Juvenile Ischemic Stroke Secondary to Cardiogenic Embolism: A Rare Case Report
Our patient was a 24-year-old male presented to the emergency department with the chief complaint of right-sided weakness without any loss of consciousness. He reported sudden onset of weakness within the previous 24 h having occurred after exercise and followed by difficulty in speech. No further specific symptoms including nausea, vomiting, vertigo, chest pain, or headache were noted prior to the emergence of sudden weakness except for a complaint of recent dyspnea on exertion (DOE). In his medical history, we detected a period of posttraumatic seizure that had been controlled with carbamazepine; he had stopped the course of medication 3 months ago. Also, a suspicious history of rheumatic fever in childhood without any documented therapy or diagnosis was present.\nIn physical examination, he was alert and oriented with obvious aphasia as he was able to obey the commands yet unable to speak. His vital signs were as follows: BP = 110/70 mm Hg, PR = 70/min, RR = 16/min, BT = 37°C. In his respiratory and cardiovascular examination, there was no specific abnormal finding. His peripheral pulses were symmetric and normal. In central nervous system examination, he had a right-sided hemiplegia with muscle force of 2/5 in upper and lower extremities; right plantar reflex was extensor, while the left plantar reflex was flexor and his deep tendon reflexes were increased up to 3+. Due to his lateralized signs, the spiral brain computed tomography (CT) scan was recommended and routine lab tests were checked simultaneously. In spiral brain CT, a hypodense lesion could be observed in the left middle cerebral artery (MCA) [].\nThe lab tests results were as follows:\nErythrocyte sedimentation rate (ESR) = 47 mm/h, PT = 14.4 s, International normalized ratio (INR) = 1.33, PTT = 30.9 s, K = 4.5 mmol/L, Na = 141 mmol/L, Blood sugar (BS) = 94mg/dL, Blood urea nitrogen (BUN) = 13 mEq/dL, Cr = 1.06mg/dL, Creatine phosphokinase (CPK) = 116 U/L, Creatine phosphokinase-MB (CPKMB) = 27U/L, lactate dehydrogenase (LDH) = 358 U/L, White blood cells (WBC) = 6700/mm3 (Neut = 57%, Lymph = 40%, Mono = 3%, Eos = 0%, BASO = 0%, BAND = 0%.), Red blood cells (RBC) = 4.32 million/mm3, hemoglobin (Hb) = 11.5g/dL, Hematocrit (Hct) = 35.5 g%, Platelet (PLT) = 221000/ mm3.\nThe NIHSS of the patient was 14; however, no intravenous thrombolysis therapy was considered due to the delayed referral to our center (more than 3-4.5 h).\nDue to his history of DOE and occurrence of his signs and symptoms exactly following exercise, echocardiography was suggested. Interestingly, echocardiography revealed multiple masses in all cardiac chambers [left atrium (LA) and Left ventricular (LV) (two separated), right ventricle (RV) and right atrium (RA) in order of largest to smallest, respectively] []. Findings were in favor of a multiple myxoma. On the basis of cardiology consultations, association of a multiple cardiac myxoma and probable cerebral emboli originating from it forced anticoagulant therapy because of high risk of hemorrhagia of lesion did not start. He was admitted at cardiac surgery intensive care unit and scheduled to undergo cardiac myxoma resection 2 days after his emergency department admission. The day following cardiac surgery, his hemiplegia resolved and he was ambulated at the time of discharge. Furthermore, muscle forces of the upper and lower limbs improved from 2/5 and 2/5 to 3/5 and 4/5 before and after operation, respectively. Postoperation imaging of the patient including brain CT scans and magnetic resonance imagings are presented in Figures -. The follow-up CT scan revealed evidences of remained ischemic injury in the left MCA 2 months after operation [].