Point 13

Intro

Receptors

Pathway

Deficits

Eyes

Eye Defic.

Overview

Problems

Contents

Anatomy

 

 

Frontal Eye Field LesionA 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 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 misalignment of the two eyes). 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!

PPRF LesionNow 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.

Abducens Nucleus LesionA 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. In such a case the neurons in the right medial rectus receive an input from a convergence center located rostral to the oculomotor complex. There will be no diplopia.

Abducens Nerve LesionWhat about a lesion of the ABDUCENS NERVE. Let's 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.

DIPLOPIA

(Gr., diplous=double + ope=sight)

DiplopiaWhen 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.

Head Rotation and Eye MovementYou 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 TOWARDS the side of the paralyzed muscle (LEFT in this example). This alleviates the double vision.

MLF LesionA 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 hypothesis regarding this condition, but we will not delve into them at this time.

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).

DON'T 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.

COWSYou also need to be aware of caloric nystagmus. If a subject tilts his or her head back (so as to get the horizontal canals 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.