A 25-year-old Chinese woman presented with headache and difficulty in speaking and moving the right arm for the last eight hours. She used oral contraceptives once ten days ago and inhaled nitrous oxide outside with friends in the last week.\nThe patient began to use oxide intermittently twenty months ago. She gradually developed numbness and weakness of distal limbs, and balance difficulty, which significantly improved after vitamin B12 intake of one month. One year ago her numbness in the distal limbs subacutely deteriorated and ascended to both proximal thighs and the upper trunk. Medical record showed she had impaired superficial sensation of both hands, feet and the thorax region from T4 to T8 dermatome, impaired deep sensation of the lower limbs, and areflexia. MRI showed hyper-intensities involving the posterior and lateral column of the spine cord ranging from T5 to T11 vertebral body on T2 sequence (not shown). A diagnosis of peripheral neuropathy and subacute combined degeneration was made and her symptoms again improved significantly with vitamin B12 intake.\nThe patient did not use other substances and had no family history.\nThe patient had significant motor aphasia, mild right facial paralysis and right deviation of tongue. Muscle strength of the right upper limb is 0/5 with reduced tendon reflex compared with the left side. No apparent abnormalities in mental status, sensations and coordination were found.\nErythrocyte sedimentation rate (34 mm/H), c-reaction protein (21.1 mg/L), D-Dimer (1.14 ug/ml) and lactate dehydrogenase (314 U/L) were elevated. Complete blood count, liver enzyme, creatinine, urea nitrogen, troponin I, protein C, protein S, antinuclear antibodies, autoantibodies to extractable nuclear antigens, antiphospholipid antibodies, anti-neutrophil cytoplasmic antibodies, and beta-HCG were all within normal limits. Folate and vitamin B12 levels were normal. Homocysteine level was within the upper limit (13.6 umol/L; normal range 6–14 umol/L). No mutation of Factor V Leiden was found. Methylenetetrahydrofolate reductase (MTHFR) genotype of C677T and A1298C, and plasminogen activator inhibitor 1 (PAI-1) genotype of 4G/5G were confirmed.\nHead CT showed hemorrhagic infarction (Fig. a&b, arrow) and subarachnoid hemorrhage (Fig. b, arrow heads) mainly involving the left parietal lobe. MR angiography and venography were normal (not shown) and excluded major abnormalities of the large and medium arteries as well as the venous sinus system. Since the patient did not experience any major symptomatic improvement during the hospital stay and there was the concern about the existence of isolated cortical vein thrombosis, MRI head with 0.1 mm thickness demonstrated expanding hematoma and edema causing cingulate herniation, and confirmed isolated cortical vein thrombosis over the frontal cortical surface in the sagittal, coronal and axial section (Fig. a-c) ten days after admission.\nVitamin B6, B12, folate, mannitol and Low Molecular Weight Heparin were initiated. The sizes of thrombus, hematoma and edema reduced continuously after treatment of five (Fig. d-f) and twelve days (Fig. g-i), respectively, and the patient achieved significant improvement in muscle strength (grade 3/5) and verbal fluency in the meantime. Anticoagulation was switched from Low Molecular Weight Heparin to oral anticoagulant after another two weeks and the patient was discharged.\nDuring the last follow-up (6 weeks after symptom onset), the patient had further improvement in muscle strength (grade 4/5) and almost normalized verbal fluency. The patient was satisfied with her recovery and no adverse effects were reported.
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.