A Case of Myasthenia Gravis Preceded by Major Depression

SIR: In some reports on the relationship between myasthenia gravis (MG) and depression, the relationship has been discussed mainly from the viewpoint that depression may occur secondarily in MG patients reacting to having a chronic disability.^1,2 The possibility that the involvement of the central nervous system in MG may play a pathogenic role in depression has been less examined and remains unclear.

We here report a case of MG occurring with depression, in which the symptomatology and progress suggested that depression stemmed from the same pathology as MG.

Case Report

A 39-year-old man developed symptoms of depression, including a depressed mood, guilt feelings, appetite loss, insomnia, and general fatigue in 1998. At this time, he had not yet experienced symptoms of MG.

Four months later, he began to feel drooping in both eyelids. Two months thereafter, he suddenly experienced difficulty with speech and, around the same time, complained of a suicidal tendency. After another two months, the patient was admitted to our psychiatry unit. A diagnosis was made of major depression according to DSM-IV, and his score on the Hamilton Rating Scale for Depression (Ham-D) was 22 points. A brain CT and an EEG were normal.

The patient was prescribed fluvoxamine 50 mg/day. However, he soon began to experience dysphagia repeatedly and suffered from aspiration pneumonia. Consequently, the medication was discontinued. He also had marked weakness of the upper limbs, which got worse in the afternoons. The diagnosis of MG was established by a consultant neurologist, in consideration of a positive result on an edrophonium (Tensilon) test. The serum titer of anti-AchR antibody was very high (25.5 pmol/ml); the level in cerebrospinal fluid was not examined.

The patient was treated with anticholinesterase drugs. At the same time, thymoma was found and a thymectomy was performed. Since then, he has shown gradual improvement in both MG and depressive symptoms. The score on Ham-D gradually decreased (from 17 at admission to 13, 10, and 9 in successive months), simultaneous with a reduction of the serum titer of anti-AchR antibody (from 25.5 to 18.7, 14.2, and 15.2 pmol/ ml).

Comment

In the present case, findings suggest that depression was not caused by the patient's reaction to disability resulting from MG, but by a pathology in common with MG. Onset of depression preceded onset of MG, and depressive symptoms associated with anxiety about MG symptoms were obscure; on the contrary, guilt feelings toward subordinates and regret over life choices, such as choosing an occupation and getting married, were more prominent. In addition, the score on Ham-D decreased parallel to decrease in the serum titer of anti-AchR antibody. This progress suggests that MG and depression in this patient had the same immunological basis.

The potential pathogenic role of anti-AchR antibody in depression has been controversial.³ This case, however, suggests that increased attention should be paid to the complications of MG with depression. Further research on the autoimmune pathology of depression may help us understand the relationship between these two diseases.