Neuromyelitis optica spectrum disorders are characterized by severe demyelination and axonal damage with autoimmune mechanisms, predominantly targeting the optic nerves and the spinal cord. Patients often test positive for anti-AQP4 antibodies, while some have anti-MOG antibodies. Double seropositivity has been described, with a variable prevalence (0 to 26%) dependent on the testing method. The clinical significance of double seropositivity remains unclear. We present the case of a 65-year-old patient, admitted to our clinic with optical neuritis, followed up approximately 10 days later by cervical myelitis, who tested positive for both anti-AQP4 and anti-MOG antibodies. The clinical onset coincided with a mild form of SARS-CoV-2 infection. The neurological symptoms were initially relatively subdued, which delayed the diagnosis. The patient was not vaccinated against SARS-CoV-2. The clinical picture was compatible with an anti-AQP4 phenotype. The patient was started on corticosteroid therapy, under which the clinical response was good. Our case reinforces the idea that SARS-CoV-2 can precipitate autoimmune demyelinating diseases since SARS-CoV-2 infection has already been demonstrated as a risk factor for NMOSD relapses. To the best of our knowledge, this is the first reported case of double seropositive neuromyelitis optica associated with COVID-19. We expect that in the near future, as the true burden of COVID becomes clearer, we shall encounter other cases which can trace their apparent clinical onset to a SARS-CoV-2 infection. Careful attention should be paid to the apparent minor neurological symptoms of COVID-19.

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.

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.

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.