Bronchial Hyperresponsiveness After Cervical Spinal Cord Injury

May-26-2014

Bronchial Hyperresponsiveness After Cervical Spinal Cord InjuryThe degree of pulmonary dysfunction following spinal cord injury is dependent upon the level of injury sustained. Lesions above the third cervical segment result in complete paralysis of all muscles of respiration and therefore necessitate mechanical ventilation, whereas lesions at lower cervical levels will, to varying extents, spare the major muscles of inspiration, ie, the diaphragm (C3-5), scalene muscles (C4-8), and intercostal muscles (Tl-12). The expiratory muscles receive their innervation from the first thoracic segment and below. Hence, transection of the cervical spinal cord (quadriplegia) renders expiratory function severely compromised. As a result, inability to clear secretions, mucous plugging, atelectasis, and respiratory infections are common pulmonary complications in this patient population.
Traumatic injury to the spinal cord causes a restrictive ventilatory impairment, the severity of which parallels the level of injury. Spirometry and measurement of static lung volumes have demonstrated reductions in vital capacity, inspiratory capacity, and expiratory reserve volume, as well as elevated residual volume. Measures of airflow, including the FEVi and mean forced expiratory flow during the middle half of the forced vital capacity (FVC), are also reduced. Because flow rates were believed to be decreased in proportion to the reduction in vital capacity in subjects with spinal cord injury, the presence of an obstructive component of respiratory dysfunction in this population was not suggested by previous investigators.” mycanadianpharmacy

Transection of the cervical spine interrupts the sympathetic innervation of the lungs, which originates from the upper six thoracic ganglia. However, the parasympathetic nerve supply, arising in the vagal nuclei of the brainstem, from which efferent cholinergic nerves pass down the vagus nerve to synapse in ganglia within the airway wall, remains intact. Such unopposed cholinergic tone might be expected to cause enhanced bronchial responsiveness. To investigate the effect of such altered innervation on airway reactivity, we performed bronchial challenge testing with inhaled methacholine in subjects with chronic cervical spinal cord lesions. In addition, we examined the effect of inhaled ipratropium bromide, a blocker of airway muscarinic receptors, on bronchial responsiveness to methacholine.