During an asthma attack, inflammation, increased mucus secretion, and smooth muscle spasm constrict airways in the lungs. These are automatic actions in response to a stimulus. This stimulus can vary, but may be increased dopamine, cortisol and adrenaline levels resulting from heightened stress, or something as simple as dust or smoke.
Just for simplicity, we’ll leave stress to one side for a moment.
Stimuli, such as dust, are detected by nerves within the posterior pulmonary plexus (a group of nerves in the lungs). This information is then relayed to the thoracic sympathetic chain (another collection of nerves), which then communicates with the spinal cord.
The levels of the spinal cord receiving this input are in the upper thoracic spine (T1-5). The spinal cord then relays this information to the brain, which stimulates increased mucus production, bronchial spasm etc, via the vagus nerve.
Fig 2. Diagram showing the relationship between the spinal cord, viscera, and sympathetic chain.
Crucially, in normal cases, the nerves in the pulmonary plexus only activate when stimulation is great enough to represent a threat. This is controlled by a neurological mechanism called “threshold”, whereby a certain degree of stimulation is required before a message (called an action potential) can sent.
Inadequate stimulation means no message is sent, and this is termed a failed initiation. A series of failed initiations have the effect of sensitising a nerve, meaning that less future stimulation is needed to generate an action potential. This is known as sensitisation and means normal stimuli can activate a nerve. In the case of asthma patients, an example could be cold air triggering bronchial constriction.