The assessment of patients with neuropsychiatric conditions follows the time-honored principles of general clinical practice and requires considerable expertise, as well as a good deal of patience and persistence. As part of the mental state examination, the motor system must be systematically addressed, alongside other physical signs of neuropsychiatric relevance. Direct observation of the patient's gait and spontaneous movements begins in the outpatient waiting room or-depending on circumstances-the ward corridor, and can be highly illuminating. In many cases, these initial informal observations can play an important role in steering the diagnostic process.

The clinical assessment of the facial structure and its expression remain a valuable, yet often underutilized, component of neuropsychiatric evaluation. Drawing on traditions spanning from internal medicine to contemporary cognitive neuroscience, careful observation of the face can yield insights into underlying psychological, neurologic, and genetic processes. While facial findings are rarely diagnostic in isolation, they may provide important information when integrated with clinical history and examination. As digital phenotyping and machine-learning tools increasingly complement bedside observation, clinicians should preserve and refine their skills in facial assessment, ensuring that technological advances augment rather than replace clinical judgment.

Although 18F-FDG PET is commonly used in the differential diagnosis of cognitive decline, synaptic vesicle glycoprotein 2A PET may offer a more direct assessment of synaptic integrity and address limitations associated with 18F-FDG, such as sensitivity to sensory stimuli and glycemic variations. In this study, a head-to-head comparison of 18F-SynVesT-1 and 18F-FDG was performed for differentiating causes of cognitive decline in a tertiary clinical setting. Methods: Patients with cognitive decline referred for 18F-FDG PET were recruited to undergo 18F-SynVesT-1 PET/MRI (49 ± 26 d after 18F-FDG PET). Diagnosis was determined by routine clinical follow-up (median, 11 mo) and classified as Alzheimer disease (AD), frontotemporal degeneration (FTD), dementia with Lewy bodies (DLB), other neurodegenerative disorders (ONDs), or nonneurodegenerative disorders (NoNDs). Volume-wise and voxelwise semiquantitative analyses were performed using tracer-specific healthy volunteers. Diagnostic accuracy for both tracers was evaluated through logistic regression and by consensus from 3 readers. Noninferiority was defined by an area-under-the-curve margin (ΔAUC) of -0.10 within a 95% CI, using the clinical follow-up diagnosis as the gold standard. Results: Ninety-four patients were included: 44 with AD, 12 with FTD, 4 with DLB, 5 with ONDs, and 29 with NoNDs. Volume-wise and voxelwise analyses showed that, in patients with AD and DLB, reductions in the temporoparietal and precuneus/posterior cingulate were less pronounced with 18F-SynVesT-1 PET than with 18F-FDG PET (e.g., posterior cingulate in AD, -10% vs. -20%). In FTD, the most impacted areas showed greater variability, typically affecting the anterior temporal and frontal cortices, depending on the FTD subtype. Visual assessment showed lower sensitivity for AD with 18F-SynVesT-1 PET than with 18F-FDG PET (0.57 vs. 0.73) with equal specificity (0.76), whereas quantitative analysis yielded a lower area under the curve (0.71 vs. 0.81; ΔAUC, -0.10; 95% CI, -0.21 to 0.01). For FTD, 18F-SynVesT-1 visual classification yielded similar sensitivity and specificity (0.58 and 0.90) compared with 18F-FDG (0.50 and 0.93) but a lower quantitative area under the curve (0.64 vs. 0.76; ΔAUC, -0.12; 95% CI, -0.27 to 0.04). Conclusion: 18F-SynVesT-1 PET enabled accurate classification of disease-specific patterns of cognitive decline. Although classification performance for FTD was similar to that of 18F-FDG PET, the lower effect size in neocortical binding resulted in lower sensitivity for AD. Larger study samples are needed to formally evaluate tracer noninferiority in this clinical context for all subgroups.

A large body of research in developmental science and comparative biology identifies social play as a fundamental driver of learning and experience-dependent plasticity in some species. Rather than rehearsing stereotyped behaviors, social play is thought to promote adaptive responses to uncertainty through dynamic, reciprocal interactions. However, whether these functional properties produce immediate cognitive benefits during early childhood remains unknown. Here, we tested whether a brief session of socio-competitive gameplay (Mario Kart™ 8 Deluxe), implementing key functional properties of social play, could transiently modulate attentional reorienting and sensorimotor learning in preschool children. Using a within-subject crossover design (n = 33), including no-play and an active object-play control (Tangram), we found that only 30minutes of socio-competitive gameplay play accelerated the emergence of inhibition of return and selectively enhanced dominant-hand sensorimotor learning. Importantly, cross-SOA attentional modulation following socio-competitive gameplay was associated with late-phase dominant-hand advantage in manual dexterity. These findings show that brief exposure to a socially contingent digital environment can rapidly modify attentional dynamics and facilitate online sensorimotor learning in five-year-old children. Although digital gameplay cannot fully reproduce the embodied nature of physical social play, our results suggest that videogames implementing key functional properties of social play may transiently engage evolved mechanisms supporting behavioral flexibility and surprise-driven learning. More broadly, the immediate cognitive benefits of play may depend less on its physical form than on the computational demands it places on the developing brain.

In recent years, the notion of Tourettic obsessive-compulsive disorder (Tourettic OCD), viewed as a distinctive endophenotype of Gilles de la Tourette syndrome, has garnered increasing attention. Despite this growing interest, clinical observations of affected patients remain sparse in the literature. This article presents the clinical case of a teenager diagnosed with Gilles de la Tourette syndrome, whose condition evolved to domination of obsessive-compulsive and behavioral disorders over the previously dominant multiple motor and vocal tics. The question of the nosological independence of Tourettic OCD, its positioning within the spectrum of neuropsychiatric disorders, and the delineation between tics and obsessive-compulsive phenomena continues to be a matter of debate. This case highlights the complexity of diagnosing these conditions and underscores the need for interdisciplinary collaboration between neurologists and psychiatrists in managing such patients.