A 32-year-old male with a known history of bipolar disorder was brought to the emergency department with altered mental status. The patient's symptoms started with slurring of speech and left-sided motor weakness a day before the presentation. The patient suffered two episodes of seizures in the emergency department, which were controlled with two intravenous doses of lorazepam. He had no prior history of seizure disorder. He had to be immediately intubated and sedated for airway protection and was transferred to the intensive care unit from the emergency department. Noncontrast computed tomography (CT) of the head was significant for an infarct in the right frontotemporoparietal region of the brain (Figure ). A CT angiogram of the head and neck revealed complete occlusion of the right middle cerebral artery (Figure ) and a nonocclusive thrombus in the right internal carotid artery (Figures -). The etiology of stroke was unclear at this time. There was no personal history of known thrombophilia and family history was not available, as he was an adopted child. Laboratory investigations were pertinent for macrocytic anemia (hemoglobin: 11.2 mg/dl, mean corpuscular volume: 105 fl/cell). The Factor V Leiden, protein C, and protein S levels were within normal limits. A urine toxicology test obtained prior to administering lorazepam to the patient was negative. The vitamin B12 and folate levels were found to be low (198 pg/ml, and 2.5 ng/ml, respectively). The methylmalonic acid level was in the normal range (0.12 mcmol/L; ref. range: 0.0-0.4 mcmol/L) while the homocysteine level was elevated (253 mcmol/L; ref range: 0-10). Laboratory findings were significant for hyperhomocysteinemia, which led us to gather more history in order to understand its etiology. It was ultimately revealed that the patient had been inhaling nitrous oxide as a recreational agent for the past five years. The patient's symptoms at presentation were past the 4.5 hour time window for thrombolytic therapy and, therefore, he was not a candidate for it. He was mechanically ventilated and oral aspirin 81 mg and atorvastatin 80 mg once daily was administered through an orogastric tube for secondary prophylaxis of ischemic stroke. He was also started on intravenous levetiracetam for seizure prophylaxis. On Day 5 of admission, the patient had a successful weaning trial and was subsequently extubated. Physical therapy and speech therapy were provided to the patient, and he was discharged home on Day 11 of admission. The patient continues to follow up in our neurology clinic. On his last follow-up, 12 months after discharge from the hospital, the patient had residual, left-sided motor weakness in both the upper and lower extremities and mild dysarthria without any signs and symptoms of peripheral neuropathy.
Sudden-onset chest pain for 1 d.\nA 29-year-old man complained of sudden precordial pain with no remission for 1 d prior to hospital admission but denied hemoptysis, dyspnea, or syncope. He sought evaluation and was admitted for the purpose of intensive examination and treatment.\nThe patient had been addicted to N2O for 1 year; as a result, peripheral neuropathy had occurred and was treated with vitamin B12 (Vit B12). His medical history included poor blood glucose control and anxiety. However, he had no history of thrombosis, malignant tumor, recent trauma, or prolonged air travel.\nThe patient has smoked over 13 pack-years and did not have alcoholism or a positive family history.\nThe initial assessment revealed that the patient was overweight and fragile, with a body mass index of 31.12 kg/m2, temperature of 36.3 °C, blood pressure of 110-120/70-80 mmHg, heart rate over 110 beats/min, respiratory rate over 30 breaths/min, and pulse oximetry of 93% when the fraction of inspired oxygen was 49%. Moreover, the physical examination indicated diminished breath sounds on both sides and the accentuation of pulmonic second sounds.\nLaboratory data showed a high leukocyte count and an increased hemoglobin level, suggested abnormal liver biochemistry and hyperlipidemia, and revealed HHcy (24.12 µmol/L), high Vit B12 (734 µmol/L), and normal folate (14.39 nmol/L). The results of the protein S, protein C, anti-thrombin III antibody, anti-cardiolipin antibody, lupus anticoagulant, anti-β2gp1 autoantibody, and other autoantibodies were within normal limits. The clotting profile was normal, other than the D-dimer value (1.13 mg/L), and thrombophilia screening was negative. As markers in the risk stratification of PE, the levels of brain natriuretic peptide (BNP) and cardiac troponin I (CTnI) were 533 pg/mL and 0.334 ng/mL, respectively. Arterial blood gas levels measured with an oxygen concentration of 49% showed the following: pH, 7.44; PaCO2, 30 mmHg; and PaO2, 74 mmHg.\nAn electrocardiogram (ECG, Figure ) showed sinus tachycardia with typical changes on SIQIIITIII (S wave in the aVL lead, Q wave and T wave in the III lead). Ultrasonic cardiogram demonstrated right ventricular enlargement with left ventricular compression. Color Doppler scans were used to explore femoral, popliteal, and calf muscular venous thrombosis in the right extremity. Computed tomographic pulmonary angiography (CTPA) revealed occlusion of the pulmonary artery trunk, lobar artery, and arterial branches on both sides and signs of increased right heart load (Figure and ).