Ignore the faces: Neural characterisation of emotional inhibition from childhood to adulthood using MEG.

The ability to effectively and automatically regulate one's response to emotional information is a basic, fundamental skill for social functioning. The neural mechanisms underlying emotion regulation processing have been assessed, however few investigations have leveraged neurophysiological techniques, particularly magnetoencephalography (MEG) to determine the development of this critical ability. The current MEG study is the first to examine developmental changes in the neural mechanisms supporting automatic emotion regulation. We used an emotional go/no-go task with happy and angry faces in a single-site cohort of 97 healthy participants, 4-40 years of age. We found age-related changes as a function of emotion and condition in brain regions key to emotion regulation, including the right inferior frontal gyrus, orbitofrontal cortices and primarily right-lateralized temporal areas. Interaction effects, including an age by emotion and condition, were also found in the left angular gyrus, an area critical in emotion regulation and attention. Findings demonstrate protracted and nonlinear development, due to the adolescent group, of emotion regulation processing from child to adulthood, and highlight that age-related differences in emotion regulation are modulated by emotional face type.

Frequency-specific neural synchrony in autism during memory encoding, maintenance and recognition.

Working memory impairment is associated with symptom severity and poor functional outcome in autistic individuals, and yet the neurobiology underlying such deficits is poorly understood. Neural oscillations are an area of investigation that can shed light on this issue. Theta and alpha oscillations have been found consistently to support working memory in typically developing individuals and have also been shown to be functionally altered in people with autism. While there is evidence, largely from functional magnetic resonance imaging studies, that neural processing underlying working memory is altered in autism, there remains a dearth of information concerning how sub-processes supporting working memory (namely encoding, maintenance and recognition) are impacted. In this study, we used magnetoencephalography to investigate inter-regional theta and alpha brain synchronization elicited during the widely used one-back task across encoding, maintenance and recognition in 24 adults with autism and 30 controls. While both groups performed comparably on the working-memory task, we found process- and frequency-specific differences in networks recruited between groups. In the theta frequency band, both groups used similar networks during encoding and recognition, but different networks specifically during maintenance. In comparison, the two groups recruited distinct networks across encoding, maintenance and recognition in alpha that showed little overlap. These differences may reflect a breakdown of coherent theta and alpha synchronization that supports mnemonic functioning, or in the case of alpha, impaired inhibition of task-irrelevant neural processing. Thus, these data provide evidence for specific theta and widespread alpha synchrony alterations in autism, and underscore that a detailed examination of the sub-processes that comprise working memory is warranted for a complete understanding of cognitive impairment in this population.

Prolonged Dexmedetomidine Infusion and Drug Withdrawal In Critically Ill Children.

OBJECTIVE: To characterise the incidence, symptoms and risk factors for withdrawal associated with prolonged dexmedetomidine infusion in paediatric critically ill patients. METHODS: Retrospective chart review in the paediatric intensive care unit and the cardiac critical care unit of a single tertiary children's hospital. Patients up to 18 years old, who received dexmedetomidine for longer than 48 hours were included. RESULTS: A total of 52 patients accounted for 68 unique dexmedetomidine treatment courses of more than 48 hours. We identified 24 separate episodes of withdrawal in the 68 dexmedetomidine courses (incidence 35%). Of these episodes 38% occurred in patients who were weaned from dexmedetomidine alone while the remaining occurred in patients who had concurrent weans of opioids and/or benzodiazepines. Most common symptoms were agitation, fever, vomiting/retching, loose stools and decreased sleep. The symptoms occurred during the latter part of the wean or after discontinuation of dexmedetomidine. A cumulative dose of dexmedetomidine of 107 mcg/kg prior to initiation of wean was more likely associated with withdrawal (this equates to a dexmedetomidine infusion running at 1 mcg/kg/hr over 4 days). Duration of opioid use was an additional risk factor for withdrawal. The use of clonidine, as a transition from dexmedetomidine, did not protect against withdrawal (p = 1). CONCLUSIONS: A withdrawal syndrome may occur after prolonged infusion of dexmedetomidine. As all our patients were also exposed to opioids this may be affected by the duration of opioid use. We identified a cumulative dose of 107 micrograms/kg of dexmedetomidine beyond which withdrawal symptoms were more likely (which equates to 4 days of use at a dose of 1 mcg/kg/hr). A protocol for weaning should be considered in this circumstance.