[Seroconversion of anti-aquaporin-4 antibody in a patient with neuromyelitis optica spectrum disorder: a case report].

We report a case of a patient with neuromyelitis optica spectrum disorder (NMOSD) who was originally treated for multiple sclerosis (MS) due to a negative anti-aquaporin-4 (AQP4) antibody test, but later the antibody titer became positive. A 58-year-old woman without prior medical history developed acute left facial pain, vomiting, and hiccups. MRI showed an intraparenchymal lesion extending from the medulla oblongata to cervical cord with high T2-weighted signal intensity. The patient responded to steroid pulse therapy. However, she developed diplopia and gait disturbance after six months, and follow-up MRI revealed a new lesion in the left middle cerebellar peduncle. The patient was diagnosed with MS due to the dissemination in the time and space of her lesions and negative anti-AQP4 antibody status. There was no relapse for three and a half years on fingolimod therapy. However, a severe relapse occurred four years later that involved optic neuritis and multiple new brain lesions. During this episode, the anti-AQP4 antibody test was positive, and the patient was diagnosed with NMOSD. This case highlights the possibility that seroconversion of anti-AQP4 antibody may occur at any time in NMOSD patients. Therefore, this diagnostically paramount antibody should be measured several times during the treatment of relapsing-remitting MS in patients with repeat frequent recurrences and uncommon symptoms of MS.

[Endogenous endophthalmitis following staphylococcus aureus meningitis].

Endogenous endophthalmitis is a rare complication of acute meningitis. A healthy 82-year-old woman suddenly developed septic bacteremia and meningitis owing to Staphylococcus aureus (methicillin-susceptible Staphylococcus aureus); she presented with a high fever and drowsiness. Improvement of these initial symptoms unveiled impaired bilateral visual acuity. Detailed ophthalmological assessments diagnosed it as probable endogenous endophthalmitis, which was immediately treated with vitrectomy. Subsequently, the patient totally recovered without any neurologic or ophthalmic sequela.

[Asystole after anesthetic induction with remifentanil].

A 45-year-old man was scheduled for laparoscopic cholecystectomy. He had hypertension controlled with beta-adrenergic, calcium channel and angiotensin II receptor blocking agents. Because he had complications of symptomatic cervical spondylosis and sleep apnea syndrome, we performed awake fiberoptic intubation with remifentanil at a dose of 0.05 microg x kg(-1) min(-1). After intubation and following administration of propofol and vecuronium, ECG unexpectedly changed to asystole. We administered atropine 1.5 mg and performed chest compressions, which successfully restored sinus rhythm within 10 seconds. However, no cardiac disease was detected by a cardiologist. The operation was scheduled a week later again. Anti-hypertensive agents were discontinued. A temporary pacing wire was inserted before surgery, and atropine 0.5 mg was administered before anesthetic induction with remifentanil. No cardiac event was noticed through the perioperative period. We suggest that even a low dose of remifentanil may cause asystole in patients taking beta-adrenergic and calcium channel blocking agents, and preemptive administration of atropine may be effective.