Numerous stretch receptors within smooth muscle cells of the airways also project via the vagus nerves to the NTS and influence the depth and duration of breathing. Afferent signals from these specialized nerve endings mediate the Hering-Breuer reflex, described in 1868—a shortened inspiration and decreased tidal volume triggered by excessive lung expansion. The Hering-Breuer mechanism seems not to be important at rest, as bilateral vagal section has no effect on the rate or depth of respiration. These aspects of afferent pulmonary modulation of breathing have been reviewed by Berger and colleagues. It is interesting, however, that patients with high spinal transections and inability to breathe can still sense changes in lung volume, attesting to a nonspinal afferent route to the brainstem from lung receptors, probably through the vagus nerves. In addition, there are receptors located between pulmonary epithelial cells that respond to irritants such as histamine and smoke. They have been implicated in the genesis of asthma. There are also “J-type” receptors in the lung interstitium that are activated by substances in the interstitial fluid of the lungs. These are capable of inducing hyperpnea and probably play a role in driving ventilation under conditions such as pulmonary edema.
Both the diaphragm and the accessory muscles of respiration contain conventional spindle receptors, but their role is not clear; all that can be said is that the diaphragm has a paucity of these receptors compared with other skeletal muscles (a property shared with extraocular muscles) and is therefore not subject to spasticity with corticospinal lesions or to the loss of tone in states such as REM sleep, in which gamma motor neuron activity is greatly diminished.
The common respiratory sensations of breathlessness, air hunger, chest tightness, or shortness of breath, all of which are subsumed under the term dyspnea, have defied neurophysiologic interpretation. In animals, Chen and colleagues from Eldridge’s laboratory have demonstrated that neurons in the thalamus and central midbrain tegmentum discharge in a graduated manner as respiratory drive is increased. These neurons are influenced greatly by afferent information from the chest wall, lung, and chemoreceptors and are postulated to be the thalamic representation of sensation from the thorax that is perceived at a cortical level as dyspnea. However, functional imaging studies indicate that various areas of the cerebrum are activated by dyspnea, mainly the insula and limbic regions.
Many of the most interesting respiratory patterns observed in neurologic disease are found in comatose patients, and several of these patterns have been assigned localizing value, some of uncertain validity: central neurogenic hyperventilation, apneusis, and ataxic breathing. These are discussed in relation to the clinical signs of coma (see
Chap. 16) and sleep apnea (see Chap. 18). Some of the most bizarre cadences of breathing—those in which unwanted breaths intrude on speech or those characterized by incoordination of laryngeal closure, diaphragmatic movement, or swallowing or by respiratory tics—have occurred in paraneoplastic brainstem encephalitis. Similar incoordinated patterns occur in certain extrapyramidal diseases. Patterns such as episodic tachypnea up to 100 breaths per minute and loss of voluntary control of breathing were, in the past, noteworthy features of postencephalitic parkinsonism.
In Leeuwenhoek’s disease, named for the discoverer of the microscope who described and was afflicted with the problem, there is an almost continuous epigastric pulsation and dyspnea in association with rhythmic bursts of activity in the inspiratory muscles—a respiratory myoclonus akin to palatal myoclonus (Phillips and Eldridge). Two such cases in our clinical material followed influenza-like illnesses and resolved slowly over months. Another patient with similar movements intermittently causing gasping sounds gave us the impression of having a psychogenic disease.