Non-pharmacological treatment of Attention Deficit Disorder with or without Hyperactivity (ADHD). Overview and report of the first international symposium on the non-pharmacological management of ADHD.

Attention Deficit Disorder with or without Hyperactivity (ADHD is a neurodevelopmental disorder which affects the day-to-day functioning of children and adults with this condition. Pharmacological treatment can reduce the symptoms associated with ADHD, but it has some limitations. The objective of this symposium is to determine the effects of non-pharmacological approaches on ADHD symptoms. Results indicate that the following intervention are promising approaches: cognitive behavioral therapy (CBT), mindfulness-based interventions (MBI), yoga, cognitive and metacognitive intervention, neurofeedback and parental training programs. Current research advocates multimodal approaches in conjunction with school or work accommodations integrating innovative technologies.

The Effect of Experimental Recuperative and Appetitive Post-lunch Nap Opportunities, With or Without Caffeine, on Mood and Reaction Time in Highly Trained Athletes.

Purpose: To investigate the effects of placebo (PLA), 20 min nap opportunity (N20), 5mg·kg-1 of caffeine (CAF), and their combination (CAF+N20) on sleepiness, mood and reaction-time after partial sleep deprivation (PSD; 04h30 of time in bed; study 1 ) or after normal sleep night (NSN; 08h30 of time in bed; study 2 ). Methods: Twenty-three highly trained athletes ( study 1 ; 9 and study 2 ; 14) performed four test sessions (PLA, CAF, N20 and CAF+N20) in double-blind, counterbalanced and randomized order. Simple (SRT) and two-choice (2CRT) reaction time, subjective sleepiness (ESS) and mood state (POMS) were assessed twice, pre- and post-intervention. Results: SRT was lower (i.e., better performance) during CAF condition after PSD (pre: 336 ± 15 ms vs. post: 312 ± 9 ms; p < 0.001; d = 2.07; Δ% = 7.26) and NSN (pre: 350 ± 39 ms vs. post: 323 ± 32 ms; p < 0.001; d = 0.72; Δ% = 7.71) compared to pre-intervention. N20 decreased 2CRT after PSD (pre: 411 ± 13 ms vs. post: 366 ± 20 ms; p < 0.001; d = 2.89; Δ% = 10.81) and NSN (pre: 418 ± 29 ms vs. post: 375 ± 40 ms; p < 0.001; d = 1.23; Δ% = 10.23). Similarly, 2CRT was shorter during CAF+N20 sessions after PSD (pre: 406 ± 26 ms vs. post: 357 ± 17 ms; p < 0.001; d = 2.17; Δ% = 12.02) and after NSN (pre: 386 ± 33 ms vs. post: 352 ± 30 ms; p < 0.001; d = 1.09; Δ% = 8.68). After PSD, POMS score decreased after CAF (p < 0.001; d = 2.38; Δ% = 66.97) and CAF+N20 (p < 0.001; d = 1.68; Δ% = 46.68). However, after NSN, only N20 reduced POMS (p < 0.001; d = 1.05; Δ% = 78.65) and ESS (p < 0.01; d = 0.71; Δ% = 19.11). Conclusion: After PSD, all interventions reduced sleepiness and only CAF enhanced mood with or without napping. However, only N20 enhanced mood and reduced sleepiness after NSN. Caffeine ingestion enhanced SRT performance regardless of sleep deprivation. N20, with or without caffeine ingestion, enhanced 2CRT independently of sleep deprivation. This suggests a different mode of action of napping and caffeine on sleepiness, mood and reaction time.

'Resurgent', 'twin' or 'silent' epidemic? A select data overview and observations on increasing psycho-stimulant use and harms in North America.

In the early 2000s, increasing prevalence of psycho-stimulant (e.g., crack/cocaine, methamphetamine) use and related harms, including severe adverse health outcomes, was observed among - mostly marginalized - populations of persons using illicit drugs in North America, underscoring an urgent need for interventions options towards improved prevention and treatment. By about 2010, however, the 'opioid crisis', featuring unprecedented use and public health burden, had accelerated into full force in North America, largely muting attention to the psycho-stimulant issue until recently. Recent surveillance data on drug use and related mortality/morbidity from the present decade has documented a marked resurgence of psycho-stimulant use and harms especially in at-risk populations, commonly in direct combination with opioids, across North America, resulting in a 'twin epidemic' comprised of opioids and psycho-stimulants We briefly review select epidemiological data indicators for these developments from the United States and Canada; in the latter jurisdiction, related evidence has been less prevalent and systematic but corroborating the same trends. Evidently, the (widely ongoing) focus on the 'opioid epidemic' as a 'mono-type' drug problem has become an anachronism that requires urgent and appropriate correction. We then briefly consider existing, evidence-based options for - prevention and treatment - interventions targeting psycho-stimulant use and harms, which are substantially more limited and/or less efficacious than those available for problematic opioid use, while presenting major gaps and challenges. The observed resurgence of psycho-stimulants may, indirectly, relate to recent efforts towards curtailing (medical) opioid availability, thereby accelerating demand and supply for both illicit opioids and psycho-stimulants. The presently unfolding 'twin epidemic' of opioids and psycho-stimulants, combined with limited intervention resources, presents an acute challenge for public health and may crucially undermine actively extensive efforts to reduce opioid-related health harms in North America.

NCS-Rapgef2, the Protein Product of the Neuronal Rapgef2 Gene, Is a Specific Activator of D1 Dopamine Receptor-Dependent ERK Phosphorylation in Mouse Brain.

The neuritogenic cAMP sensor (NCS), encoded by the Rapgef2 gene, links cAMP elevation to activation of extracellular signal-regulated kinase (ERK) in neurons and neuroendocrine cells. Transducing human embryonic kidney (HEK)293 cells, which do not express Rapgef2 protein or respond to cAMP with ERK phosphorylation, with a vector encoding a Rapgef2 cDNA reconstituted cAMP-dependent ERK activation. Mutation of a single residue in the cyclic nucleotide-binding domain (CNBD) conserved across cAMP-binding proteins abrogated cAMP-ERK coupling, while deletion of the CNBD altogether resulted in constitutive ERK activation. Two types of mRNA are transcribed from Rapgef2 in vivo. Rapgef2 protein expression was limited to tissues, i.e., neuronal and endocrine, expressing the second type of mRNA, initiated exclusively from an alternative first exon called here exon 1', and an alternative 5' protein sequence leader fused to a common remaining open reading frame, which is termed here NCS-Rapgef2. In the male mouse brain, NCS-Rapgef2 is prominently expressed in corticolimbic excitatory neurons, and striatal medium spiny neurons (MSNs). Rapgef2-dependent ERK activation by the dopamine D1 agonist SKF81297 occurred in neuroendocrine neuroscreen-1 (NS-1) cells expressing the human D1 receptor and was abolished by deletion of Rapgef2. Corticolimbic [e.g., dentate gyrus (DG), basolateral amygdala (BLA)] ERK phosphorylation induced by SKF81297 was significantly attenuated in CamK2α-Cre+/- ; Rapgef2cko/cko male mice. ERK phosphorylation in nucleus accumbens (NAc) MSNs induced by treatment with SKF81297, or the psychostimulants cocaine or amphetamine, was abolished in male Rapgef2cko/cko mice with NAc NCS-Rapgef2-depleting AAV-Synapsin-Cre injections. We conclude that D1-dependent ERK phosphorylation in mouse brain requires NCS-Rapgef2 expression.