The gut microbiota is involved in the development of the immune system and can modulate the risk for immune-mediated disorders such as multiple sclerosis (MS). Dysbiosis has been demonstrated in MS patients and its restoration by disease-modifying treatments (DMTs) is hypothesized. We aimed to study the changes in gut microbiota composition during the first 6 months of treatment with dimethyl fumarate (DMF), an oral DMT, and to identify the microorganisms associated with DMF side effects. We collected and analyzed the gut microbiota of 19 MS patients at baseline and after 1, 3, and 6 months of DMF treatment. We then cross-sectionally compared gut microbiota composition according to the presence of gastrointestinal (GI) symptoms and flushing. Overall, the gut microbiota biodiversity showed no changes over the 6-month follow-up. At the genus level, DMF was associated with decreased Clostridium abundance after 6 months. In subjects reporting side effects, a higher abundance of Streptococcus, Haemophilus, Clostridium, Lachnospira, Blautia, Subdoligranulum, and Tenericutes and lower of Bacteroidetes, Barnesiella, Odoribacter, Akkermansia, and some Proteobacteria families were detected. Our results suggest that gut microbiota may be involved in therapeutic action and side effects of DMF, representing a potential target for improving disease course and DMT tolerability.

Nonalcoholic fatty liver disease (NAFLD) exponentially affects the global healthcare burden, and it is currently gaining increasing interest in relation to its potential impact on central nervous system (CNS) diseases, especially concerning cognitive deterioration and dementias. Overall, scientific research nowadays extends to different levels, exploring NAFLD’s putative proinflammatory mechanism of such dysmetabolic conditions, spreading out from the liver to a multisystemic involvement. The aim of this review is to analyze the most recent scientific literature on cognitive involvement in NAFLD, as well as understand its underlying potential background processes, i.e., neuroinflammation, the role of microbiota in the brain–liver–gut axis, hyperammonemia neurotoxicity, insulin resistance, free fatty acids, and vitamins.

Hepatitis C Virus (HCV), despite being a hepatotropic virus, is the causative agent of many systemic disorders, such as vasculitis, autoimmune diseases, lymphoproliferative disorders, and a broad spectrum of neurological and psychiatric manifestations. Although symptoms have been misdiagnosed or underdiagnosed, only recently, evidence of direct (inflammatory) or indirect (immune-mediated) HCV-dependent cerebral effects has been established. HCV infection can promote acute inflammatory response, pro-coagulative status and ischemic disorders, and neurodegeneration. These effects rely on cerebral HCV replication, possibly mediated by blood–brain barrier alterations. Further study is needed to better understand the HCV-related mechanisms of brain damage.

Background: Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular transitory condition characterized by severe headache, possible concomitant acute neurological symptoms, evidence of diffuse multifocal segmental constriction of cerebral arteries, and usually spontaneously resolving within 3 months. Putative causes and/or precipitating factors are vasoactive drugs—e.g., antidepressants, α-sympathomimetics, triptans—post-partum, and immunosuppressants. Case presentation: We report the case of a middle-aged woman referred to the emergency room (ER) with a 7-day long intense headache and vomit. Cerebral non-contrast computed tomography (CT) was negative for acute ischemic lesions or intracranial bleedings. She was again referred to ER 7 days later with additional fluctuating episodes of weakness in left arm and both lower limbs. A new brain CT was negative. Due to worsening headache, a transcranial color-coded Doppler (TCCD) was performed, which showed diffuse multifocal blood flow acceleration in all principal intracranial vessels, and particularly on the right hemisphere. These findings were subsequently confirmed at MR angiogram and digital subtraction angiography. Conclusion: TCCD imaging is a non-invasive and relatively inexpensive tool which provides real-time information on cerebrovascular function, blood flow velocities, and hemodynamic changes. TCCD may be a powerful tool in the early detection of acute infrequent cerebrovascular conditions, as well as in monitoring their course and the therapeutic response.

Background: Increasing evidence supports the existence of a somatosensory subtype of tinnitus, in which craniocervical–craniomandibular structures can modulate tinnitus perception also through central auditory pathways. Despite growing mechanistic evidence, no targeted pharmacological intervention has been validated for this subtype. Objectives: This study aimed to synthesize the anatomical and neurophysiological rationale linking masseter hyperactivity to somatosensory tinnitus and to discuss BoNT/A as a hypothesis-generating therapeutic option requiring clinical validation. Methods: A PRISMA-ScR-guided scoping review was conducted in MEDLINE and EMBASE, using three complementary search lines (last search: 31 May 2026). Results: Of 284 records screened, four studies met eligibility criteria: three from the search strategy on BoNT/A and tinnitus and one from the search strategy on tinnitus and masticatory dysfunction. One additional record (Ranoux and Levine, 2024) was identified through manual search, describing tinnitus improvement following periauricular and splenius capitis BoNT/A injections, with masseter/temporalis injection proposed as an alternative site in the same protocol. Conclusions: Current anatomical and neurophysiological evidence supports a plausible link between masseter hyperactivity and somatosensory tinnitus in selected patients. BoNT/A is established for reducing masseter hyperactivity and may theoretically reduce abnormal somatosensory input; however, direct clinical evidence for tinnitus improvement remains insufficient. Its use should be considered experimental or hypothesis-based, within a multidisciplinary framework and with standardized outcome assessment. Prospective controlled trials are needed.

The optic nerve (ON), as an extension of the central nervous system, reflects multiple sclerosis (MS) pathological processes. Transorbital sonography (TOS) is emerging as a novel technique to detect ON changes. Our aim was to investigate retrobulbar ON morphometric changes in MS and their relationship with prior history of optic neuritis. 122 MS subjects were enrolled, 68 with and 54 without history of optic neuritis. ON diameters without and with sheath were measured at 3 mm (OND3 and ONSD3) and 5 mm (ONSD5) posterior to the optic disc; myelination index (MI=ONSD3/ONSD5) was calculated. To account for intrasubject dependencies, linear mixed models (LMMs) for repeated measures were employed, adjusting for age at onset and body mass index. ONs with history of inflammation (I-ON) exhibited significantly reduced diameters versus companion nerves in both measurements with and without sheath (OND3: p = 0.002; ONSD3: p = 0.010; ONSD5: p = 0.046). All ONs diameters progressively decreased with increasing neuritis frequency, demonstrating a dose-response effect. Significant measurement reductions in OND and ONSD3 were observed in I-ON of patients with Expanded Disability Status Scale >3, whereas no significant differences emerged for progression index (PI) > 0.20 among ONs with and without history of optic neuritis. TOS reliably captures ON morphometric changes related to inflammatory history and chronic neuroaxonal injury in MS, supporting its role as a promising biomarker of disability burden and progression independent of relapse activity (PIRA).