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NYSTAGMUS
Normally with the head at rest, in the neutral position the resting discharges in the two
vestibular nerve are equal. Vestibulomotor (vestibuloocular and vestibulospinal) reflexes are
elicited when inputs from the two vestibular organs or their central projection are made equal,
that is, they are unbalanced. Such unbalancing can occur by an abnormally involving one side
to a greater degree than the other. In this case we term the resultant vestibular reflex –
spontaneous. Vestibular input from 2 sides can also be unbalanced by stimulating 1 or both of
the vestibular organs. When a vestibular input imbalance is large or prolonged a constellation
of stereotyped responses occurs. These responses are as follow: head turning, falling,
swaying, vertigo, past pointing and nystagmus.
Nystagmus involves a rhythmic back and forth eye movement with slow phase in one
direction and fast phase in the opposite direction. Nystagmus is named by the direction of fast
phase of nystagmus because this movement can be easily observed. . Nystagmus is called leftbeating when fast phase is left-directed and right- beating when fast phase is right-directed.
The head turning, falling, past pointing and nystagmus slow phase are in the same direction,
that is, away from the ear with the greater output.
Vestibular responses can be generates by rotational or caloric stimulation of the vestibular
organ. Vestibular nystagmus occurs when the semicircular duct system is overstimulated. For
example if the head is continuously rotated in one direction, whereby the semicircular duct initiated compensatory eye movement, becomes a rotational nystagmus. Because slow
compensatory eye movement phase of the nystagmus comes from the semicircular duct
system it is called the vestibular or slow phase of the nystagmus. Conversely, because the fast
back eye movement comes from the brain, it is called the central or fast phase of the
nystagmus. Postrotational nystagmus is directed to the opposite side compared to rotational
nystagmus. After stopping the semicircular canal on the opposite side is stimulated.
Rotatory nystagmus.
Rotatory movement of the head to the left generates an ampullopetal movement of endolymph
in the left labyrinth. It will result in stimulation of the hair cells in the crista of the left
horizontal semicircular canal and inhibition of the hair cells in the right horizontal
semicircular canal.
Head movement to the right generates endolymph movement to the left in the right duct. This
is toward the ampulla and therefore increases the right vestibular nerve discharge rate. The
increased vestibular nerve output causes eyes deviation away from the side stimulated, that is,
to the left, which is opposite to the direction of head movement. Head movement to the right
generates also ampullofugal movement in the left duct, which decreases neural activity of the
left vestibular nerve.
Stimulation of the hair cells in the right horizontal semicircular canal will result in an increase
in the number of action potentials in the right vestibular nerve which causes increased firing
of cells in the right vestibular nuclei, an increase in firing of neurons in the left PPRF
(Paramedian pontine reticular formation), an increase in firing of both small and large neurons
in the left abducens nucleus and reflex results in the movement of the left eye to the left (via
left lateral rectus; C.N. VI) and the right eye to the left (via ascending MLF input to the right
medial rectus; C.N. III). This is called the VESTIBULO-OCULAR REFLEX (VOR), which
is a critically important reflex for stabilizing visual images in the presence of a continuously
moving head. It is named (i.e., right beating or left beating) by the direction of fast (rapid)
phase.
The results of a lesion in the LEFT vestibular nerve on eye movements.
Lesion in the left vestibular nerve (or labirynth) puts the right (intact) vestibular nerve in
“control.” This imbalance results in the eyes being pushed slowly to the left (right vestibular
nerve turns on right vestibular nuclei, which turns on the left PPRF, which turns on the left
abducens, which turns both eyes to the left). When the eyes are pushed as far left as possible,
they move back very quickly to the right by mechanisms not fully understood. The eyes then
slowly move to the left again, and this vicious cycle continues. Lesion of the left vestibular
nerve will result in a right nystagmus.
The results of a lesion in the LEFT vestibular nerve on vestibulospinal reflex.
Lesions involving the vestibular nerve, nuclei, and descending pathways will result in
problems such as stumbling or falling towards the side of the lesion. Think of the normal side
as being in control and pushing against the weak side. For example, if you have a patient with
a lesion that has destroyed the left labyrinth, the left vestibular nerve, the left vestibular nuclei
and the left lateral vestibulospinal tract are “tuned” down. Meanwhile, the normal right nerve
is fine and firing away and thus the right lateral vestibulospinal tract is also in good shape.
The two lateral vestibulospinal tracts usually counteract each other functionally, but now the
right side takes over. Falling to the weak side, in this case to the left. The increased activity in
the right vestibular nuclei can affect the body musculature via the right lateral vestibulospinal
tract. This will result in increased activity in the right arm and leg. The cells of origin of the
lateral vestibulospinal tract lie in the lateral vestibular nucleus. Axons arising from this
nucleus descend through the caudal brain stem and upon reaching the spinal cord course
within the ventral funiculus and innervate neurons for the entire length of the cord. This
projection is uncrossed. Through this tract, the vestibular apparatus influences on those
muscles that restore and maintain upright posture (trunk extensors and proximal extensors of
arm
and
leg).
Caloric nystagmus.
COWS – The Cold stimulus causes nystagmus to the Opposite direction. The Warm stimulus
causes nystagmus to the Same direction.
If a subject tilts his or her head back (so that the horizontal canals are oriented vertically), and
one ear is irrigated with either warm or cold water, nystagmus will result due to movement of
endolymph in semicircular canals. Caloric nystagmus is produced by a temperature change in
the vestibular apparatus. In the clinical laboratory, the temperature change is usually produced
by irrigation of the external auditory canal by warm or cold water. The temperature change is
conducted through bone to semicircular canals. The warm caloric irrigation heats endolymph.
This warm endolymph become less denser and thus flow up toward the utricle causing the
depolarization of hair cells in irrigated ear. In result the eyes rotate (slow phase) to the
opposite ear (vestibuloocular reflex). The cold caloric irrigation cools the endolymph in
horizontal duct. This cold endolymph become slightly denser and thus falls, causing the
hiperpolarization of hair cells in the labirynth of the irrigated ear, thereby the opposite
labirynth is overstimulated (resting discharge). In result the eyes rotate toward (slow phase)
the irrigated ear.
For instance, irrigation of the right ear with warm water will turn on the receptors in the right
horizontal canal (because the endolymph flows towards the ampulla and hair cells are
depolarizated). Thereby the eyes will go slowly to the left and then move back to the right (a
right nystagmus; warm =nystagmus same side). Irrigation of the right ear with cold water
would give the opposite results.
Figure 49 (below) is draw to reflect the fact that increased neural activity from a horizontal
semicircular duct rotates the eyes horizontally away from the duct.
Optokinetic reflex (OKR)
OKR is driven by visual signals, which are processed much more slowly than vestibular
signals. The OKR is more effective for slow rotations that continue over many seconds, but is
much less effective for very fast rotations.
The visual stimulus for posture control is derived from optic flow of the retinal image. The
retina contains diretion – selective ganglion cells that respond exclusively to motion in certain
directions. This information passes along the optic nerve, decussates at the chiasm and goes
to the cortex via the geniculate body (LGN) or to the midbrain via the accessory optic
tract. This tract has several nuclei in the pretectum. One pair of these nuclei, the nucleus of
the optic tract (NOT), is tuned to horizontal target motion. The lateral terminal nuclei (LTN)
are tuned for vertical OKN.
Neurons in these nuclei have large receptive fields and respond
to large textured stimuli moving in specific directions. Stimulation of the right NOT with
rightward motion causes following movements of the eyes to the right or ipsilateral side, and
similarly stimulation of the left NOT with leftward motion causes leftward following
movements. Neurons in the pretectum and accessory optic nuclei project to the vestibular
nuclei, where these visual signals join the same final pathways used by the VOR.
Schematic diagram depicting optokinetic pathways. Cortical input to temporally directed
movement, which is present only in frontal-eyed animals, requires the establishment of
normal binocular cortical connections. Direct crossed pathways from the eye to the nucleus of
the optic tract provide subcortical optokinetic responses even when binocular cortical
connections are absent (R and L represent monocularcortical cells corresponding to the right
and left eyes, respectively). Note that the nucleus of the optic tract (NOT) relays horizontal
visuo-vestibular information to the vestibular nucleus (VN), where it is integrated with
horizontal vestibular input from the labyrinths to establish horizontal extraocular muscle
tonus. LGN - lateral geniculate nucleus;
CC - corpus callosum;
V1 - abducens nucleus;
III - oculomotor nucleus;
LR - lateral rectus muscle;
MR -medial rectus muscle;
AC - anterior canal;
PC - posterior canal;
HC – horizontal canal.