sixt

editi
142 I CHAPTER 4

,-4i"~~
P ,

c
Figure 4-15. Clinical findings with trochlear (IV) nerve lesion. The affected (right) eye is elevated on forward gaze
(A). The extent of elevation is increased with adduction (B) and decreased with abduction (e). Elevation increases
with head tilting to the affected side (0) and decreases with head tilting in the opposite direction (E).

can be overcome by caloric stimulation. Its pathophysi-
ology and causes are discussed more fully in the section
on gaze palsy. Mild impairment of upgaze is not un-
common in asymptomatic elderly subjects.
A gence. Its causes are discussed later (see Internuclear
3. Internuclear ophthalmoplegia-This disorder re-
sults from a lesion of the medial longitudinal fasciculus,
an ascending pathway in the brainstem that projecrs
from the abducens to the contralateral oculomolOr
nerve nucleus. As a consequence, the actions of the ab-
ducens and oculomotor nerves during voluntary gaze
or caloric-induced movement are uncoupled. Excursion
of the abducting eye is full, but adduction of the con-
tralateral eye is impaired (Figure 4-17). Internuclear
ophthalmoplegia cannot be overcome by caloric srimu-
!ation; it can be distinguished from oculomotor nerve
palsy by noting preservation of adduction with conver-
Ophthalmoplegia) .
4. One-and-a-half syndrome-A pontine lesion af-
fecting both the medial longitudinal fasciculus and me
ipsilateral paramedian pontine reticular formation (larer~

8
- Gaze
Figure 4-16. Clinical findings with abducens
nerve lesion. The affected (right) eye is adducted
(A) and cannot be abducted (B).
gaze center) produces a syndrome that combines imernu-
clear ophthalmoplegia with an inability to gaze toward
the side of the lesion (Figure 4-18). The ipsilateral eyeis
immobile in the horiwntal plane and movemenr of me
(VI) contralateral eye is restricted to abduction, which maybe
at rest associated with nystagmus. The causes include ponrine
infarct, multiple sclerosis, and pontine hemorrhage.
 DISTURBANCES OF VISION I 143

B. DIPLOPIA TESTING
When the patient complains of diplopia, maneuvers to

-
test eye movement should be used to determine its
Gaze anatomic basis. The patient is asked to fix his or her vi-
sion on an object, such as a flashlight, in each of the six
cardinal positions of gaze (see Figure 4-5). With nor-
Nystagmus Impaired adduction
mal conjugate gaze, light from the flashlight falls at the
same spot on both corneas; a lack of such congruency
confirms that gaze is disconjugate. When the patient
notes diplopia in a given direction of gaze, each eye

Impairedadduction
-Gaze

Nystagmus
Right
INO
should be covered in turn and the patient is asked to re-
port which of the two images disappears. The image
displaced farther in the direction of gaze is always refer-
able to the weak eye, because that image will not fall on
the fovea. A variation of this procedure is the red glass
Figure 4-77. Eye movements in internuclear ophthal- test, in which one eye is covered with translucent red
moplegia(INO) resulting from a lesion of the medial glass, plastic, or cellophane; this allows the eye respon-
longitudinal fasciculus bilaterally. sible for each image to be identified.

A B

- Gaze
R
••
I
I
••\
\
-
Gaze
L

I
I

I
" To left medial rectus " To right I
I \ medial rectus I
I
I To left
~ I
I lateral
I rectus
Abducens (VI)
muscle
nucleus

Medial
longitudinal
fasciculus

Paramedian
pontine
reticular
formation
Pons Pons

R L R L

Figure 4-78. One-and-a-half syndrome. This results from a pontine lesion (shaded area) involving the paramedian
pontine reticular formation (lateral gaze center) and medial longitudinal fasciculus, and sometimes also the
abducens (VI) nucleus, and affecting the neuronal pathways indicated by dotted lines. Attempted gaze away from
the lesion (A) activates the uninvolved right lateral gaze center and abducens (VI) nucleus;the right lateral rectus
muscle contracts and the right eye abducts normally. Involvement of the medial longitudinal fasciculus interrupts
the pathway to the left oculomotor (III) nucleus, and the left eye fails to adduct. On attempted gaze toward the lesion
(B),the left lateral gaze center cannot be activated, and the eyes do not move. There is a complete (bilateral) gaze
palsy in one direction (toward the lesion) and one-half (unilateral) gaze palsy in the other direction (away from the
lesion), accounting for the name of the syndrome.