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.
A 27-year-old man of North African descent attended the emergency room of our tertiary percutaneous coronary intervention centre because of chest pain. Since 12 h, he had experienced severe retrosternal chest pain with sweating, nausea, and vomiting. Electrocardiography demonstrated ST-elevation in the anterior leads (Figure ). Detailed history revealed that in the hours prior to presentation, he had been recreationally using high amounts of N2O by inhalation from balloons. For the last 24–48 h, he had been sleep-deprived and, while sitting in a car, he had inhaled approximately 3.3 kg (or 420 balloons) of N2O and smoked 4 joints of cannabis. The patient had not experienced recent trauma, had no co-morbidities and was not under any prescription. He had never experienced chest pain before, there were no signs of acute heart failure. Besides smoking nicotine and cannabis, he did not have any other cardiovascular risk factors. There was no family history of coronary disease or sudden cardiac death. Drug screening upon presentation was positive for tetrahydrocannabinol (THC). Patient admitted to regularly smoke cannabis but denied consumption of alcohol or any other recreational drugs.\nAs per hospital protocol, he received 180 mg ticagrelor orally, 300 mg aspirin intravenously (i.v.) and 5000 EH heparin i.v. and was referred for immediate coronary angiography (CAG). This showed a normal aspect of the left main, right coronary and circumflex artery. The distal left anterior descending artery (LAD) was totally occluded, and thrombus was angiographically visible in the proximal segment, with maintained flow (TIMI 3) (Figure and ). Despite successful wire passage into the distal LAD and multiple balloon dilatations, no recanalization was achieved. Therefore, mechanical thrombectomy by means of AngioJet was attempted without distal recanalization, nor angiographical resolution of the proximal thrombus. Optical coherence tomography of the proximal LAD confirmed the presence of residual thrombus but excluded atherosclerotic media thickening. Plaque/endothelial erosion underneath the thrombus could not be excluded (Figure and ). Because of a minimal lumen area of 10.75 mm2 no further intervention was undertaken. The procedure was discontinued, and the patient received tirofiban i.v. for 48 h, on top of standard dual antiplatelet therapy (DAPT: ticagrelor and aspirin).\nThe first high-sensitive troponin T and CK-MB levels were 0.418 μg/L and 77 μg/L, peaking at 5.35 μg/L (upper limit of reference range: 0.014 μg/L) and >300 μg/L (upper limit of reference range: 7.6 μg/L). Transthoracic echocardiogram (TTE) showed a reduced (30–40%) left ventricular ejection fraction (LVEF) with apical and mid septal akinesia, a normal right ventricular function and no valvular abnormalities (). Migration of a venous thromboembolism due to intracardiac right-left shunt was excluded by using right-sided contrast. Vitamin B12 (114 pmol/L; reference range: 160–700 pmol/L), folic acid (7.7 nmol/L; 8.8–40 nmol/L), and homocysteine (205 μmol/L; <15 μmol/L) levels were measured upon admission.\nAfter 5 days, serum homocysteine levels had decreased to 86 μg/L. Additional analysis excluded the presence of a methylenetetrahydrofolate reductase (MTHFR)-gene polymorphism. To evaluate the effect of the initiated antiplatelet therapy CAG was repeated after 7 days. The size of the thrombus in the proximal LAD was slightly reduced, but the distal LAD remained occluded. (Figure and ). After initiation of heart failure medication, he was discharged with the advice to take DAPT for 1 year, discontinue drug abuse and take oral folic acid and vitamin B12 supplementation. Upon discharge persistent ST-elevation with negative T- (V2–V6) and pathological Q-waves (V2–V6) in the anterior leads was shown on the electrocardiogram (Figure ).\nAfter 3 months, a repeat TTE showed improvement of LVEF (53%), with remaining anteroseptal wall motion abnormalities (). He did not report recurrent angina or symptoms of heart failure.