What question did this study set out to answer?

The aim is to explore recovery of respiratory control post-hemorrhagic stroke in a pediatric patient with sleep-disordered breathing.

May 10, 2026

1333 What Was Lost Can Be Found: Recovery of Respiratory Control After Stroke in a Pediatric Patient

Key Points

The aim is to explore recovery of respiratory control post-hemorrhagic stroke in a pediatric patient with sleep-disordered breathing.
Case report of a 13-year-old female with hemorrhagic stroke and sleep apnea caused by atrioventricular malformation rupture.
Monitoring of respiratory status and polysomnography (PSG) assessments were conducted throughout her recovery period.
Therapy involved tracheostomy, mechanical ventilation, and subsequent non-invasive ventilation adjustments.
Initial PSG showed moderate obstructive sleep apnea (oAHI 7.3 events/hr) and central sleep apnea (CSAI 6.2 events/hr).
After one year, follow-up PSG showed improvement to mild obstructive sleep apnea (oAHI 1.7 events/hr) with no significant CSA (CSAI 2.8 events/hr).
MRI revealed no residual AVM and evidence of encephalomalacia in specific brain regions.

Abstract

Abstract Introduction Hemorrhagic stroke can lead to sleep-disordered breathing (SDB), typically central sleep apnea (CSA), by damaging the brain’s respiratory control centers. We present a pediatric case of obstructive (OSA) and CSA secondary to hemorrhagic stroke in the setting of atrioventricular malformation (AVM) rupture, and the evolution of imaging findings that accompanied loss and subsequent recovery of breathing control. Report of case(s) A 13-year-old previously healthy female presented with new-onset headache and altered mental status secondary to an acute hemorrhagic stroke. A ruptured posterior fossa/cerebellar AVM was discovered as the etiology. She suffered acute respiratory failure requiring tracheostomy placement and mechanical ventilation. With clinical improvement, capping trials were attempted but failed due to apneas secondary to the underlying traumatic brain injury. 6 months after the initial injury, she was discharged on BPAP ST with settings of 10/5 cmH2O with a rate of 14 breaths per minute (bpm). One month after discharge, she had an accidental decannulation and her tracheostomy was unable to be re-established. A polysomnogram (PSG) at this time showed moderate obstructive (oAHI 7.3 events/hr) and central sleep apnea (CSAI 6.2 events/hr). She was discharged on non-invasive ventilation on BPAP ST 9/4 cmH2O with a backup rate of 12 bpm. After a year of therapy, she had shown clinical improvement, regaining the ability to speak in full sentences and near-complete functionality of her left hemibody. A repeat baseline PSG showed improvement to mild OSA (oAHI 1.7 events/hr) with no significant CSA (CSAI 2.8 events/hr), after which BPAP ST was discontinued. A follow-up MRI brain showed no evidence of AVM residual with encephalomalacia in the left cerebellum, medial right cerebellum, and brainstem. Conclusion Although hemorrhagic stroke can lead to SDB, it is important to monitor and re-evaluate sleep apnea, which may improve as a result of neuroplasticity. Support (if any)

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