Twenty Nine Flashcards
What are the two functions of the vestibular system? What are the chief connections of the vestibular system? What may abnormal stimulation of the vestibular system result in?
The two chief functions of the vestibular system are to keep the head and body lined up
on an even keel and to keep the eyes fixed on a target when the head is moving. In other
words, the vestibular system is intimately involved in mechanisms that maintain
equilibrium and visual fixation. Vestibular system connections are made chiefly with
spinal motoneurons and ocular motor neurons, although extensive connections also exist
with the cerebellum and the brainstem reticular formation. Ordinarily, the vestibular
system functions subconsciously but abnormal vestibular stimulation may reach
conscious levels in the form of vertigo (dizziness).
What 3 things keep the maintain the balance of the body? How many are needed to accomplish balance? How is this tested?
Input from three sources plays a role in maintaining balance: the eyes which provide
awareness of surroundings; the muscles of the neck, back, and limbs which provide
awareness of body position; and, last but not least, the vestibular receptors in the internal
ear that respond to changes in the position of the head. Balance can be maintained with
any two of these inputs, but not with only one. Thus, an individual with tabes dorsalis,
degeneration of the dorsal columns of the spinal cord, while standing and closing the
eyes, will lose balance and sway and fall. This is the Romberg sign and occurs because
two of the inputs for balance have been lost (proprioception and vision) and now only
vestibular remains.
What are the vestibular receptors for balance? Where are they located? Where do they synapse? Where do these neurons synapse and what movements do they influence?
The vestibular receptors for balance are in the maculae of the utricle and saccule.
The maculae are static receptors and by monitoring the position of the head they trigger
the mechanisms that control balance. They exert their influence via the vestibular nerve
and its connections with the inferior, lateral, and medial vestibular nuclei.
The lateral, medial, and inferior vestibular nuclei influence the spinal motor nuclei via
the lateral and medial vestibulospinal tracts (Fig. 1). The lateral vestibulospinal tract
has a very strong influence on extensor movements in the ipsilateral limbs. The medial
vestibulospinal fibers descend bilaterally and influence movements of the head and neck.
What is the vestibulo-ocular reflex? What does it result in? What is the pathway like including the location of the neurons and the axons in the pathway?
Rotation of the head in any direction results in reflex turning of the eyes in the opposite direction.
The anatomical substrate for this phenomenon is the very strong vestibulo-ocular reflex (VOR) which includes three groups of neurons: 1) afferent neurons in the vestibular
ganglion, 2) interneurons in the vestibular nuclei, and 3) efferent or lower motor neurons in the oculomotor, trochlear, and abducens nuclei (Fig. 2).
The afferent neurons in the vestibular ganglion are bipolar cells. Their peripheral branches innervate the ampullary crests, vestibular receptors in the semicircular ducts
that are stimulated by rotary movements of the head. The central branches or axons of
the vestibular ganglion cells reach the brainstem in the vestibular nerve and synapse in
the superior and medial vestibular nuclei. These two nuclei project chiefly via the
medial longitudinal fasciculus (MLF) to the alpha motoneurons of cranial nerves III, IV,
and VI in such an organized manner that the eyes will always turn directly opposite to the
direction of the head rotation.
What is nystagmus? How is it named? How can it be induced? What happens when it’s induced? What does this induction initiate? What causes slow movements? Fast movements? Which side nystagmus will cold induce? Warm?
Nystagmus refers to involuntary rhythmic movements of the eyes that include two
components: a slow drifting away from the target and a fast return to the target.
Nystagmus is described according to the fast phase since it is much more obvious than
the slow phase. Nystagmus can be induced by stimulating the vestibular apparatus either
by rotation (vestibular or rotatory nystagmus) or by placing cold or warm water in the ear
(caloric nystagmus). Both methods induce currents in the endolymphatic fluid in the
semicircular ducts, the rotation because of the fluid inertia and the thermal because of
convection currents. Both stimulate the hair cells of the ampullary crests and initiate the
powerful vestibulo-ocular reflex. The slow phases of the vestibular and caloric
nystagmus are caused by this vestibulo-ocular reflex, whereas the fast phases are
triggered by the cerebral cortex. In the case of caloric nystagmus, cold induces the fast
phase of the nystagmus to the opposite side, warm to the same side (COWS).
How is the vestibulocular reflex used to test levels of brain stem damage in comatose patients?
Clinical use of the vestibulo-ocular reflex to assess levels of brainstem damage in a
comatose patient is common. When such a patient’s head is briskly turned to one side or
the other, or is tilted up or down, the eyes turn in the opposite direction. This
phenomenon, referred to as the oculocephalic reflex or Doll’s eye movements, is
indicative of an intact pathway subserving the vestibulo-ocular reflex. Normally these
reflex movements are suppressed by the cerebral cortex. In the comatose patient,
however, the reflex is disinhibited and its presence shows that the central parts of the
tegmentum of the midbrain and rostral pons are intact.
Likewise, such eye movements can be induced in comatose patients by irrigating the
external auditory canal with warm or cold water. With cold water both eyes turn toward the side irrigated, while with warm water they turn toward the opposite side. These movements are also manifestations of the vestibulo-ocular reflex and are comparable to the slow phase of the nystagmus induced by caloric stimulation in normal individuals.
In comatose patients, what will be the results of these tests if the whole brain stem is intact? If the Medial Longitudinal fasciculus is damaged somehwere between cranial nerves 6 and 3/4 (caudal pons and midbrain)? If the brainstem if damaged below the caudal pons (CNVI)?
If its all intact, the oculomotor reflex will be completely intact (both eyes respond)—>decorticate, arm flexing due to red nuclei. If its in the MLF, eyes will only move laterally (CNVI). If its below CNVI, there will be no response—>decerebate, all extension.
What connections exist between the vestibular system and the cerebellum? Where do vestibular signals to the cerebellum and originate and end and vice versa.
As described in the chapter on the cerebellum, direct and indirect connections exist
between the vestibular system and the cerebellum. Direct connections are made via the
vestibular nerve, while indirect connections are made through the vestibular nuclei. Both
types of connections enter the cerebellum through the juxtarestiform body, the medial
part of the inferior cerebellar peduncle, and pass chiefly to the flocculonodular lobe and
adjacent parts of the vermis. Collateral branches from the vestibulocerebellar fibers
terminate in the fastigial nuclei. The flocculonodular lobe coordinates the muscular
activity associated with equilibrium and eye movements through the fastigial nuclei
which project chiefly to the vestibular nuclei.
What are some connects between the vestibular nuclei and the brainstem reticular formation?
The vestibular nuclei have widespread connections with motor and autonomic centers in
the brainstem reticular formation. Paths from the vestibular nuclei ascend and descend to
various pontine reticular and medullary reticular nuclei that influence motor neurons in
the brainstem and spinal cord. Likewise, vestibuloreticular connections are made with
autonomic centers such as the vomiting center in the medulla. This connection accounts
for the nausea and vomiting associated with motion sickness.