Many conditions can induce ventilation asymmetry, including pulmonary disorders responsible for side-to-side differences in lung size and/or mechanical properties, such as lobectomy, local fibrosis, atelectasis, and unilateral emphysema. Ventilation may also be asymmetric when the two lungs are subjected to different pleural pressures because of extrapulmonary factors, such as pleural effusion, or of parietal anomalies, such as scoliosis. Hemidiaphragmatic contraction usually results in expansion of the lower rib cage, both via the direct effect of the muscle insertions with the abdominal contents serving as a fulcrum and via expansion of the abdomen due to the caudal motion of the hemidiaphragm.33 Paralysis of the hemidiaphragm impairs these mechanisms, causing asymmetry of rib cage expansion. However, because the mediastinum is mobile between the two hemithoraces, there is no simple correlation between chest expansion asymmetry and lung inflation asymmetry. To elucidate the interactions between the lungs and chest wall under normal and pathologic conditions, Loring et al34 and Lin et al35 developed a model consisting of two lungs, which could have different properties, enclosed in a chest wall and separated by a compliant mediastinum. They evaluated situations of asymmetric lung injury with symmetrical chest-wall expansion.35 Because the mediastinum between the hemithoraces was compliant, it was displaced by pressure differences between the two sides, allowing transmission of these pressures. Thus, inflation of one lung tended to increase the contralateral pleural pressure, limiting inflation of the other lung and promoting asymmetric lung expansion, whereas chest-wall expansion remained symmetrical. Consistent with this model, a study in which De Groote et al32 used OEP and CT scanning in patients with single-lung transplantation for emphysema showed asymmetric ventilation between the two lungs with symmetrical volume changes of the two hemithoraces. To our knowledge, no study has explored the volume changes of the two hemithoraces in situations of asymmetric lung injury with decreased compliance of one lung, such as lobectomy, unilateral fibrosis, or atelectasis. We, therefore, do not know if, contrary to the condition of unilateral emphysema, asymmetric ventilation is associated with asymmetric rib cage motion. The result of asymmetric ventilation probably depends on the severity of the disease and, therefore, on the mechanical properties of the different components of the model developed by Lin et al.35 Situations characterized by major modifications in local lung compliance, such as severe atelectasis, can probably result in asymmetric chest-wall expansion. However, in such situations standard investigations readily exclude unilateral diaphragmatic weakness as the cause of the asymmetry. Another limitation to the usefulness of OEP is mediastinal stiffness due, for instance, to radiotherapy or heart surgery. In this case, a less severe asymmetric lung injury may result in detectable chest-wall motion asymmetry due to insufficient mediastinal displacement during breathing. Therefore, in these situations, chest-wall motion asymmetry might lack specificity for the diagnosis of hemidiaphragmatic weakness. Nevertheless, because the mediastinum has at least some degree of mobility between the two hemithoraces, at a given degree of ventilation asymmetry, the chest-wall motion asymmetry should be greater than the ventilation asymmetry when the underlying cause is hemidiaphragmatic weakness and less than the ventilation asymmetry when the underlying cause is asymmetric lung injury.