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.
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 ).