Clinical usability of telephone-based cognitive screening tests in Parkinson's disease Angelica De Sandi, Edoardo Nicolò Aiello, Federica Verardo, Denise Mellace, Angelica Marfoli, et al. Journal of Parkinson S Disease, 2026 Background Accessible screening tools are crucial for the early detection of cognitive impairment in Parkinson's disease (PD), especially in contexts where in-person assessments are not feasible. Objective To assess the clinical usability of telephone-based cognitive screening (TBCS) tools in PD patients. Methods Forty-two non-demented PD individuals and N = 103 healthy controls (HCs) underwent a TBCS battery including the Telephone Interview for Cognitive Status (TICS), the Telephone-based Frontal Assessment Battery (t-FAB) and sub-tests from the Telephone-based Verbal Fluency Battery (t-VFB) and Telephone Language Screener (TLS). PD individuals were also administered the Montreal Cognitive Assessment (MoCA) in person and assessed for behavior and cognitive-driven functional independence via caregiver-report questionnaires administered over the telephone (Neuropsychiatric Inventory, NPI and Amsterdam IADL Questionnaire – 30-item version, A-IADL-Q-30, respectively). Correlations were run to test the construct and ecological validity of TBCS tests in PD individuals; ROC analyses were run to test the capability of TBCS tests to discriminate PD individuals from HCs and PD individuals with a defective MoCA from those performing normally (PD-MCI vs. PD-CN). Results The vast majority of TBCS measures were significantly associated with the MoCA and A-IADL-Q-30 scores, supporting convergent and ecological validity, respectively; TBCS measures also diverged from the NPI. TBCS measures of global cognition and executive-attentive measures discriminated PD individuals from HCs with acceptable accuracy (AUC = 0.71–0.75), showing, by contrast, a better performance in differentiating PD-MCI from PD-CN groups (AUC = 0.74–0.89). Conclusion TBCS tests are clinimetrically sound tools for identifying cognitive deficits in PD.
The Emotional Landscape of Multiple System Atrophy: A Preliminary Personality-Based Perspective Eleonora Zirone, Giulia Franco, Federica Arienti, Roberta Ferrucci, Alessandro Di Maio, et al. Journal of Clinical Medicine, 2025 Background: Multiple System Atrophy (MSA) is a rapidly progressing neurodegenerative movement disorder characterized by autonomic failure, parkinsonism, and cerebellar ataxia. While its non-motor symptoms are well-documented, personality features in MSA remain underexplored. This study characterizes the personality traits of non-demented patients with MSA and explores their association with clinical variables. Methods: Twenty-six patients with MSA were assessed using the Minnesota Multiphasic Personality Inventory-2-Restructured Form (MMPI-2-RF). Dementia was excluded by Montreal Cognitive Assessment. Descriptive statistics and non-parametric analyses were conducted to examine clinical, demographic, and MMPI-2-RF variables. Results: Patients commonly showed elevated scores in somatic domains: Somatic Complaints (39%), Malaise (58%), and Neurological Complaints (85%), as well as in internalizing emotional traits: Low Positive Emotions (39%), Introversion (46%), Suicidal Ideation (46%), and Hopelessness (54%). Externalizing behavioral traits were absent, with only 4–8% of patients showing elevations in aggression or behavioral dysfunction. Strong correlations were found between somatic and emotional traits (r = 0.656, p < 0.001), and between Neurological Complaints and disease duration (r = 0.662, p < 0.001). Conclusions: This exploratory study reveals a distinct personality pattern in MSA, characterized by marked suicidal ideation, emotional vulnerability with internalizing coping, and absence of externalizing behaviors. These features highlight the need for suicide risk screening, interventions to alleviate psychological suffering, and tailored multidisciplinary care. Larger, longitudinal studies are warranted to confirm these preliminary results and clarify whether these traits reflect premorbid personality, early disease manifestations, or secondary responses, as well as their prognostic and clinical relevance.
Exploring the relationship between dystonia and STN-DBS in Parkinson’s disease: insights from a single-centre cohort Luigi G. Remore, Delia Gagliardi, Linda Borellini, Alfonso Fasano, Valeria Lo Faso, et al. Neurological Sciences, 2025 Introduction Motor side effects may emerge after deep brain stimulation (DBS) of the subthalamic nucleus (STN) in Parkinson’s disease (PD) patients. Out of 60 PD patients, we observed 16 patients displaying de novo dystonic symptoms after the implantation and 11 dystonic PD patients without benefit from the stimulation. We hypothesized that a common neural pathway may cause dystonia in both conditions. Our study aims to investigate the clinical and connectivity substrates of dystonia after STN-DBS. Methods We divided our cohort into four groups: 16 patients displaying dystonia after STN-DBS, 11 patients with previously known dystonia not improving after surgery, 14 patients with dystonic symptoms relieved by the stimulation and 19 controls who never experienced dystonia. MANOVA was used to compare clinical data and the distance of the active contact center from the STN border among the four groups. Finally, we reconstructed the “sour” spots for dystonic symptoms and the associated structural and functional connectivity using a Parkinsonian normative connectome. Results De novo dystonic and not-improved dystonic patients had a statistically significant longer PD duration before surgery (p = 0.001) and a greater active contact-STN distance (p < 0.001). Moreover, the “sour” spots were similar in both groups and structural and functional connectivity profiles were associated with brain areas correlated with dystonia pathophysiology (cerebellum, midbrain, parietal and temporal cortices). Conclusions We formulated a two-hit model for dystonia after STN-DBS: a clinical feature of Parkinsonian patients causes predisposing altered plasticity contributing to dystonic symptoms development when coupled with the stimulation of dystonia-related subcortical and cortical structures.