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Abstract Aims The evidence supporting the efficacy of dietary preventive therapy in migraine is rising, particularly regarding the ketogenic diet. However, less evidence exists for the Low-Glycemic Index Diet and the 2:1 KD. This retrospective single-center real-life study aims to evaluate the efficacy of a 2:1 ketogenic diet and a Low-Glycemic-index Diet in chronic and high-frequency episodic migraine. Methods Sixty patients with high-frequency episodic and chronic migraine were treated with either a Low-Glycemic-index diet (39 patients) or a 2:1 (21 patients) ketogenic diet for three months. We collected data on the migraine frequency and intensity and the MIDAS and HIT-6 scores through the headache diary. Anthropometric measurements (BMI, fat mass, free fat mass, and weight) were also collected and analyzed similarly. Data obtained at the baseline and after three months of each diet were compared. Results Migraine intensity, frequency, MIDAS and HIT-6 scores, fat mass, weight, and BMI improved in both diet groups. Conclusions Both diets are effective in reducing migraine symptoms and migraine-related disability.

Fatigue, defined as a subjective lack of physical and/or mental energy, is a clinical symptom highly characterizing multiple sclerosis (MS). The present study utilized a novel approach to the study of fatigue, examining first person-mental imagery of the symptom. Eighteen right-handed patients with MS (14F, 4 M, mean age 45.8 ± 8.15 years) were evaluated and were compared to nineteen healthy controls (10F, 9 M, mean age 43.15 ± 8.34 years) Patients were all in relapsing remitting form and no patient had presented relapses in the 6 months prior to inclusion in the study. We evaluated their behavioral performance and fMRI activations. We used an fMRI paradigm used to trigger first person-mental imagery of fatigue, through short sentences describing the principal manifestations of fatigue. Participants were asked to imagine the corresponding sensations (Sensory Imagery, SI). As a control, they had to imagine the visual scenes (Visual Imagery, VI) described in short phrases. They made a vividness rating by pressing the corresponding button.Behaviorally, we found that patients’ mean scores at the Multidimensional Fatigue Symptom Inventory for the general scale, physical scale, and mental scale were significantly higher than healthy controls (p = 0.05, p = 0.002, p = 0.006 respectively), but not for the emotional scale and for vigor scale (p = 0.207, n.s., p = 0.06, n.s.). In the imagery fMRI task, patients were significantly slower (mean reaction times and standard deviation: 2.24 s ± 0.33) than controls (mean reaction times and standard deviation: 1.918 s ± 0.455) for the SI task (Z=-2.058, p = 0.040), while no significant difference was found for the VI task.Regarding brain mapping, our main result is a group by task interaction. The SI task (vs. VI task) in healthy controls (relative to patients) increased activation in the left inferior parietal lobule. These preliminary results indicate that fatigue is related to dysfunctions in higher-order aspects of motor control, given the role of the posterior parietal lobe in motor planning and multisensory integration.

The pathogenesis of cerebral small vessel disease (CSVD) is largely unknown. Endothelial disfunction has been suggested as the turning point in CSVD development. In this study, we tested the effect of plasma from CSVD patients on human cerebral microvascular endothelial cells with the aim of describing the pattern of endothelial activation. Plasma samples from three groups of young subjects have been tested: PTs (subjects affected by early stage CSVD); CTRLs (control subjects without abnormalities at MRI scanning); BDs (blood donors). Human Brain Endothelial Cells 5i (HBEC5i) were treated with plasma and total RNA was extracted. RNAs were pooled to reduce gene expression-based variability and NGS analysis was performed. Differentially expressed genes were highlighted comparing PTs, CTRLs and BDs with HBEC5i untreated cells. No significantly altered pathway was evaluated in BD-related treatment. Regulation of p38 MAPK cascade (GO:1900744) was the only pathway altered in CTRL-related treatment. Indeed, 36 different biological processes turned out to be deregulated after PT treatment of HBEC5i, i.e., the cytokine-mediated signaling pathway (GO:0019221). Endothelial cells activate inflammatory pathways in response to stimuli from CSVD patients’ plasma, suggesting the pathogenetic role of neuroinflammation from the early asymptomatic phases of cerebrovascular disease.

There is limited information regarding the severity of COVID-19 in immunocompromized patients. We conducted a retrospective cohort study considering the period from 1 March 2020 to 31 December 2020 to determine whether previously existing lymphopenia increases the risk of hospitalization and death after SARS-CoV-2 infection in the general population. The laboratory and hospital discharge databases of the Azienda Sanitaria Universitaria Friuli Centrale were used, and 5415 subjects infected with SARS-CoV-2 and with at least one recent absolute lymphocyte count determination before SARS-CoV-2 positivity were included. In total, 817 (15.1%) patients had severe COVID-19. Patients developing severe COVID-19 were more frequently males (44.9% of the severe COVID-19 group vs. 41.5% in the non-severe COVID-19 group; p < 0.0001) and were older (73.2 ± 13.8 vs. 58.4 ± 20.3 years; p < 0.0001). Furthermore, 29.9% of the lymphopenic patients developed severe COVID-19 vs. 14.5% of the non-lymphopenic patients (p < 0.0001). In a logistic regression model, female sex remained a protective factor (OR = 0.514, 95%CI 0.438–0.602, p < 0.0001), while age and lymphopenia remained risk factors for severe COVID-19 (OR = 1.047, 95%CI 1.042–1.053, p < 0.0001 for each additional year of age; OR = 1.715, 95%CI 1.239–2.347, p = 0.0011 for lymphopenia). This provides further information to stratify the risk of COVID-19 severity, which may be an important element in the management of immunosuppressive therapies.

Cladribine is an effective disease-modifying treatment for relapsing-remitting multiple sclerosis that acts as an immune reconstitution therapy and is administered in a pulsed manner. Despite its efficacy, severe disease reactivation early after treatment represents a serious clinical problem, and clear evidence to guide the management of such a situation is lacking. Here, we describe the case of a patient experiencing considerable disease activity during the 1st year after the initiation of cladribine treatment. The patient was switched to alemtuzumab and, therefore, received double immune reconstitution therapy. Data regarding this approach are lacking, and real-world observations may be of interest. Despite achieving good control of disease activity, we observed several serious infectious complications. Our results suggest that sequential immune reconstitution therapies may be effective; however, at the price of higher susceptibility to infections.

Background Subacute sclerosing panencephalitis is a progressive neurodegenerative disorder caused by a latent and mutant measles virus which is extremely rare in developed countries. The lack of effective treatments leads to the research of other anti-inflammatory and neuroprotective treatments.Case Here we present a case of a 17-year-old patient affected by subacute sclerosing panencephalitis who manifest a dramatic improvement in neurological and general clinical conditions, as well as an arrest in the progression of demyelinating process in the central nervous system, after the beginning of a high ratio ketogenic diet.Conclusions Given its anti-inflammatory, antioxidant and metabolic effects, we believe that ketogenic diet utilisation could be a rational approach, can be considered a safe add-on therapy, carrying on with only a minimal risk of adverse effects or interactions.

Headaches are among the most prevalent and disabling neurologic disorders and there are several unmet needs as current pharmacological options are inadequate in treating patients with chronic headache, and a growing interest focuses on nutritional approaches as non-pharmacological treatments. Among these, the largest body of evidence supports the use of the ketogenic diet (KD). Exactly 100 years ago, KD was first used to treat drug-resistant epilepsy, but subsequent applications of this diet also involved other neurological disorders. Evidence of KD effectiveness in migraine emerged in 1928, but in the last several year’s different groups of researchers and clinicians began utilizing this therapeutic option to treat patients with drug-resistant migraine, cluster headache, and/or headache comorbid with metabolic syndrome. Here we describe the existing evidence supporting the potential benefits of KDs in the management of headaches, explore the potential mechanisms of action involved in the efficacy in-depth, and synthesize results of working meetings of an Italian panel of experts on this topic. The aim of the working group was to create a clinical recommendation on indications and optimal clinical practice to treat patients with headaches using KDs. The results we present here are designed to advance the knowledge and application of KDs in the treatment of headaches.