In July, 2008, a 67-year-old woman with refractory depression was referred to our institute. In 2006, she had a thymectomy for thymoma. In January, 2008, after experiencing family discord, she lost her appetite, and her bodyweight decreased by 5 kg in 1 month. She became pessimistic and self-recriminating and made several suicide attempts. CT showed no evidence of a recurrence of the thymoma. Neurological examination showed only slight muscle weakness of her limbs, but the cause of her anorexia remained unclear despite further in-hospital examinations such as gastrointestinal tract endoscopies and systemic contrast-enhanced CT. She was diagnosed as having depression and was transferred to a regional psychiatric hospital, where she was treated sequentially with sertraline, paroxetine, clomipramine, and nortrip tyline, and augmentation lithium. These treatments were ineff ective, and her body weight decreased from 60 kg to 33·5 kg. She was then transferred to us. Her depressed mood, decreased interests, hypogeusia, anorexia, insomnia, anxious restlessness, decreased energy and fatigue, guilty feelings, poor concentration, and suicidal ideation persisted. She fulfi lled the DSM-IV diagnostic criteria for major depressive disorder. Her total score on the 17-item Hamilton Depression Rating Scale (total-HDRS) was 40. She could walk and had no ocular and bulbar symptoms, but neurological examinations showed mild proximal muscle weakness and atrophy of her limbs. Blood test results indicated hypoalbuminaemia (albumin 3·4 g/dL); other investi gations including CT chest, tumour markers, electro encephalography, and brain MRI were normal. Ten sessions of electroconvulsive therapy (ECT) were done in September, but the depressive symptoms persisted. She stopped taking medication, other than quetiapine as required (prescribed by us), but at the end of October, she suddenly developed impaired con sciousness with a reduced respiratory rate. A blood gas analysis showed carbon dioxide narcosis, and she was immediately placed on a ventilator. No evidence of pulmonary disease was found, and a diagnosis of myasthenic crisis was made on the basis of a high acetylcholine receptor antibody (AchR-Ab) titre (120 nmol/L), waning on the Harvey-Masland test, and a history of thymoma. She was treated with plasmapheresis and immunoadsorption followed by prednisolone treatment (maximum dose, 50 mg/day). Her respiratory function subsequently improved, and she was extubated. In December, she was treated with pyridostigmine (180 mg/day). As the anti-AchR-Ab titre decreased, totalHDRS score improved substantially without antidepressant therapy (fi gure). Her long-lasting depressive symptoms improved completely, and her bodyweight recovered to 40 kg; she was discharged in July, 2009. When last seen in September, 2009, both her depression and myasthenia gravis were in remission. The pathology of depressive symptoms associated with myasthenia gravis, including the hypothalamo-pituitaryadrenal axis dysfunction resulting from chronic stress and central cholinergic defi cit, is controversial and remains to be elucidated. Although some patients with major depressive disorder complicated with myasthenia gravis improve after ECT, the potential to misdiagnose myasthenia gravis as depression has been highlighted. 20% of people with myasthenia gravis are initially diagnosed as having a psychiatric disorder, and improvements in depressive symptoms associated with improvements in myasthenia gravis have been reported. Whether depressive symptoms in individual cases are attributable to myasthenia gravis or major depressive disorder should be investigated. Since the AchR-Ab titre and the depressive symptoms improved over time in our case, we concluded that the patient’s depressive symptoms could predominantly be attributed to myasthenia gravis. When managing treatment-resistant depressive patients, the medical history must be suffi ciently considered.