
Probably yes. - JR
Clipboard: 6Remove all items
Sleep Breath. 2011 May;15(2):179-84. doi: 10.1007/s11325-011-0505-1. Epub 2011 Mar 25.
Efficacy of rapid maxillary expansion in children with obstructive sleep apnea syndrome: 36 months of follow-up.
Sleep Breath. 2011 May;15(2):173-7. doi: 10.1007/s11325-010-0419-3. Epub 2010 Sep 17.
Sleep Med. 2009 Apr;10(4):471-8. doi: 10.1016/j.sleep.2008.04.003. Epub 2008 Aug 26.
NREM sleep instability changes following rapid maxillary expansion in children with obstructive apnea sleep syndrome.
Sleep. 2008 Jul;31(7):953-7.
Orthodontic expansion treatment and adenotonsillectomy in the treatment of obstructive sleep apnea in prepubertal children.
- Sleep. 2009 Jan 1;32(1):table of contents.
- At the request of the corresponding (first) author, the editors of Sleep are retracting the following paper and erratum: Guilleminault C, Quo S, Huynh NT, Li K. Orthodontic expansion treatment and adenotonsillectomy in the treatment of obstructive sleep apnea in prepubertal children. Sleep;31(7):953-957 and Erratum to Guilleminault C, Quo S, Huynh NT, Li K. Orthodontic expansion treatment and adenotonsillectomy in the treatment of obstructive sleep apnea in prepubertal children. Sleep;31(7):953-957, in Sleep 2009;32(1):6.[Sleep. 2010]
- [PubMed - indexed for MEDLINE]
J Laryngol Otol. 2008 Dec;122(12):1318-24. doi: 10.1017/S002221510800279X. Epub 2008 Jun 25.
Sleep. 1998 Dec 15;21(8):831-5.
- [PubMed - indexed for MEDLINE]
Thursday, June 11, 2015
For children with autism, there are differences in brain activity during sleep in comparison with typically developing children, say Canadian researchers, whose findings underline the relationship between sleep quality and cognitive performance in all children and adolescents.
The researchers found that stage 2 sleep spindles, which are important for taking sleep into deeper phases and have been linked to learning potential, are shorter and of lesser frequency among autistic children, even when these children do not have overt sleep problems.
The investigators believe that the results, which showed a differential effect on subsequent performance on IQ tests, could result from differences in cortical organization and information processing in children affected by the condition.
"This is an important discovery that confirms the major role of sleep in consolidating cognitive abilities," said Roger Godbout, PhD, director of the Sleep Research Laboratory at the Hôpital Rivière-des-Prairies, who is also a professor at Université de Montréal, Canada, in a release.
"This study establishes beyond a doubt that children and adolescents are particularly affected by a lack of sleep, especially because they are in an important developmental period. This is also an important finding given that 10% to 25% of Canadian children and adolescents — and 45% to 85% of autistic children — have sleep problems."
The research was published in the July issue of the International Journal of Psychophysiology.
The researchers studied 13 typically developing and 13 high-functioning autistic children who did not complain of poor sleep. They slept two consecutive nights in a sleep laboratory. Non–rapid eye movement sleep, sleep spindles, and sigma activity were measured using electroencephalography (EEG).
Stage 2 sleep spindles were identified visually on C3, C4 (central), and Fp1, Fp2 (frontal) leads. They were defined as bursts of EEG activity at 12-16 Hz lasting 0.5-2.0 seconds. Sigma activity was also recorded on the C3, C4, Fp1, and Fp2 EEG leads during stage 2 sleep, with total sigma (12-15.75 Hz), slow sigma (12-13 Hz), and fast sigma (13.25-15.75 Hz) frequencies determined.
The children also completed the French–Canadian version of the Wechsler Intelligence Scale for Children–IV test on the morning after each of the sleep recording nights.
Although autistic and typically developing children spent the same length of time in stage 2 sleep, for the autistic children, sleep spindle density was significantly lower and sleep spindles were of shorter duration at the Fp1 electrode for both the total and second quarter of the night (P < .05 for all).
In the last 2 hours of the night, fast sigma EEG activity was significantly lower at the C3 and C4 electrode in autistic than in typically developing children (P < .05 for both).
There was a negative correlation between verbal IQ and sleep spindle density at the Fp2 electrode in typically developing children. In contrast, there was a negative correlation between verbal and full-scale IQ scores with C3 sleep spindle density in autistic children.
The duration of sleep spindles at C4 was positively correlated with verbal IQ, but only in typically developing children. There was a positive correlation between performance IQ and fast sigma activity at C4 during the latter part of the night, again only in typically developing children.
Lead author Sophie Tessier, a student in the Sleep Laboratory and Clinic, Hôpital Rivière-des-Prairies, in Montreal, said that it was important that they studied children without sleep difficulties.
She explained that differences in the density and duration of sleep spindles suggest that autistic children have differences in cortical functioning, even when their sleep appears to be unaffected.
The findings also raise questions about the nature of autism.
"Our aim is really to understand what autism is and what its consequences are," Tessier said. "We are still wondering about the etiology and what it affects, and so we're still understanding how the brain network is connected and how it works."
She said that it is clear that the learning and cognitive processing are different between autistic and unaffected children during the day, and now it is known that their sleep patterns are "completely different."
"We also see that sleep doesn't support cognition, and the resources for learning are not available in the same way, so we are trying to understand what is autism and where it has consequences...to find the target of intervention eventually," Tessier told Medscape Medical News.
A Good First Step
Commenting on the findings for Medscape Medical News, Shalini Paruthi, MD, fellow of the American Academy of Sleep Medicine and director of the Pediatric Sleep and Research Center at SSM Cardinal Glennon Children's Medical Center, in St. Louis, Missouri, said that the study was a "very interesting" descriptive study.
Although noting that the children included in the study were not typical of the autistic population, in whom sleep problems are extremely common, she added: "I think it's definitely a good first start at trying to understand their EEG sleep patterns and see if that correlates with their cognitive processing."
Dr Paruthi would like to see the study repeated in a larger group of children.
"Once you have a larger sample size, you can really see if those differences are becoming significant and something that can distinguish the typically developing normal children vs those children who have autism," she told Medscape Medical News.
She explained that it will also be important to look at different groups of children with autism, including those who are low functioning, and determine how EEG differences relate to daytime functioning.
If the impact of sleep is replicated in further studies, Dr Paruthi believes that it may help identify which specific types of services a child would benefit from to improve their functioning at a faster rate.
"The best outcome that we can hope for by doing any kind of research in kids who do have autism is how closely can we get them to learn how to communicate better, communicate more effectively, and communicate more frequently, and how we get them to really function in life.
"I think it's really important that we continue to do research on children who have autism. Everything takes time, so starting with small groups, starting with the kids who are more high functioning...I think that is totally an appropriate step, because we know that so many children are diagnosed with autism," she said.
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