Respiratory complications are the leading cause of death during the initial year after acute
SCI, and the third leading cause of death thereafter. Complete or partial loss of respiratory
muscle innervations in individuals with cervical and high thoracic injuries leads to
inadequate ventilation and inability to effectively clear secretions, often prompting
supportive ventilation following initial injury. Development of atelactasis, pneumonias and
respiratory failure are the most common respiratory complications observed during the acute
phase of injury. It is well known that a restrictive ventilatory defect, dependent upon the
level and completeness of injury, is apparent in individuals with chronic cervical SCI.
Respiratory functional impairment might be further compromised in these individuals, the
majority of whom share many aspects of obstructive airway physiology commonly associated with
asthma. The asthma-like features that individuals with chronic cervical SCI demonstrate have
been hypothesized to be due to overriding cholinergic airway tone carried by intact vagal
(parasympathetic) nerve fibers arising from the brainstem, whereas sympathetic innervations
is interrupted at the level of the upper thoracic spinal cord. Whether airway narrowing and
AHR in chronic cervical SCI is also related to chronic airway inflammation is unknown,
although it is conceivable that repeated respiratory infections or, possibly, a neurogenic
component, could contribute to chronic airway inflammation.
Therefore, the investigators aim to assess how long-acting bronchodilator (tiotropium
bromide) affects various indices of lung function, including: pulmonary function tests,
levels of inflammation and cough strength across 24 hours after receiving study drug. Results
will be analyzed for baseline, 1 hour, 3 hours, 20 hours and 24 hours post drug inhalation
for both active medication and non-active placebo.