Mrs. T was a 67-year-old woman who had no past history of physical disease and had no psychiatric family history. In June 2008, she experienced depressed mood, decreased energy, anxiety, agitation, and insomnia, and she visited a psychiatric clinic. She was diagnosed with MDD. She took milnacipran (30
mg/day), but her depressive symptoms became more serious gradually without a change of the medication around December 2008. She completely lost interest in her leisure activity. In April 2009, she developed physical symptoms such as a respiratory discomfort. She was examined in many physical hospitals, but no abnormal results were found. She developed hypochondriacal delusions and delusions of poverty gradually. Her appetite decreased, and her body weight was decreased by 12
kg in a year.
She was admitted to a regional psychiatric hospital in May. She had severe agitation and complained, “I cannot breathe.” It was difficult for her to keep still, and she wandered about the hospital ward. She was treated sequentially with fluvoxamine (100
mg/day), amitriptyline (30
mg/day), sulpiride (50
mg/day), and augmentation olanzapine (10
mg/day), but it was impossible to use adequate doses because of her strong apprehension in regard to psychotropics. Finally, the neuroleptics and antidepressants were discontinued, and minor tranquilizers were prescribed, but her agitation did not improve. In October, paroxetine monotherapy (40
mg/day) was started, and she was transferred to us in November 2009.
Severe anxiety, agitation, depressed mood, decreased energy, loss of appetite, decreased body weight, insomnia, hypochondriacal delusions, and delusions of poverty were noted, and she fulfilled the DSM-IV diagnostic criteria for MDD with psychotic features. Total score on the 17-item Hamilton Rating Scale for Depression (HRSD) was 31. The physical examination and neurological examination revealed only low body mass index of 16.6. The blood examination revealed only anemia (hemoglobin 11.4
g/dL). An electrocardiogram, electroencephalogram, and brain MRI revealed no abnormalities.
ECT was done because she had severe depressive symptoms with psychotic feature. Anesthesia consisted of atropine sulfate (0.25
mg) intravenously with propofol (0.9
mg/kg) by intravenously bolus. Succinylcholine (0.9
mg/kg) was given intravenously as a muscle relaxant after induction of anesthesia. Thymatron IV system was used, and bifrontal brief pulse ECT was performed twice a week. The seizure threshold was determined by the half-age method. Paroxetine (40
mg/day), zolpidem (10
mg/day), and bromazepam (4
mg/day), those she had been taking at the previous hospital, were continued.
Confusion persisted soon after awakening from anesthesia at the initial ECT session. 30 minutes later, she failed to respond to our calling and fell into a substupor. Concurrently she developed autonomic symptoms, including pyrexia (38.6°C), tachycardia (160/min), elevated blood pressure (160/70
mmHg), and severe hyperhidrosis, and neurological symptoms, including severe generalized rigidity, palpebral and labial myoclonus, tremors of all limbs, and generalized hyperreflexia. Her total score on the Serotonin Syndrome Scale (SSS) [2
] was 20, and she was diagnosed with the serotonin syndrome. Except for leukocytosis (12,250/μ
L) and anemia (hemoglobin 9.9
g/dL), the blood examination revealed no abnormalities, including serum creatinine, blood urea nitrogen, creatinine phosphokinase, or electrolytes. The electroencephalogram revealed no paroxysmal abnormalities. In the same day, all oral medication including paroxetine was discontinued. Fluid administration was started under general management. Flunitrazepam (2
mg) was administered intravenously, and the neurological symptoms and autonomic symptoms were alleviated, but the benefit lasted only about 2
hr. The symptoms were gradually alleviated subsequently, and 24
hr later all vital signs except the pyrexia became normal. 48 hours later, the symptoms of serotonin syndrome including pyrexia and substupor resolved completely.
We continued the discontinuation of paroxetine, and performed the second ECT session 5 days after the initial session. We performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of serotonin syndrome were observed. Finally, her MDD remitted. The time-courses of the total scores on SSS and HRSD are shown ().
Time-course of changes in total score on Serotonin Syndrome Scale and Hamilton Rating Scale for Depression.