VESTIBULAR NUCLEI AND ABDUCENS NUCLEUS
You are probably wondering why we suddenly have TWO nuclei under ONE point. Well, over the years Ive learned that it is much easier to cover them both at the same time because of their close functional association in the control of eye movements. This is a very long and tough point, but hang in there!
There are four vestibular nuclei within the brain stem (superior, lateral, medial, and inferior). All four can not be seen in the same cross section, since they are present for a considerable rostrocaudal distance from the rostral medulla to the middle of the pons. You only have to be able to identify the MEDIAL and INFERIOR vestibular nuclei, both of which are present at level #4 (shown below on the left).
The vestibular nuclei receive their primary input from the vestibular portion of C.N. VIII (vestibular-auditory). The axons in the vestibular nerve are the central processes of neurons that lie in the vestibular or Scarpas ganglion which lies in the internal auditory meatus. These central processes terminate in the vestibular nuclei and the cerebellum. The peripheral processes of these cells receive information from the receptors of the vestibular labyrinth, i.e. hair cells located in the semicircular canals and the saccule and the utricle (otolith organs).
The three (on each side) membranous semicircular canals lie within the bony labyrinth and contain endolymph. As shown in two of the drawings below, the canals, one horizontal and two vertical, lie in three planes that are perpendicular to each other. The HORIZONTAL or lateral canals on the two sides lie in the same plane, while the plane of each anterior canal is parallel to that of the posterior canal of the opposite side. The horizontal semicircular canals communicate at both ends with the utricle, which is a large dilation of the membranous labyrinth. The vertical canals (anterior and posterior) communicate with the utricle at one end, and join together at the other end (the common canal communicates with the utricle).
At one end of each semicircular canal is a dilation called the ampulla (L., little jar, is labeled amp in the upper right drawing below). The ampulla of a horizontal semicircular canal has been enlarged in the drawing below (upper left). Each ampulla contains a crista (crista ampullaris; ridge), which is a transversely oriented ridge of tissue. The upper surface of the crista contains ciliated sensory hair cells that are embedded in a gelatinous material called the cupula (L., little tube). These ciliated sensory hair cells contain vesicles that possess neurotransmitter. When the neurotransmitter is released from the hair cell, the peripheral process of a cell in the vestibular ganglion is turned on. Interestingly, the hair cells release transmitter even when they are not stimulated, so the axons in the vestibular nerve are always firing at a baseline rate.
Each hair cell of the crista possesses several shorter stereocilia and a single tall kinocilium at one margin of the cell as shown in the lower figure. Deflection of the stereocilia TOWARD the kinocilium results in an INCREASE in the firing rate of the vestibular fiber associated with the hair cell, while deflection AWAY from the kinocilium results in a DECREASE in the firing rate of the vestibular fiber.
The kinocilia associated with the hair cells in the horizontal semicircular canal lie on the utricle side of the ampulla. For instance, rotation of the head to the RIGHT will result in stimulation of the hair cells in the crista of the RIGHT horizontal semicircular canal and inhibition of the hair cells in the LEFT horizontal semicircular canal. 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. This is easy, RIGHT HEAD ROTATION-RIGHT HORIZ. SEMICIRC. CANAL-RIGHT VESTIBULAR NERVE-RIGHT VESTIBULAR NUCLEI TURNED ON OR TUNED UP. All of this is in response to ANGULAR ACCELERATION of the head to the RIGHT, the stimulus needed to turn on the hair cells of the RIGHT horizontal semicircular canal.
UTRICLE AND SACCULE
While semicircular canals respond to angular acceleration in specific directions, hair cells in the utricle and saccule respond to linear accelerations. The utricle and saccule are saclike structures that contain a patch of sensory hair cells called the macula (L., spot). The hair cells in the macula, which are similar to those in the cristae, are embedded in the otolith (ear stone) membrane, a gelatinous structure that contains a large number of hexagonal prisms of calcium carbonate called otoconia (ear dust). Since the density of the otoconia is greater than the surrounding endolymph, the otolith membrane will be displaced by the force of gravity or other linear accelerations. Such displacement bends the stereocilia and, depending on the polarity of the cell, either causes an increase or a decrease in the number of impulses in the associated vestibular fiber.
Once vestibular input from the semicircular canals and otolith organs has reached the vestibular nuclei, the information is used to maintain balance and to stabilize the visual image on the retina during head movements. First we will consider only the projections of the vestibular nuclei that reach the spinal cord in order to help us maintain our BALANCE. For example, lets say that you are walking to lecture this morning and slip on the icy sidewalk. Your feet fly to the RIGHT and your upper body and head fly to the LEFT (left ear down). Information coming out of your semicircular canals will be related to the accelerating head. This particular angular acceleration affects several different canals (beyond what you need to know for this course), but what I want you to know is that the LEFT vestibular nuclei are turned on. Once your head is not moving the information will come from the utricles. Again, you do not have to know the specific pattern from each side, but only that the LEFT vestibular nuclei are turned on.
The increased activity in the LEFT vestibular nuclei can affect the body musculature via the LEFT LATERAL VESTIBULOSPINAL TRACT. This will result in increased activity in the LEFT arm and leg in order to right ourselves after slipping. The cells of origin of the lateral vestibulospinal tract lie in the lateral vestibular nucleus (you can not see this nucleus in your sections). Axons arising from this nucleus descend through the caudal brain stem (you dont see these fibers on the cross sections) 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 apparatuswhich detects whether the body is on an even keelexerts its influence on those muscles that restore and maintain upright posture. Such muscles are proximal rather than distal.
REMEMBERLATERAL VESTIBULAR NUC.LATERAL VESTIBULOSPINAL TRACTUNCROSSEDENTIRE LENGTH OF CORDVENTRAL FUNICULUSPROXIMAL MUSCLESMAINTAINS BALANCE BY ACTING MAINLY ON LIMBS
The increased activity in the LEFT vestibular nuclei can also affect body musculature via a second, smaller, descending pathway to the spinal cord. This smaller pathway is called the MEDIAL VESTIBULOSPINAL TRACT (or descending medial longitudinal fasciculus [MLF]). Cells within the medial vestibular nucleus possess axons that descend bilaterally (the ipsilateral projection is denser) in a position just off the midline near the dorsal surface of the pons and medulla. These descending axons course caudally and enter the spinal cord, where they lie within the medial part of the ventral funiculus. This pathway makes connections with cervical and upper thoracic motor neurons that play a role in maintaining the normal position of the head via innervation of spinal cord neurons that innervate neck musculature. Thus when your head flies to the LEFT, it will reflexively be brought to an upright position via information flowing out of the LEFT medial vestibular nucleus. REMEMBERMEDIAL VESTIBULAR NUCLEUSMEDIAL VESTIBULOSPINAL TRACTBILATERALCERVICAL AND UPPER THORACIC SPINAL CORD ONLYMAINTAINS HEAD ERECT.
Now we can do some problem solving. 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 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. The end result? STUMBLING AND FALLING TO THE WEAK SIDE, IN THIS CASE TO THE LEFT.
At the very onset of vestibular problems there may be a Romberg sign. Postural instabilities are kept in check by visual inputs however, closing the eyes with the feet together will reveal the unstable condition.
Imbalance in the vestibulospinal tracts can be demonstrated in healthy medical students. Put a penny on the floor and stand directly over it so that it lies between your feet. Bend your head forward to stare at the penny. While staring at the penny, turn to the RIGHT five complete turns. At the end of the five turns stop and try to stand erect and hold your arms straight ahead. Now, the LEFT vestibular nerve is dominating, so which way do you stumble? Following this spinning exercise, you might also experience some nausea, autonomic disturbances and vertigo (you are spinning, or the room is spinning). In addition, there will be an involuntary to and fro oscillation of the eyes. This is called nystagmus and demonstrates the CONNECTIONS BETWEEN THE VESTIBULAR APPARATUS AND NUCLEI IN THE BRAIN STEM THAT INNERVATE MUSCLES THAT MOVE THE EYES IN THE HORIZONTAL DIRECTION.
We now need to look at the ABDUCENS nucleus. The abducens lies just off the midline within the dorsal part of the pons, just under the fourth ventricle. (Dont let the pons scare you, its pretty easy!) C.N. VI fibers pass ventrally from the abducens nucleus, exit at the pontomedullary junction and eventually reach the lateral rectus (LR6). We will evaluate the effects of lesions involving this nucleus and nerve later in this point, but first we need to talk about how the vestibular system influences horizontal eye movements.
Eye movements induced by the vestibular apparatus are compensatory. That is, they oppose head movements or changes in head position and act to keep the fovea of the retina on an object of interest. For example, a quick turn (or push) of your head to the RIGHT will result in a compensatory reflex turning of the two eyes to the LEFT. You already know some of the receptors and pathways underlying this reflex. Thus a quick rotation of the head to the RIGHT will turn on the hair cells in the RIGHT horizontal semicircular canal, increase the firing of the right vestibular nerve and increase the firing of neurons in the RIGHT vestibular nuclei.
Now for a new pathway! Cells in the RIGHT vestibular nuclei send their axons across the midline to the contralateral PARAMEDIAN PONTINE RETICULAR FORMATION (PPRF). The PPRF, which lies within the medial portion of the pontine tegmentum, ventral to the abducens nucleus, is an integrative region involved in the generation of horizontal eye movements. Neurons in the LEFT PPRF project to the LEFT ABDUCENS nucleus. It contains two types of neurons. The larger motor neurons in this nucleus possess axons that pass ventrally through the pons to exit on the ventral surface of the brain stem (at the pontomedullary junction). Axons of C.N. VI then innervate the ipsilateral LATERAL RECTUS (LR6). There are also other smaller neurons in the abducens nucleus whose axons do not leave the brain stem, but rather CROSS and ASCEND in the medial longitudinal fasciculus (MLF) to terminate in the oculomotor nucleus (C.N. III). Never, I said never, forget the MLF!!! In particular, these crossed axons from the abducens nucleus end only upon those neurons within the oculomotor nucleus that innervate the MEDIAL RECTUS muscle. Remember, neurons in the oculomotor nucleus that innervate other eye muscles, as well as the preganglionic parasympathetic neurons that innervate the ciliary ganglion, do not receive this crossed input from the abducens nucleus. Only those neurons that innervate the medial rectus muscle receive this ascending, crossed input.
Now you can see how a rotatory movement of the head to the RIGHT results in an increase in the discharge of the RIGHT vestibular nerve, an increase in firing of the RIGHT vestibular nuclei, an increase in firing of neurons in the LEFT PPRF, an increase in firing of both small and large neurons in the LEFT abducens nucleus and reflex turning 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.
So; lets examine the results of a lesion in the LEFT vestibular nerve on eye movements. Such a lesion puts the RIGHT 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 snap 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. This nodding back and forth is called NYSTAGMUS (to nod). It is named (i.e., right or left) by the FAST direction. For instance, a lesion of the LEFT vestibular nerve will result in a RIGHT nystagmus. Thus, the RIGHT (intact) vestibular nerve is driving the LEFT PPRF and LEFT ABDUCENS to move the eyes slowly to the LEFT, after which they reflexively snap back to the RIGHT (i.e., the direction of the nystagmus).
Now we need to consider pathways involved in VOLUNTARILY turning both of our eyes horizontally to the LEFT in order to see a new object of interest. This is called a left horizontal saccade (jerk). We already know that to do this we need to have the LEFT lateral rectus and the RIGHT medial rectus contract synchronously. The two eyes will then move together (conjugately) to the LEFT. To VOLUNTARILY do this, we use a pathway that begins in the frontal eye fields of the cerebral cortex (area 8). This is a cortical area that lies rostral to the primary motor area (area 4; where the corticospinal axons begin). To voluntarily move your eyes to the LEFT, information from your RIGHT frontal eye fields is conveyed to the LEFT (contralateral) PPRF. You should know the rest from here, but Ill help! The RIGHT frontal eye field will tell your LEFT PPRF to turn on both large and small neurons in the LEFT abducens nucleus. Two things will then happen. The LEFT eye will turn LEFT (laterally) and the RIGHT eye will turn LEFT (medially). This is a voluntary LEFT horizontal saccade.
A lesion in the RIGHT frontal eye fields will mean that the first part of the circuit involved in voluntarily turning the eyes to the LEFT is fouled up. Therefore immediately after such a lesion in area 8 on the RIGHT, the intact (LEFT) cortex takes over and pushes both eyes to the RIGHT. If the cortical lesion also involves area 4 (which is not too far away from area 8) of the RIGHT cortex, the hemiplegia (due to damage to the corticospinal tract) will be on the LEFT. Thus THE EYES LOOK AWAY FROM THE HEMIPLEGIA (the eyes look at the normal intact extremities). This is especially true when the patient is comatose. Once out of the coma, recovery usually occurs and the patient is able to make saccades into the opposite half field. However, saccades are less frequent in such patients. You should know by now that there is NO atrophy of any eye muscles following a cortical lesion. Also there is NO diplopia (no double vision due to the misalignment of the two eyes; we will cover this later). Remember, the motor neurons in the abducens and oculomotor nuclei are not dead and the eyes are turned conjugately to the right just after the lesion!
Now for a lesion in the PPRF. A lesion of the LEFT PPRF will result in the inability to make a VOLUNTARY saccade that moves the eyes to the LEFT of the midline. There is no atrophy of the lateral rectus or diplopia (no misalignment of the two eyes). Sometimes the eyes will be deviated to the RIGHT due to the unopposed normal circuitry for making RIGHT horizontal saccades. If a lesion in the pons is big enough to also involve the corticospinal fibers on the same side, the deviating eyes will LOOK TOWARDS THE HEMIPLEGIA.
A lesion of the LEFT ABDUCENS NUCLEUS will result in atrophy of the
LEFT LATERAL RECTUS and the inability to turn the LEFT eye laterally. Also, the small cells in the LEFT abducens nucleus are dead, so the ascending input to the RIGHT (contralateral) oculomotor nucleus, and in particular to the neurons innervating the medial rectus, is lost. This results in the inability to turn the RIGHT eye medially when attempting to look to the LEFT. THERE IS NO ATROPHY OF THE RIGHT MEDIAL RECTUS. WHY? BECAUSE THE NEURONS INNERVATING THE RIGHT MEDIAL RECTUS ARE NOT DEAD. THEY HAVE JUST LOST AN INPUT TELLING THEM TO FIRE DURING A LEFT HORIZONTAL SACCADE. They will fire for example during convergence (simultaneous contraction of both medial recti). In such a case the neurons in the right medial rectus receive an input from a convergence center located rostral to the oculomotor complex. The left lateral rectus has atrophied and the neurons innervating the right medial rectus have only lost an input. Thus the left eye will deviate further to the right then the right eye. Thus to ameliorate double vision the patient will rotate their head to the left (toward the abducens nucleus lesion).
What about a lesion of the ABDUCENS NERVE? Lets examine the results of a lesion of the LEFT C.N. VI (for instance in the cavernous sinus). Such a lesion will result in atrophy of the LEFT lateral rectus muscle. Due to the unopposed action of the LEFT medial rectus, the LEFT eye will be deviated MEDIALLY. This will result in double vision, since the two eyes are not aligned (the fovea are not looking at the same point in space). There is further information regarding diplopia on the next page.
(Gr., diplous=double + ope=sight)
When looking at an object (such as your finger, as in the drawing below), its image falls upon the fovea of both retinae. The fovea lies at the posterior pole of the retina and is the part of the retina where visual acuity is greatest. Misalignment of the visual axes causes the image to fall on non-corresponding areas of the two retinae and two images are seen instead of one. For instance, hold your RIGHT finger out in front of you and place your LEFT index finger upon your LEFT lateral canthus (see drawing below). Press gently with your LEFT finger and you should obtain diplopia. If the pushing deviates your LEFT eye medially, (as in a lesion of the LEFT LR) you will see the false image to the LEFT of the true image. You will notice that the false image moves, and is not as clear as the true image. Also, you will notice that the further you move your RIGHT finger to the LEFT (towards the bad eye in the case of a LEFT LR lesion) the greater the separation of the two images. This is called horizontal diplopia. Vertical diplopia in which the images are separated in the vertical (up and down) axis.
You know that following a lesion of the LEFT lateral rectus the LEFT eye will be deviated medially or to the RIGHT. As a way of avoiding the diplopia (which is greatest on LEFT gaze), the patient will turn their head TOWARD the side of the paralyzed muscle (LEFT in this example). This alleviates the double vision.
A lesion in the RIGHT MLF involving the ascending axons of the neurons in the LEFT abducens will result in the inability to turn the RIGHT eye medially when attempting to look to the LEFT. This is called INTERNUCLEAR OPHTHALMOPLEGIA (INO; between the nuclei [6+3], paralysis of eye muscles). Because the RIGHT medial rectus has lost its drive (from the LEFT abducens) the RIGHT eye will deviate a little to the RIGHT when looking straight ahead and there will be diplopia. Turning the head to the left will ameliorate the diplopia. A final interesting finding in INO is that following a lesion of the (for example) right MLF, when the patient attempts to look left, the left eye will exhibit nystagmus. There are several hypotheses regarding this condition, but we will not delve into them at this time. Think about why this might happen.
We can produce nystagmus in people with normal vestibular circuitry. For example, you can elicit vestibular nystagmus by seating a subject in a darkened room (it is dark so the patient cannot fixate on objects to reduce the nystagmus, like a figure skater), and rotating him/her in one direction. For example, if you rotate the subject to the RIGHT, the eyes will move to the LEFT and snap back to the RIGHT (a RIGHT NYSTAGMUS). Motion to the RIGHT turns on the hair cells in the RIGHT horizontal semicircular canal and I know you can take it from here! Realize that when the subject spins to the RIGHT, he/she will initially have a RIGHT nystagmus, but after rotation at a constant speed for a while, the endolymph will catch up and the nystagmus will cease. When the subject is brought to an abrupt halt the hair cells in the LEFT horizontal semicircular canals will now be turned on. Like those in the RIGHT ampulla of the RIGHT horizontal semicircular canal, the hair cells are polarized towards the utricle. This will make the LEFT side the driving side, thus pushing the eyes slowly to the RIGHT after which they snap back to the LEFT (i.e., there is a LEFT nystagmus).
DONT FORGET THE DESCENDING VESTIBULOSPINAL PATHWAYS. THINK ABOUT THE DRIVING SIDE CAUSING THE ARMS AND LEGS TO BE SO ACTIVE THAT THEY PUSH YOU TOWARDS THE OPPOSITE SIDE. THUS A PERSON WITH A LEFT NYSTAGMUS (LEFT SIDE IS DRIVING) WILL FALL OR STUMBLE TO THE RIGHT.
You also need to be aware of caloric nystagmus. 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. 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 utricle). This will result in the RIGHT side driving the system. RIGHT side dominance means that the eyes will go slowly to the LEFT and then snap back to the RIGHT (a RIGHT NYSTAGMUS; warm=nystagmus same side). Cooling the RIGHT ear would give the opposite results. Just remember COWS = cold opposite, warm same. You should understand COWS under normal conditions. I WILL NOT, REPEAT, WILL NOT, ask you questions on the exam regarding the results of caloric testing following the various lesions I have just presented. This is beyond the scope of this course.