Sleep deprivation versus melatonin to induce sleep during paediatric electroencephalography

Abstract

signature of such social anxiety. For example, constraining eye contact leads to exaggerated increase of amygdala activation in ASD. Interestingly, the administration of bumetanide (a substance acting on choride channels and restoring GABA inhibition) normalizes the level of amygdala activation during constrained eye contact and increases the time spent in spontaneous eye gaze in patients with ASD. This data could support the excitatory/inhibitory dysfunction hypothesis in ASD. Truly, amygdala response to oxytocin has been sometimes inconsistent in ASD, but it might reflect a differential effect of this substance depending on the level of social anxiety in this population. NF1 is the most common single gene disorder that affects brain function. Patients with NF1 present an enhanced predisposition for attention-deficit–hyperactivity disorder (ADHD). We know that children with ADHD can show difficulties in recognizing emotions in faces. In this context, visual perception deficits in patients with NF1 are not likely to be due to problems in low-level stimulus processing but rather might be related to deficits in allocation of attention. In conclusion, subtyping both NF1 and ASD based upon prominent symptoms could be very useful. Comorbidity is very high between NF1 and ASD symptomatology on the one hand, and with ADHD symptomatology on the other hand. The former type of symptoms might benefit from methylphenidate, while the latter could improve with oxytocin or bumetanide, leading to more personalized treatment and aiming to improve the social interactions of these patients.