Abstract Introduction Obstructive and central sleep apnea syndromes often coexist with periodic limb movement disorder (PLMD), but the underlying mechanisms linking these phenomena remain incompletely understood. Mixed sleep apnea in a non-obese individual with minimal daytime sleepiness along with restless legs and PLMD presents a unique diagnostic and pathophysiologic challenge. We report a case that highlights the potential role of prior neurotoxic drug exposure and iron deficiency in the genesis of such a mixed phenotype. Case Description A 65-year-old non-obese male (BMI 22.5 kg/m²) presented with a 15-year history of witnessed apneas, non-refreshing sleep, and restless sensations in the legs. His wife reported nightly apneic events. The patient denied excessive daytime sleepiness (Epworth Sleepiness Scale = 0). He had longstanding sensorineural hearing loss since early adulthood, attributed to prolonged childhood exposure to streptomycin and quinine. His STOP-Bang score was 4, and serum ferritin was 21.5 µg/L, suggesting low iron stores.Overnight polysomnography revealed a total apnea–hypopnea index (AHI) of 15.4 events/hour, with 24 obstructive apneas, 17 central apneas, and 3 mixed apneas. Sleep efficiency was high (94.6%), with a mean SpO2 of 95% and nadir of 79%. The limb movement index was 21.7/hour, with 7 limb movement–related arousals, confirming coexistent PLMD. Treatment included positional therapy and oral iron supplementation. After two months, limb sensations and movements improved up to some extent, and witnessed apneas persisted. He was offered CPAP therapy. Discussion This case represents an uncommon phenotype of mixed sleep apnea in a lean, non-sleepy patient. The coexistence of central events and PLMD suggests a possible shared neurophysiologic dysfunction, potentially linked to drug-induced neuronal damage or respiratory muscle impairment from historical streptomycin/quinine exposure. Given the patient’s history of prolonged exposure to these agents, it is biologically plausible that cumulative damage to neuromuscular junctions, respiratory motor neurons, or central respiratory control circuits contributed to his mixed apnea phenotype. Iron deficiency may have further exacerbated the PLMD component. Recognizing such atypical etiologies expands the clinical spectrum of sleep-disordered breathing and underscores the importance of personalized diagnostic and therapeutic strategies. This abstract is funded by: None
Khara et al. (Fri,) studied this question.