Depression is one of the most prevalent psychiatric disorders and a leading cause of disability worldwide. Although the pathogenesis of depression remains far from fully understood, current research suggests a potential role for vitamin D due to its involvement in brain functioning. Moreover, vitamin D supplementation has shown promising results in the treatment of patients with depression. Therefore, the present study aimed to systematically review the available research investigating the association between vitamin D levels and the onset of depression. This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and the protocol was registered in the PROSPERO database (registration number: CRD42024515918). A search was performed across PubMed/Medline, SCOPUS, and Web of Science databases, yielding a total of 8,052 potentially eligible articles. After the removal of duplicates and ineligible records, and exclusion based on title and abstract screening, 297 original full-text articles were assessed according to the inclusion and exclusion criteria. Ultimately, 66 articles were included in this systematic review. Most of the included studies employed a cross-sectional design (N = 46). Overall, the data analyzed in this review indicate an association between depression and vitamin D serum levels, particularly in studies using cross-sectional designs. Only a few longitudinal studies demonstrated that lower vitamin D levels are associated with an increased risk of developing depressive symptoms or major depressive disorder, highlighting an important research gap. However, it remains to be established through future research whether acute or chronic vitamin D supplementation could have a protective effect against the development of depression.

Chorea is a hyperkinetic movement disorder, accompanied by dystonia, myoclonus, tics, stereotypies, and tremors. It is characterized by excessive, purposeless movements that are distressing, irregularly timed, and randomly distributed. Chorea can be present in many diseases, such as hereditary, metabolic disturbance, drug-induced, and functional disorders, and, rarely, genetic, autoimmune, and infectious diseases. Primary myelofibrosis (PMF) is a myeloproliferative neoplasm that leads to ineffective clonal hematopoiesis, fibrous tissue deposits in the bone marrow, extramedullary hematopoiesis, and splenomegaly. In rare cases, following uncertain pathological mechanisms, it can present with chorea, particularly affecting the limbs, head, and orofaciolingual muscles. We present a case of a male patient with evolving PMF over several years who was admitted for progressive cognitive impairment and generalized involuntary movement disorder. We also present a review of all cases of myeloproliferative disorders presenting with chorea published in the last 40 years.

Background and Clinical Significance: Statins are a widely used drug class associated with a plethora of muscular side effects ranging from the subclinical elevation of creatine kinase to fulminant rhabdomyolysis. Cardiac myopathy secondary to statin treatment is rare and was recently reported as a part of statin-induced necrotizing autoimmune myopathy (SINAM). Its occurrence outside of this context is still debated. Case Presentation: We present the case of a 60-year-old male who developed atorvastatin-induced rhabdomyolysis, without associated hydroxymethyl glutaryl coenzyme A reductase (HMGCR) antibodies, with clinical findings of cardiac failure and severe ECG anomalies. The symptoms slowly regressed with statin withdrawal, and the patient made a full recovery. We discuss the recently proposed statin-associated cardiomyopathy (SACM) and the possible mechanisms. We compare our case to the three other cases of statin-induced cardiac myositis found in the literature. Conclusions: We believe that in vulnerable patients, as was our case, statins can determine significant subacute cardiac toxicity. This would seem to occur in the context of severe skeletal muscle injury, probably due to higher metabolic resistance on the part of the myocardium. Also, the available evidence suggests myocardial involvement should be actively investigated in SINAM patients, preferably by cardiac MRI.

We set out to assess the diagnostic utility of the split hand index (SHI) for amyotrophic lateral sclerosis (ALS) and also to see if and how it can be applied to severely atrophied muscles, a frequent finding in this setting. We enrolled 38 patients from our clinic, 19 diagnosed with ALS and 19 controls, matched for age and sex. The SHI was calculated, on both sides, for all the patients. We calculated a SHI of 0 when the abductor pollicis brevis muscle (ABD) or first dorsal interosseous muscle (FDI) compound muscle action potentials (CMAPs) were unobtainable, and we allotted a value of 0.1 mV to abductor digiti minimi muscle (ADM) CMAP, for mathematical purposes, when the value would have been 0. The means differences were large between groups, with a significant variance heterogeneity. We performed a ROC analysis and obtained an accuracy of 0.83 for a SHI of 7.2, p-value < 0.0001. In conclusion, we reaffirm the utility of the SHI in the diagnosis of ALS, especially in limb onset cases, and we think that it can be safely extended to severely atrophied muscles with absent or very low CMAP values, without endangering the sensitivity or specificity.

Behçet’s disease (BD) is a systemic vasculitis that frequently presents with a relapsing–remitting pattern. CNS involvement (Neuro-Behçet) is rare, affecting approximately 10% of patients. Its etiological mechanisms are not yet fully understood. The most commonly accepted hypothesis is that of a systemic inflammatory reaction triggered by an infectious agent or by an autoantigen, such as heat shock protein, in genetically predisposed individuals. Mycobacterium tuberculosis is known to be closely interconnected with BD, both affecting cell-mediated immunity to a certain extent and probably sharing a common genetic background. We present the case of a 34-year-old Caucasian woman who had been diagnosed with tuberculous meningitis 15 months prior, with significant neurological deficits and lesional burden on MRI with repeated relapses whenever treatment withdrawal was attempted. These relapses were initially considered as reactivation of tuberculous meningoencephalitis, and symptoms improved after a combination of antituberculous treatment and corticosteroid therapy. After the second relapse, the diagnosis was reconsidered, as new information emerged about oral and genital aphthous lesions, making us suspect a BD diagnosis. HLA B51 testing was positive, antituberculous treatment was stopped, and the patient was started on high doses of oral Cortisone and Azathioprine. Consequently, the evolution was favorable, with no further relapses and slow improvements in neurological deficits. To our knowledge, this is the first report of Neuro-Behçet’s disease onset precipitated by tuberculous meningitis. We include a review of the available literature on this subject. Our case reinforces the fact that Mycobacterium tuberculosis infection can precipitate BD in genetically predisposed patients, and we recommend HLA B51 screening in patients with prolonged or relapsing meningoencephalitis, even if an infectious agent is apparently involved.