Background: Wernicke-Korsakoff encephalopathy is a metabolic disease caused by vitamin B1 deficiency that predominantly affects alcoholic patients. Its clinical picture is characterized mainly by altered mental status with memory deficits, ophthalmoparesis, and ataxia, although other clinical manifestations may also be present. The current case presents certain clinical difficulties regarding the diagnosis when confronting an atypical presentation of a classical disease in an acute setting when a decision to administer an intravenous thrombolytic agent needs to be made.Case presentation: This case involves a young male patient, with a history of chronic alcohol abuse, malnourished, and in poor general health, who presented with right-sided hemiparesis and language disturbance of acute onset, suggesting a left hemispheric stroke. The psychological examination was difficult due to a mix of confusion and aphasia, the latter being challenging to assess as the patient had a dismissive and highly deflective attitude toward the examiner. The initial cerebral computed tomography scan was unremarkable, in line with early imaging in ischemic stroke patients. On subsequent magnetic resonance imaging, lesions were observed in the medullo-pontine tegmentum, around the aqueduct of Sylvius, in the mamillary bodies, in the medial thalami, but also extensive bilateral cortical involvement in the frontal lobes. After receiving intravenous vitamin B1 treatment, the patient made a slow, but full, recovery, after eight weeks of hospitalization, and was subsequently transferred to a psychiatry clinic for treatment of his addiction.Conclusion: Atypical Wernicke-Korsakoff encephalopathy can closely mimic stroke, usually akin to a vertebro-basilar lesion. Our case is the first report we are aware of Wernicke-Korsakoff encephalopathy feigning a left hemispheric stroke with aphasia and right hemiparesis. This has implications for the emergency medicine doctor, neurologist and the stroke specialist when considering an emergency differential diagnosis for a patient with an initial normal computed tomography scan, especially in regard to deciding acute therapy.

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.