Hemispheric stroke lesions impair contralateral diaphragmatic function: A comparative ultrasound-based cross-sectional study with healthy controls

Abstract

Introduction: The diaphragm is the primary respiratory muscle, responsible for about 75% of the airflow into the lungs, physically separating the thoracic cavity from the abdominal cavity. The diaphragm has several functions besides ventilation, including trunk stabilization and balance control. This dual function of the diaphragm (ventilation and posture) is performed simultaneously and is independent of the phase of respiration, which suggests that the response may be pre-programmed by the central nervous system. Ventilation is activated voluntarily through the corticospinal pathway or automatically through the bulbospinal pathway. There are hypotheses that hemiplegia caused by a lesion superior to the brainstem will impair diaphragmatic movement. Objective: To investigate whether hemispheric stroke lesions affect contralateral diaphragmatic function and respiratory capacity using comprehensive ultrasonographic assessment compared to healthy controls. Design: Cross-sectional observational study with matched healthy controls. Participants: Forty-two patients with hemispheric stroke (27 ischemic, 15 hemorrhagic; mean age 66.43 ± 6.41 years; 23 women) and 42 age- and sex-matched healthy controls (mean age 65.15 ± 5.62 years; 21 women). Main Outcome Measures: Spirometry (FVC, FEV1, FEV1/FVC), maximum inspiratory pressure (MIP), and comprehensive diaphragmatic ultrasound assessment including thickness at rest and maximum inspiration, thickening fraction (TFDI), and excursion at rest and maximum inspiration. Results: Stroke patients demonstrated significant respiratory impairment compared to healthy controls, with reduced MIP (62.83 ± 5.24 vs 78.65 ± 7.62 cmH2O, p < 0.001), FVC (2.12 ± 0.42 vs 3.28 ± 0.65 L, p < 0.001), and altered FEV1/FVC ratio (104.64 ± 4.22 vs 86.80 ± 6.40% predicted, p < 0.01). Within the stroke group, despite differences in functional limitations between ischemic and hemorrhagic stroke types, no significant differences were found between stroke mechanisms in respiratory or diaphragmatic variables (p > 0.05). However, significant contralateral impairments were consistently observed compared to the ipsilateral side: reduced diaphragmatic thickness at rest (-0.11 cm, p < 0.001, Cohen's d = 0.58) and maximum inspiration (-0.14 cm, p < 0.001, d = 0.77), decreased thickening fraction (-10.12%, p = 0.004, d = 0.51), and limited excursion at rest (-0.64 cm, p < 0.001, d = 0.85) and maximum inspiration (-2.07 cm, p < 0.001, d = 0.72). Interestingly, the ipsilateral hemidiaphragm showed preserved function similar to healthy controls across most parameters.

Conclusions: Hemispheric stroke lesions significantly impair contralateral diaphragmatic function regardless of stroke type, with moderate to large effect sizes indicating substantial clinical relevance. The ipsilateral hemidiaphragm maintains near-normal function, suggesting effective compensation mechanisms. These findings support the neuroanatomical basis of crossed cortico-diaphragmatic control pathways and highlight the importance of targeted respiratory assessment and rehabilitation focusing on the affected hemidiaphragm in stroke patients.