Cotard’s syndrome with schizophreniform disorder can be successfully treated with electroconvulsive therapy: case report

Case

Mr. G, a 27-year-old single man, was referred to our outpatient clinic by his gastroenterologist for evaluation and treatment of his psychiatric symptoms. He presented with a 1-month history of symptoms that included shortness of breath, heartburn and refusal to eat solid food, leading to a weight loss of 12 kg (from 75 kg to 63 kg). He had constipation, lack of appetite, abdominal distension, ideas of gastrointestinal system malfunction, shortness of breath and headache. According to his mother, he was complaining of constipation, anorexia, weight loss, stomach and heart problems, insomnia and self-induced vomiting.

The patient reported that his headaches had started 2 years previously and that he had visited a neurologist who prescribed various analgesics, which he had taken until recently. His parents had observed during the last 2 years the patient’s low mood, social withdrawal and failure in his job. Because of the cardiac and gastrointestinal complaints that had started 1 month before, cardiologic and gastrointestinal examinations were performed; they revealed no organic pathology that might result in such symptoms. Although all the patient’s test results were normal, he was given an appointment for endoscopic examination by his gastroenterologist because of his persistent ideas of stomach and intestine malfunction. From the history taken both from him and from his parents, the characteristic symptoms of schizophrenia were understood to have started within the preceding month.

Mr. G underwent a psychiatric outpatient examination and was diagnosed with schizophreniform disorder according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV),5 and thereafter he was admitted to hospital. He was prescribed haloperidol, 10 mg/d. He escaped from the inpatient unit 3–4 hours after admission, while the nurse was closing the secure door. He was seized by police officers at a shopping centre some 3–4 miles away from the hospital. He declared that the reason for his escape was the lack of oxygen in the clinic. The next morning, he attempted to escape through the ventilation area of the lavatories, but he was not successful because of the secured doors of the ventilation system. The haloperidol dosage was increased to 20 mg/d, and zuclopenthixol acetate, 50 mg, was administered by intramuscular injection.

In his first week in the hospital, the patient refused solid food and preferred to drink only water and fruit juices. His nihilistic delusional ideations were that he had no stomach and a nonfunctional gastrointestinal system, that his stomach had connected with his heart, which had no beat, and that he could not excrete feces. He used these ideas to explain his rejection of solid food. With the antipsychotic therapy, he showed some improvement and started to eat some solid food.

No neurologic or psychiatric disease was present in his family history. His past medical history revealed that when he was 6 years old, he had meningitis after mumps, from which he fully recovered after 25 days of in-hospital treatment. He had done well at school. There was no history of habitual cigarette or alcohol use.

The results of routine hematologic and biochemical tests, including thyroid hormone tests, were all normal. Two cranial computed tomographic (CT) images acquired 1 month and 2 years before the admission to hospital both demonstrated dilatation of the lateral and third ventricles. Magnetic resonance imaging (MRI) showed central atrophy and bilateral atrophic dilatation at the temporal horns of the lateral ventricle. The findings of an electroencephalogram were normal. Single-photon emission computed tomography (SPECT) was performed, and the brain image (technetium 99m hexamethylpropyleneamine oxime SPECT) revealed left temporal, left inferior frontal and left parietal hypoperfusion.

Because of the extrapyramidal side effects of haloperidol, biperiden was added, 4 mg/d, and the dosage was increased to 6 mg/d in the second week. At the end of the sixth week, the severity of the extrapyramidal side effects led to the decision to change the antipsychotic medication; quetiapine was started and haloperidol was tapered over 1 week. Quetiapine was increased up to 800 mg/d, then the patient started to gain weight and show improvement. However, despite improvement in social function, he continued to show somatic delusions after 2 weeks of quetiapine treatment.

Because of the severity of the presentation and the lack of response to medication, Mr. G was referred for a course of ECT. He received a total of 12 bilateral ECT treatments (Thymatron DGx, Somatics, Lake Bluff, Ill) at a rate of 3 per week. ECT dosage was selected according to the standard settings of device percent energy (percent energy 30, frequency 50 Hz, stimulus duration 1.68 s, number of pulses 168, charge delivered 151.2 mC). All treatments were performed under general anesthesia with propofol and succinylcholine chloride. At the end of the first week of ECT treatment, the patient showed improvement, and after 12 treatments the patient was back to his premorbid status. Thereafter, ECT was stopped and olanzapine, 10 mg/d, started. Posttreatment SPECT performed the following week showed total improvement of left inferior frontal and left parietal hypoperfusion and revealed minimal hypoperfusion at the left temporal lobe.

After discharge from the hospital, no somatic or psychotic symptoms were reported by both the patient and his relatives, and he was still in remission and had good occupational and social functioning at 4 months’ follow-up.