Atypical Depression: A Clinical Alert for Obstructive Sleep Apnea Screening

Obstructive sleep apnea (OSA) syndrome (OSAS) is a prevalent yet frequently underdiagnosed condition, particularly in young patients with mood disorders, due to the overlap of complaints such as fatigue, hypersomnia, irritability, and concentration deficits.^1,2 Depression and anxiety affect 20%–35% of OSA patients, suggesting a bidirectional relationship between these conditions.^3,4 The atypical depression phenotype, characterized by hypersomnia, hyperphagia, weight gain, and fatigue, has been specifically identified as a clinical context wherein systematic OSA screening is strongly recommended.^5,6

Case Report

A 28-year-old married woman and mother, who was employed and had a high school education, had been managed in general practice for depressive symptoms since age 16 years. She had a history of antidepressant use but no prior psychiatric or psychological follow-up. During her pregnancy at age 24 years, she discontinued her medication without an apparent recurrence of psychiatric symptoms.

At age 26 years, her depressive symptoms resurfaced, including low mood, anhedonia, marked fatigue, and social withdrawal. These symptoms were accompanied by binge-eating episodes and worsening migraines. Her general practitioner reintroduced her previous antidepressant, escitalopram (titrated to 20 mg/day), and referred her to the neurology department, where topiramate 100 mg at bedtime was started for migraine prophylaxis.

During this period, she experienced a progressive weight gain of approximately 40 kg (88 lb), leading to class III obesity (body mass index: 46.6 kg/m²) and significant functional impact. Due to persistent mood complaints and their effect on her global functioning, she was referred for a psychiatric evaluation.

Initial psychiatric assessment highlighted subdepressive mood, hypobulia, adynamia, difficulty concentrating, hypersomnia with daytime sleepiness, and hyperphagia (including binge-eating episodes without compensatory behaviors). These findings confirmed a diagnosis of atypical depression.

A switch from escitalopram to fluoxetine was performed to target binge-eating control, and topiramate was titrated to 150 mg/day. Fluoxetine was eventually increased to 60 mg/day, which led to significant improvements in mood, volition, and energy levels. By the fourth month of treatment, there was also a notable reduction in the frequency and intensity of binge-eating episodes.

Despite this partial recovery, the patient continued to report impaired concentration, irritability, intense daytime fatigue, nonrestorative sleep, and snoring (noted by her partner). Trazodone 100 mg at bedtime was added but provided only slight improvement in subjective sleep quality.

Given the persistent residual symptoms and multiple risk factors (obesity, hypersomnia, nonrestorative sleep, and snoring), she was referred for a sleep study and a pulmonology consultation. The patient scored 12/24 on the Epworth Sleepiness Scale,⁷ indicating moderate excessive daytime sleepiness. Full polysomnography revealed severe OSAS, with a respiratory disturbance index of 30.8 events/hour and a T90 of 0.4%.

Targeted treatment with automatic positive airway pressure (APAP) was initiated. The patient adapted well within the first few weeks, showing significant improvement in daytime sleepiness, nonrestorative sleep, irritability, and concentration; notably, her migraines also went into remission. Following psychiatric re-evaluation, she remained clinically stable on fluoxetine 40 mg/day in sustained remission. She is concurrently followed by a multidisciplinary obesity team with high adherence to the treatment plan.

Discussion

This case illustrates several critical points at the intersection of psychiatry and sleep medicine. It demonstrates how young patients with atypical depression, marked weight gain, and snoring can go years without formal OSA screening, contributing to underdiagnosis within psychiatric care.^6,8

Furthermore, the partial response to optimized antidepressant therapy, characterized by persistent fatigue, hypersomnia, and cognitive deficit, aligns with clinical recommendations to screen for OSA in cases of resistant or partially responsive depression.^6,9

It is noteworthy that the functional improvement following APAP initiation is consistent with evidence showing that continuous positive airway pressure/APAP treatment reduces daytime sleepiness and improves depressive symptoms on average, particularly in patients with high device adherence.^10–12

Finally, the case reinforces the well-recognized difficulty in distinguishing the core symptoms of major depressive disorder from OSAS manifestations, requiring an integrated and collaborative approach between general practice, psychiatry, neurology, and pulmonology.^13,14

This case highlights how severe OSAS can mimic or exacerbate atypical depressive symptoms, leading to a state of pseudoresistance to antidepressants. To prevent diagnostic delays, clinicians should implement systematic screening (eg, STOP-Bang or neck, obesity, snoring, age, sex) for any patient exhibiting the triad of atypical depression, obesity, and persistent fatigue.^8,10,13,15 Recognizing this comorbidity is vital for shifting the clinical trajectory toward full remission.

Article Information

Published Online: September 29, 2026. https://doi.org/10.4088/PCC.26cr04237
© 2026 Physicians Postgraduate Press, Inc.
Prim Care Companion CNS Disord 2026;28(5):26cr04237
Submitted: March 22, 2026; accepted May 18, 2026.
To Cite: Lourenço A, Ribeiro M. Atypical depression: a clinical alert for obstructive sleep apnea screening. Prim Care Companion CNS Disord 2026;28(5):26cr04237.
Author Affiliations: Department of Psychiatry, Unidade Local de Saúde de Santa Maria, Lisbon, Portugal.
Corresponding Author: Ana Lourenço, MD, Department of Psychiatry, Unidade Local de Saúde de Santa Maria Av. Prof. Egas Moniz, 1649-028 Lisbon, Portugal ([email protected]).
Financial Disclosure: None.
Funding/Support: None.
Patient Consent: Consent was received from the patient to publish the case report, and information has been de-identified to protect patient anonymity.