PATIENTS WITH SCHIZOPHRENIA, especially older patients, show a higher incidence of obstructive sleep apnea (OSA), a chronic condition characterized by frequent episodes of upper airway collapse during sleep, than healthy controls.1 Obesity, male gender and chronic neuroleptic administration are risk factors for OSA in patients with schizophrenia.2 Here we present a case of a male patient diagnosed with simple schizophrenia who experienced a reduction in the severity of symptoms, such as blunted affect and psychomotor poverty, following treatment of previously unrecognized OSA. Written informed consent was obtained from the patient.
A 44-year-old Japanese man, who had been diagnosed with depression and treated with antidepressants, was initially seen and admitted to a psychiatric inpatient unit for his sleep difficulty and depressed mood at 36 years of age. He had no family history of psychiatric disorders. After graduating from junior high school, he had worked for his father's company until 23 years of age. Then he began to experience depressed moods, was easily fatigued and experienced sleepiness during the daytime through his twenties, and could only work part time. At 32 years of age, he fainted once for 20 min. Although a magnetic resonance imaging (MRI) scan showed mild brain atrophy, no evidence was found to explain the onset of his disturbance of consciousness. He gradually withdrew from others and he could not work at all by 35 years of age. At his first admission at 36 years of age, there was a lack of progression of brain atrophy in the MRI. He was rediagnosed as suffering from simple schizophrenia based on the ICD-103 criteria with slowly progressive manifestation of negative symptoms from his twenties and the medication was switched from antidepressants to antipsychotics. Because of his persistent depressive mood, fatigue and insomnia, although they were not enough to meet ICD-10 criteria of depressive episodes, he was readmitted at 44 years of age. A detailed interview found that he had had troublesome snoring for many years. Furthermore, the polysomnography showed that his apnea-hypopnea index (AHI) was 43.6 events/hour. No abnormalities in the soft palate or upper airways were found by a trained otolaryngologist in our hospital. Before the treatment with continuous positive airway pressure (CPAP), his weight and body mass index were 72 kg and 24.3 kg/m2, respectively. Therefore his symptoms satisfied the diagnostic criteria of adult OSA. Polysomnography showed the AHI ≥ 15 events/hour with evidence of respiratory effort during all or a portion of each respiratory event and the disorders were not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder.4 After the treatment with CPAP, his sleep improved dramatically. CPAP reduced the AHI from 43.6 to 2.3 events/hour. Accordingly, the symptoms, including the blunted affect, psychomotor poverty, and fatigue, also partially improved as the sleep disturbance improved. The severity of negative symptoms, assessed using the Positive and Negative Syndrome Scale,5 and the general assessment of his quality of life, assessed with the Global Assessment of Functioning,6 were improved as the change from 34 to 20 and from 31 to 38, respectively.
A significant portion of his apparent negative symptoms was accounted for by the symptoms of OSA, and the treatment by CPAP improved his quality of life. The present case report is in line with previous reports, including a patient with delusional schizophrenia showing an improvement of negative symptoms7 and a case with hebephrenic schizophrenia showing complete remission of auditory hallucinations after successful treatments of OSA with CPAP.8