On October 7, Spectrum News, an online autism magazine from Simons Foundation, published a feature entitled, “Wide awake: Why children with autism struggle with sleep” by Ingfei Chen. Chen described an ongoing study of sleep disorders, which are common in children with Autism Spectrum Disorder (ASD). The Stanford University associate professor involved in the study, Ruth O’Hara, is one in a group of professionals who hypothesize that a dysregulation with the hormone melatonin might be to blame as an upset to the body’s circadian rhythm. It is also possible in O’Hara’s view that other factors, such as gastrointestinal upset, medication side effects, neurological issues such as epilepsy, or breathing issues may play roles in the sleep disorder issues that plague ASD patients.
In her article, Chen also reported that some studies suggest that up to 83% of children with autism have problems falling asleep. They spend less time in REM sleep than their neurotypical peers, and have a higher incidence of micro arousals during sleep than their control counterparts.
Research into sleep is essential, as lack of restorative sleep compounds cognition, behavioral, and other issues related to ASD. The problem is that while they are struggling with wiring children with non-verbal ASD up for home and clinic polysomnography tests, scratching their heads at the abnormal results, and coming up with more conflicting theories, they might already have some concrete answers and treatments if doctors shared research and read one another’s research more readily. Clearly there is a disconnect when it comes to great discoveries that might have benefit to all.
CT disorder sleep research
Enter Dr. Alan G Pocinki: Internist, Cornell grad, and Clinical Associate Professor at George Washington University Medical Center. Pocinki studies sleep disorders in people with genetic collagen disorders, which also have problems with their autonomic nervous system, specifically those with a disorder called Ehlers-Danlos Syndrome (EDS).
Pocinki noticed that his patients who suffered from joint laxity were also being diagnosed with anxiety disorders and were not getting better with psychiatric treatment. They were also suffering from pain, fatigue, gastrointestinal issues, and other autonomic dysfunction symptoms such as proprioception issues or orthostatic intolerance. Upon reviewing sleep study results, Pocinki realized that even in the absence of narcolepsy or sleep apnea that these patients were suffering from high amounts of micro arousals, occasional elevations of heart rate, and lack of deep sleep.
“Poor sleep can cause irritability and fatigue, which in turn can trigger more adrenaline (to try to overcome the fatigue),” says Pocinki, “which in turn can make sleep worse.”
He employs the use of beta blockers to block adrenaline from exciting the overactive sympathetic nervous system. He treats the chronic pain caused by the collagen disorder, and uses medications such as diazepam to further slow the nervous system. Patients get better. Within months, they have polysomnography results that more closely resemble those of normal people. They have less anxiety, more mental focus, and fewer bouts with fatigue.
While there have not yet been any controlled studies proving a higher rate of ASD in EDS, there are currently multiple case studies describing abnormalities in body type, gait, joints, marfanoid features, and ligament laxity in ASD. GI Issues, anxiety, high autonomic reactivity, and enlarged amygdala have been reported in both groups, in addition to a slew of other overlapping symptoms. Anecdotal evidence worthy of study suggests a higher rate of ASD in EDS, both disorders have seen a spike in diagnosis rates in recent years, and neither have clear evidence of genetic causation.