Paolo Solla

What are the main findings?Migraine care in Italy is characterized by a mismatch between healthcare resource utilization and clinical needs, with limited primary-care involvement, repeated specialist consultations, and healthcare nomadism.Healthcare resource utilization is substantial, including extensive diagnostic testing—predominantly brain imaging—as well as emergency department visits, detoxification cycles, and repeated access to headache centers.

Background: The definition of motor conduction block (CB) and proximal temporal dispersion (TD) for the diagnosis of CIDP and MMN remains debated, particularly regarding whether CB should be based on amplitude or area reduction, and whether proximal TD is best assessed using negative peak or total CMAP duration. Methods: Nerve conduction waveforms from 106 CIDP, 87 MMN, and 234 controls were analyzed. Motor CB was defined by ≥ 30%, ≥ 40%, or ≥ 50% amplitude or area reduction. Proximal TD was defined as a ≥ 30% increase in negative peak duration, total CMAP duration, or either criterion. Sensitivity, specificity, and inter‐rater reliability were analyzed. Results: Across both CIDP and MMN, a ≥ 30% reduction in CMAP amplitude showed diagnostic performance comparable to area‐based CB definitions and outperformed higher cutoff values. Requiring CB in multiple nerves increased specificity but reduced sensitivity. For proximal TD, negative peak duration was the most robust single parameter. Total CMAP duration identified additional abnormalities and, when combined with negative peak duration, improved diagnostic sensitivity in both disorders while maintaining high specificity. Total CMAP duration demonstrated good inter‐rater agreement at the patient level. CMAP morphology showed substantial overlap between CIDP and MMN and limited discriminatory value. Conclusions: A ≥ 30% reduction in CMAP amplitude can be used as a universal definition of motor CB in both CIDP and MMN, providing diagnostic performance comparable to area‐based criteria with greater simplicity. In addition, proximal TD assessed using total CMAP duration may represent a complementary electrophysiological criterion in both disorders.

Background/Objectives: COVID-19 has triggered a global health crisis with sequelae extending beyond the acute phase of infection. Long COVID-19 is characterized by the persistence or new onset of symptoms weeks to months after the initial infection, including fatigue, cognitive impairment, and chemosensory dysfunction. Despite growing clinical evidence, the underlying pathophysiological mechanisms remain incompletely understood. This study aimed to evaluate the prevalence, distribution, and evolution of symptoms during the post-acute phases, with particular emphasis on olfactory and gustatory alterations. Methods: An observational study used a structured online questionnaire to collect demographic and clinical data from individuals with prior SARS-CoV-2 infection. Participants (n = 798) with persistent symptoms beyond 4–8 weeks were included. A subgroup of participants living in Sardinia underwent objective chemosensory assessment using the Sniffin’ Sticks test and the Taste Strips test for olfactory and gustatory function, respectively. Results: A high percentage of participants reported persistent symptoms consistent with long COVID-19, including fatigue, dyspnea, cognitive impairment, and chemosensory alterations. Olfactory and gustatory dysfunctions were among the most frequent manifestations. Objective assessments confirmed the presence and severity of these deficits, in accordance with data obtained using self-reported questionnaires. Symptom profiles evolved, suggesting possible central nervous system involvement and persistent inflammatory mechanisms. Conclusions: Long COVID-19 is a complex multisystem condition with a significant impact on quality of life. Chemosensory dysfunctions may serve as useful clinical markers for patient monitoring and stratification. Integrating subjective and objective data improves diagnostic accuracy and supports the development of targeted therapeutic strategies.

Background/Objectives: Continuous subcutaneous foslevodopa/foscarbidopa infusion (CSFLI) improves motor fluctuations in advanced Parkinson’s disease (PD), but some patients continue to experience residual motor and non-motor fluctuations despite optimized infusion parameters. We describe two patients receiving CSFLI in whom the addition or reintroduction of opicapone was associated with improvement in persistent fluctuations. In one patient, clinical findings were further explored using wearable sensor monitoring. Methods: Two patients with advanced PD treated with CSFLI and residual fluctuations received add-on opicapone. Clinical evaluation included neurological examination, assessment of motor fluctuations, and documentation of antiparkinsonian therapy before and after opicapone introduction. In one patient, motor performance was additionally evaluated with wearable sensor monitoring during the Timed Up and Go test and the 6-minute walk test before (T0) and three months after opicapone introduction (T1). Results: In both cases, opicapone 50 mg once daily was associated with rapid improvement in residual motor and non-motor fluctuations during CSFLI therapy. In the first patient, freezing episodes and unpredictable akinesia resolved. In the second patient, the reintroduction of opicapone improved morning slowness, axial symptoms, and dorsal pain. Wearable sensor analysis showed increased walking distance during the 6-minute walk test, higher walking speed, reduced Timed Up and Go duration, increased step length, and reduced step length variability. Conclusions: These preliminary observations suggest that opicapone may deserve further investigation as a potential adjunctive strategy in selected patients receiving CSFLI who continue to experience residual fluctuations despite optimized infusion therapy. Wearable sensor monitoring may provide objective support for treatment assessment in this setting.

Objective: Helicobacter pylori infects nearly half of the global population and has traditionally been viewed as a pathogen restricted to the gastric mucosa. Growing evidence, however, suggests that chronic infection may exert systemic effects extending to the central nervous system. This review critically examines the potential neurological implications of H. pylori infection within the emerging framework of the gut–brain axis. Methods: We performed a narrative, hypothesis-generating review of human observational and interventional studies complemented by mechanistic experimental research. The literature was evaluated with particular attention to study design, heterogeneity, and potential confounding in reported associations between H. pylori infection and neurological disorders. Results: Across multiple studies, H. pylori infection has been linked to a modestly increased prevalence of Parkinson’s disease and dementia, although findings remain heterogeneous. In Parkinson’s disease, infection may exacerbate motor fluctuations and reduce levodopa bioavailability, with partial clinical improvement reported following eradication in selected patients. Experimental studies further demonstrate that bacterial outer membrane vesicles can access the brain and promote neuroinflammatory and amyloidogenic processes, supporting biological plausibility. By contrast, several epidemiological studies report an inverse association with multiple sclerosis, suggesting potential immunomodulatory effects. Evidence relating H. pylori to migraine and mood disorders remains inconsistent. Conclusions: Current data do not support H. pylori as a primary cause of neurological disease. Instead, the infection may act as a context-dependent modifier within the complex inflammatory and immunometabolic networks of the gut–brain axis. Clarifying this relationship will require prospective studies integrating microbial strain profiling, biomarker-defined neurological phenotypes, and adequately powered interventional trials.

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, and it is considered one of the major challenges in contemporary neuroscience

In the 2023 diagnostic criteria, supporting clinical/MRI features are required to diagnose myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in patients at high risk of false MOG-IgG positivity (low/unavailable titer, cerebrospinal fluid-restricted), to help differentiation from multiple sclerosis (MS). However, overlap is possible and determining the frequency of the MOGAD supporting features at MS onset may help prevent misdiagnosis. We assessed the frequency of the MOGAD supporting features and potential risk of misdiagnosis at first attack of MS/clinically isolated syndrome (CIS). In this observational study, we retrospectively identified consecutive patients hospitalized between 2021 and 2024 at 2 Italian centers, with: (1) relapsing-remitting MS/CIS, and (2) first attack MRI available. The frequency of the MOGAD supporting features was assessed at MS/CIS presentation, and potential risk of misdiagnosis determined based on the probability of concurrent false MOG-IgG positivity. Other clinical-MRI features typical of MOGAD but not included in the 2023 diagnostic criteria were also evaluated. A total of 244 patients with MS/CIS were included (median age, 34 [range, 13-78] years; 66% were female). Overall, 65/244 (27%) patients with MS/CIS showed at least 1 MOGAD supporting feature during the presenting attack. "Central cord lesion" (27/82 [33%]) and "deep gray nuclei involvement" (24/86 [28%]) were more represented than other supporting features (0%-7%); p < 0.001. MOG-IgG was tested in 207/244 (85%) patients, showing false positivity in 3 (1.4%) patients. The combined probability of detecting a false MOG-IgG positivity and meeting 1 of the MOGAD supporting features was 0.4%. Among other typical MOGAD features not included in the diagnostic criteria, the following had a 0% frequency at MS/CIS presentation: (1) encephalopathy, (2) marked CSF pleocytosis (>50 cells/mm³), (3) wheelchair need during myelitis, and (4) MRI T2-lesion resolution postattack. Although the MOGAD supporting features can be met in one-fourth of patients at MS/CIS presentation, the risk of misdiagnosis in similar unselected cohorts remains low. Future refinements of the MOGAD supporting features should take into account their relative frequency in MS/CIS and possible integration with additional clinical-MRI features that are more specific for MOGAD.

Background: The role of dietary factors as risk or protective factors for Parkinson's disease (PD) remains debated. Objective: This retrospective case-control study aimed to evaluate the associations between foods identified through a data-driven analysis and PD, and to compare the relevance of dietary versus non-dietary factors as contributors to PD risk. Methods: The study included 680 PD patients and 612 matched controls recruited from six Italian neurology centers. Dietary data were collected using a validated 77-item food frequency questionnaire, and factor analysis was conducted to identify groups of correlated foods (i.e., factors). Logistic regression models were used to assess the associations between these factors and PD, while non-dietary factors were subsequently included in the model for comparison. Results: Seven factors were identified, four of which were significantly associated with PD. High consumption of sweets (Factor 1), red meat (Factor 3), and processed meats (Factor 6) was associated with an increased PD risk, whereas a high fruit intake (Factor 2) was protective. These associations remained significant after adjusting for other known non-dietary risk/protective factors. While the increased PD risk associated with dietary factors was weaker than that of non-dietary factors, protective dietary and non-dietary factors showed comparable effects in reducing PD risk. Conclusions: Data-driven analysis identified foods potentially influencing PD risk, although non-dietary factors demonstrated a greater impact on PD risk. These findings highlight the need to integrate both diet and lifestyle habits into future PD research and prevention strategies.