Problem:
A key role of the central nervous system is to provide for homeostasis,
or a stable internal milieu. One of the most profound challenges to
homeostasis occurs when a human or other animal moves or changes
posture. In particular, some movements, such as standing in humans or
nose-up body pitch in quadrupeds, can threaten the maintenance of
stable blood pressure and blood oxygenation. Unless compensation takes
place quickly, these movements produce (1) blood pooling in the lower
body that results in orthostatic hypotension and (2) a change in the
resting length of the respiratory muscles that results in decreased air
flow through the lungs. Many body sensors, including arterial
baroreceptors, receptors in the heart, receptors in limb veins,
receptors in the lungs, stretch receptors in respiratory muscles, and
central and peripheral chemoreceptors, detect disturbances in
homeostasis and trigger appropriate compensatory responses. However,
effective maintenance of homeostasis would seem to require that
compensation for the effects of movement on circulation and respiration
begin even before the internal environment has been affected. One
mechanism for accomplishing this would be through the actions of the
vestibular system, which detects head position and head movements, and
could thus provide "feed-forward" information to the brainstem
autonomic centers, resulting in corrections in blood pressure and
ventilation during changes in body position. The major research in our
laboratory looks at the role of the vestibular system in adjusting
blood pressure and respiration during movement and changes in posture.
We are also determining the neural pathways through which vestibular
signals influence the sympathetic nervous system (which controls blood
pressure) and respiratory motoneurons. Finally, we are interested in
determining which neural pathways are responsible for producing an
aberrant autonomic effect that can result from vestibular stimulation:
motion sickness.
Techniques:
This research involves many different techniques. In looking at the
physiological role of vestibular influences on respiration and
circulation, our research makes use of recordings of blood pressure,
blood flow, blood catecholamine levels, activity of sympathetic and
respiratory nerves, and activity of respiratory muscles. When
determining the neural pathways that are responsible for mediating
vestibular influences on respiration and circulation and for producing
motion sickness, we use conventional and transneuronal neuroanatomical
techniques as well as single-unit in vivo recordings. Our laboratory
has a unique complement of devices for producing natural vestibular
stimulation in 3 dimensions, which allows for sophisticated studies of
vestibular processing.
Our facilities permit studies on a variety of animal species, and allow the use of anesthetized, decerebrate and chronic preparations.
Significance:
This research has a number of important practical implications. The
fact that vestibular stimulation has autonomic effects is of relevance
to all vestibular researchers. Autonomic effects of vestibular
stimulation, or changes in autonomic functioning resulting from
vestibular lesions, can indirectly have effects on other vestibular
reflexes. For example, fluid loss associated with vestibular-induced
emesis or orthostatic hypotension resulting from vestibular lesions
could result in lightheadedness during rapid and unexpected changes in
posture. This lightheadedness could indirectly have effects of
vestibulo-spinal and vestibulo-ocular reflexes. Furthermore, motion
sickness and dysfunction in vestibular autonomic regulation can result
in distress and reduced attention to environmental stimuli, and thereby
alter other vestibular reflexes.
Connections between the vestibular system and brainstem autonomic centers can also be important in clinical medicine. As discussed above, vestibular lesions can increase the susceptibility for orthostatic hypotension and may decrease the ability to rapidly adjust respiration during movement. Neuroanatomical studies showing direct connections between the vestibular nuclei, the locus coeruleus, and brainstem pathways that process visceral sensory information also provide a potential neural substrate for the autonomic and affective signs and symptoms often associated with vestibular dysfunction. Clinical studies have shown a close linkage between generalized anxiety, panic disorder, agoraphobia and vestibular dysfunction. Common to patients with panic disorder and agoraphobia are heightened sensations of discomfort with motion and with changes in body position in space. Thus, alterations in vestibular functioning may contribute to some psychiatric disorders.
Vestibular autonomic regulation also has important implications for the space life sciences. Substantial data already indicate that vestibular-autonomic pathways are at least partially responsible for space motion sickness, and plastic changes in the vestibular system during space flight also may be partially responsible for postflight orthostatic intolerance. Other physiological problems experienced by astronauts, including sleep disturbances, could additionally be linked with microgravity-related changes in the vestibular system. Further research is required to determine the relationship between changes in vestibular functioning and alterations in a number of physiological processes during and subsequent to spaceflight.
With the longer duration space flights planned for the future, including the International Space Station assignments of 90-180 days and missions to Mars, which may require three years, vestibular-autonomic disturbances may become of even greater significance to NASA. A Mars mission will be further complicated by the requirement for crew members to egress in the partial-gravity environment of Mars without assistance after a flight of many months. Thus, it is imperative that we better understand the implications of changes in vestibular autonomic regulation during space flight, and that we develop countermeasures to prevent or compensate for these changes.