Short-term intervention complemented by wearable technology improves Trichotillomania – A naturalistic single-case report

There is a growing interest in using wearable technology for the treatment of body-focused repetitive behaviors (BFRBs), such as Trichotillomania. Yet, to our knowledge, few studies address the applicability and use of wearable technology as a therapeutic element in more naturalistic situations. Here we would like to introduce its potential use combined with a Habit-Reversal Training in a single-case experimental design. In practice, individuals with BFRBs frequently show complex constellations of psychiatric disorders. Accordingly, the here presented participant was diagnosed with Trichotillomania as well as comorbid ADHD and examination phobia. The participant was offered to wear an unobtrusive and user-friendly vibration device that sent an alarm when her critical hairpulling behaviors occurred. The complementing Habit-Reversal Training included an Awareness Training supported by the vibration alarm of the wearable device. It further included a Competing Response Training by learning benign behaviors that could replace the hairpulling behavior. The frequency of hairpulling episodes was assessed using daily self-reports and by using the monitoring function of the wearable device. The intervention procedure was implemented into the participant’s everyday life and evaluated over the course of 214 days. The results indicated a significant reduction in the daily episodes of hair pulling. Our preliminary findings suggest that the here applied intervention has the potential to effectively treat Trichotillomania in individuals with comorbid disorders in psychotherapeutic outpatient care. Certainly, group-studies will need to further validate the approach’s effectiveness

IRS-2 Deficiency Impairs NMDA Receptor-Dependent Long-term Potentiation

The beneficial effects of insulin and insulin-like growth factor I on cognition have been documented in humans and animal models. Conversely, obesity, hyperinsulinemia, and diabetes increase the risk for neurodegenerative disorders including Alzheimer's disease (AD). However, the mechanisms by which insulin regulates synaptic plasticity are not well understood. Here, we report that complete disruption of insulin receptor substrate 2 (Irs2) in mice impairs long-term potentiation (LTP) of synaptic transmission in the hippocampus. Basal synaptic transmission and paired-pulse facilitation were similar between the 2 groups of mice. Induction of LTP by high-frequency conditioning tetanus did not activate postsynaptic N-methyl-D-aspartate (NMDA) receptors in hippocampus slices from Irs2−/− mice, although the expression of NR2A, NR2B, and PSD95 was equivalent to wild-type controls. Activation of Fyn, AKT, and MAPK in response to tetanus stimulation was defective in Irs2−/− mice. Interestingly, IRS2 was phosphorylated during induction of LTP in control mice, revealing a potential new component of the signaling machinery which modulates synaptic plasticity. Given that IRS2 expression is diminished in Type 2 diabetics as well as in AD patients, these data may reveal an explanation for the prevalence of cognitive decline in humans with metabolic disorders by providing a mechanistic link between insulin resistance and impaired synaptic transmission