1396 Biot’s Breathing Revealed on Polysomnography in Secondary Progressive Multiple Sclerosis Without Radiographic Brainstem Lesions

Abstract Introduction Biot’s breathing, characterized by clusters of irregular respirations interrupted by abrupt central apneas, is classically associated with medullary injury. Although multiple sclerosis (MS) can produce central sleep apnea (CSA) through brainstem demyelination, Biot’s respiration is rarely documented on polysomnography (PSG), particularly in the absence of radiologic brainstem abnormalities. We report a case of secondary progressive MS (SPMS) in which PSG revealed Biot’s breathing despite stable imaging and discuss the differentiation from baclofen-induced respiratory depression. Report of case(s) A 61-year-old woman with SPMS (diagnosed 1998) presented with excessive daytime sleepiness and sleep attacks. Her comorbidities included migraine, coagulopathy, and prior obstructive sleep apnea (intolerant to CPAP due to cranial pain). She was neurologically stable on ocrelizumab. Serial MRIs from 2019–2024 demonstrated extensive chronic supratentorial demyelination without active lesions or brainstem involvement. In-lab PSG (2025) showed an AHI of 19.6 events/hour, almost entirely central (central AHI 17.5). The respiratory pattern consisted of irregular clusters of respirations with sudden, short central apneas, consistent with Biot’s breathing. Snoring and obstructive events were minimal. Oxygen saturation nadir was 77%, with 80 minutes 88%. No arrhythmias were identified. The patient was taking baclofen 20 mg four times daily and had documented autonomic dysfunction (acral discoloration, dysphagia), raising the question of baclofen-related hypoventilation. However, multiple PSG features supported medullary respiratory generator instability rather than drug effect: (1) abrupt central apneas with preserved tidal effort between apneas; (2) normal chest and abdominal movement without the shallow, uniform hypoventilation typical of baclofen; (3) apnea-linked, discrete desaturations; and (4) preserved EEG architecture without sedation patterns. These findings favored true Biot’s respiration related to MS. The patient declined PAP titration due to prior intolerance; no alternative therapy has been initiated. Conclusion This case highlights the diagnostic utility of PSG in detecting Biot’s breathing as a manifestation of subclinical medullary dysfunction in SPMS, even when MRI is unrevealing. Distinguishing Biot’s respiration from medication-induced hypoventilation is essential, and preserved tidal effort with abrupt apneas can aid differentiation. PSG may reveal clinically significant respiratory instability in chronic MS, underscoring the need for tailored management approaches for CSA in this population. Support (if any)