We report a case of a 56-year-old man who presented initially with a sudden onset of right-sided facial droop and weakness, aphasia, and confusion with no associated fever, chills, syncope, fatigue, weight loss, night sweats, nausea, vomiting, diarrhea, odontalgia, palpitations, cough, or dyspnea. Code stroke was called and the patient received tissue plasminogen activator (tPA) with subsequent resolution of his symptoms. Cranial magnetic resonance imaging showed left frontal punctate cortical restricted diffusion consistent with subacute to acute infarction. Transesophageal echocardiogram showed a severely thickened anterior mitral valve leaflet with a shaggy echodensity consistent with a vegetation. Blood cultures grew Bacillus cereus sensitive to clindamycin, trimethoprim sulfamethoxazole, and vancomycin. He was initially treated with ampicillin, clindamycin, and vancomycin and was eventually maintained solely on vancomycin. He had complete return of his neurological function and was discharged on intravenous antibiotic to complete a 6-week course.

We present a case of a 47-year-old female with a history of anxiety, depression, and alcohol dependence with history of alcohol withdrawal seizures, who presented after a witnessed seizure episode. She admitted to drinking only copious amounts of black tea 1 week prior to presentation in an attempt to quit alcohol. She was subsequently found to be severely hyponatremic with a serum sodium level of 112 mEq/L and was admitted to the intensive care unit. Approximately 48 h after admission, she experienced sudden-onset of dizziness, diaphoresis, and nausea, with a heart rate of 42 beats/min and blood pressure of 70/40 mm Hg. STAT EKG revealed new T-wave inversions in the lateral and precordial leads and troponin was elevated to 5.99 ng/ mL. Treatment was initiated for NSTEMI with continuous heparin infusion, aspirin, clopidogrel, carvedilol, and lisinopril. Transthoracic echocardiogram revealed apical and mid ventricular dyskinesia with hyperkinesis of the basal walls, with an estimated left ventricular ejection fraction of 35%. Cardiac catheterization revealed no significant coronary disease with ejection fraction 30-35% and similar areas of hypo and hyperkinesis, classic for apical ballooning syndrome. This case not only illustrates the rare phenomenon of hyponatremiainduced Takotsubo cardiomyopathy, but is one of the only incidents caused by primary polydipsia.