&nbs=
p; =
; =
&=
nbsp; <=
/P>
The=20
pupillary light reflex: =
Light=20
stimulates the retinal photo receptor and initiates =
pupillo-constriction=20
as well as visual impulses. =20
Pupil motorfibers are transmitted via the optic nerves; =
they=20
undergo a hemi-decussation at the chiasm. They exit from the optic =
tracts=20
before the lateral geniculated body and enter the brainstem via =
the=20
brachium of the superior colliculus. =20
After synapsing in the prectectal area, fibers are =
distributed to=20
the ipsilateral and contralateral Edinger Westphal nuclei. The efferent pupillary =
fibers=20
travel via the III nerve to synapse in the ciliary ganglia after =
exiting=20
the ciliary ganglion. =
Short=20
ciliary nerves then go the iris sphincter and ciliary =
body.
Dilator of the Pupil Sympathetic =
Pathway
=20
The =
sympathetic system also supplies the pupil. This pathway is perhaps =
less well=20
defined but probably originates in the hypothalamus. It descends uncrossed, =
to the=20
level of C8-T2 and it exits from the spinal cord via the =
perivertebral=20
sympathetic chain to synapse in the superior cervical ganglion and =
follow=20
the carotid plexus to join the ophthalmic division of the =
trigeminal=20
nerve. It reaches =
the ciliary=20
body and the dilator of the iris, via the long ciliary nerves.
=20
=20
=20
=20
B. =20
Examination of the pupils: =
1. =
; =20
Note the size and shape in darkness and in light.
2. =
; =20
Check for the light reflex in each eye individually.
3. =
; =20
Look for an afferent pupillary defect (RAPD - also known as =
Marcus=20
Gunn Pupil) by:
a. =20
The Swinging Flash Light Test
b. =20
The pupils must react to light in order to perform the =
test
c. =20
Not a test of the pupil per se=97but we do the test when we =
look at=20
the pupil
d. =20
Tests the optic nerve function
e. =20
Relies on a difference between the two optic nerves=97one =
must be=20
different from each other
=20
![](3D"http://umed.med.utah.edu/neuronet/lectures/2002/neuro_opthpics/Bas=)
=20
4.Check=20
the near reflex by bringing the patients own finger toward his =
nose.
=20
C. =20
Recording the pupils examination:
1. =
; =20
Record the actual size of the pupil OD (right eye) and OS =
(left=20
eye). For example: =
pupils in=20
darkness 8 mm OU (both eyes), in light 3 mm OD and 2.5 mm OS. No relative afferent =
pupillary=20
defect (no RAPD). =
Good near=20
reflex.
D. =20
The pathology involving the pupil.
1. =20
Lesions of the parasympathetic system cause a dilated pupil =
(greater anisocoria in light).
a. =
; =20
An acute third nerve palsy: =20
may signal compression of the third nerve due to a =
posterior=20
communicating artery aneurysm. =20
A third nerve palsy will be usually associated with other =
signs of=20
dysfunction including ocular motility disturbances and =
ptosis. An isolated dilated =
pupil does=20
not usually signify a III nerve palsy. =
b. =
; =20
Tonic pupil or Adie's pupil is characterized by a dilated =
pupil=20
with very poor or no light reaction with tonic constriction to =
near and=20
tonic redilation. =
Under the=20
slit lamp sectoral palsies of pupillary sphincter may be seen with =
light=20
stimulation. =
Because the=20
abnormality is post-ganglionic (that is, damage to the ciliary =
ganglion),=20
one can demonstrate supersensitivity of the sphincter muscle to=20
pilocarpine 1/10%. =
An acute=20
Tonic pupil usually a condition seen in young women who have =
asymptomatic=20
anisocoria. Adie's =
syndrome=20
consists of a tonic pupil and loss of deep tendon reflexes. The lesion causing =
pupillary=20
dysfunction is generally thought to be in the ciliary ganglion and =
the=20
cause is basically unknown.
c. =
; =20
Argyll Robertson pupil is characterized by small and =
unreactive=20
pupils (usually bilateral). =20
"Light-near" dissociation exists, i.e.; the pupil does not =
react to=20
light but will react to near (frequently the pupils are =
irregular). This pupil is associated =
with=20
syphilis. In order =
to=20
diagnosis this a VDRL and FTA be drawn. The anatomic cause is=20
unknown. A =
long-standing=20
Adie's Tonic pupil can occasionally be confused with this =
pupil.
d. =
; =20
Light-near dissociation can be seen in lesions in the=20
mid-brain.
=20
=
; =20
2. =
; =20
Lesions of the sympathetic system cause a small pupil =
(increased=20
anisocoria in darkness) Horner=92s Synd. =
a. =
; =20
Horner's Syndrome, consists of pupillary meiosis which is =
more=20
accentuated in darkness; light and near reactions are intact. There is ipsilateral =
ptosis due to=20
paresis of Muller's muscle (not the levator muscle of the =
eyelid). There is an =
apparent=20
enophthalmos because there is also an upside/down ptosis. Occasionally anhydrosis =
of the=20
face will also be seen.
b. =
; =20
Pharmacologic testing, to confirm the diagnosis of a =
Horner's=20
syndrome, a pharmacologic test may be done.
1) =20
Cocaine test, ten percent cocaine is instilled into the =
eye. The cocaine prevents the =
re-uptake=20
of norepinephrine into the normal nerve and hence the =
norepinephrine will=20
cause dilation of the pupil. =20
If there is a lesion anywhere along the sympathetic =
pathway, there=20
will be less norepinephrine coming down the nerve to be released;=20
therefore cocaine will not dilate the eye with a sympathetic =
defect.
2) =20
Hydroxyamphetamine test, to localize whether the Horner's =
syndrome=20
is preganglionic (that is before the superior cervical ganglion) =
or=20
postganglionic (after the cervical ganglion), Hydroxyamphetamine=20
(Paredrine) is instilled into both eyes at another time. Hydroxyamphetamine =
actively=20
releases norepinephrine from the nerve endings. If the lesion is =
preganglionic,=20
there will be normal norepinephrine store present at the iris and=20
therefore the pupil dilates. =20
A dilation to Hydroxyamphetamine in a Horner's eye means =
the lesion=20
is preganglionic. =
If the=20
pupil does not dilate, the lesion is postganglionic because there =
is no=20
norepinephrine to be released.
c. =20
Causes of pre-ganglionic Horner's:
=20
Central: =20
Stroke (Wallenburg syndrome)
Dissection=20
of vertebral artery with brain stem
&nbs=
p; =
; =
&=
nbsp; =20
Pre-ganglionic: =
Apex of=20
lung mass
&nbs=
p; =
; =
&=
nbsp; &n=
bsp; &nb=
sp; =20
Cervical spine abnormality
&nbs=
p; =
; =
&=
nbsp; &n=
bsp; &nb=
sp; =20
In children, neuroblastoma
&nbs=
p; =
; =20
d. =20
Causes of post-ganglionic Horner's:
&nbs=
p; =
; =
<=
/SPAN> =20
Dissection of carotid artery
&nbs=
p; =
; =
&=
nbsp; =20
Cluster Headache
3. =20
Pharmacologic Blocade.
a. =20
Can occur due to accidental exposure of the iris to a =
dilating=20
agent (e.g. Jimson weed; scopolamine patch)
b. =20
Test with pupillary constricting drug=97Pilocarpine 1%--if =
no=20
reaction=97likely pharmacologic blockade
=20
III. =20
VISUAL FIELDS
Visual=20
fields can localize a lesion in the visual sensory pathway.
A. =
; =20
Testing the visual field.
1. =
; =20
Visual fields to confrontation
a. =
; =20
Each eye is covered separately. You tell the patient to =
cover the=20
untested eye with the palm of the hand. Be sure the patient is =
not peeking=20
through the fingers. =
Ask the=20
patient to fixate on your nose and then you present fingers =
rapidly in all=20
four quadrants of his vision while he is fixating on your nose and =
he=20
counts the fingers.
b. =
; =20
Hand-to-hand comparison when both hands are presented in =
the=20
inferior field or the superior field. Ask the patient which he =
sees=20
better.
c. =
; =20
One can test the field with a red object and ask the =
patient if=20
he/she sees both objects as red in both the superior and inferior=20
fields.
d. =
; =20
Double simultaneous stimulation. One can test double =
simultaneous=20
stimulation by having the patient fixating on the nose with both =
eyes open=20
and by wiggling the fingers in the outside quadrants. Obviously one can pick =
up a gross=20
hemianopia or and extinction to simultaneous stimulation. However, this form of =
visual field=20
testing is not adequate for the routine examination. Each eye must be tested=20
separately.
2. =
; =20
When testing the visual field in the lethargic patient, the =
examiner may use a light or hand to elicit a blink. =
3. =
; =20
Other ways of visual field testing:
a. =
; =20
Tangent screen
b. =
; =20
Goldmann visual field perimetry
c. =
; =20
Automated perimetry
B. =
; =20
Recording the visual field
Pretend you are superman, burning the patient's =
visual field=20
into the page. By =
convention,=20
we recorded the left eye on the left and the right eye on the =
right (CF=3D=20
count fingers).
C. =20
Anatomy and Lesions:
Anatomy of=20
the visual field afferent system. =20
The afferent system starts at the retina, progresses =
through the=20
optic disc, optic nerve, optic chiasm, lateral geniculate body, =
optic=20
radiation's to the occipital cortex. =20
Lesions along this pathway cause characteristic visual =
field=20
defects.
| =
=20
|
=20
Diagram=20
showing the effects on the fields of vision produced by =
lesions at=20
various points along the optic pathway: A: Complete blindness =
in left=20
eye; B: The =
usual=20
effect is a left junction scotoma in association with a =
right upper=20
quadrantanopia. The=20
later results from interruption of right retinal =
nasal fibers=20
that project =
into the=20
base of the left optic nerve (Wilbrand's knee). A left nasal =
hemianopia=20
could occur from a lesion at this point but is exceedingly =
rare;=20
C: Bitemporal =
hemianopia; D: =
Right=20
homonymous =
hemianopia;=20
E and F: Right upper and lower quadrant hemianopia; and =
G: Right homonymous=20
hemianopia. =
From Victor=20
& Adams: =
Neurology |
IV. =
; =20
OCULAR MOTILITY
A. =
; =20
Testing extra-ocular muscles and motility.
1. =
; =20
Extra-ocular movements, observe the normal relationships of =
the=20
eyes to the head and lids to the cornea and look for ptosis. Look for spontaneous =
movements of=20
the eye. Then test =
the=20
cardinal directions of gaze saying, "Follow my finger with just =
your eyes"=20
and present your finger in the form of the letter H.
=20
=20
Remember that the third nerve supplies the =
following=20
muscles: Inferior, =
oblique,=20
superior rectus, inferior rectus and medial rectus as well as the =
levator=20
of the lid. The =
fourth=20
supplies the superior oblique. =20
The sixth nerve supplies lateral rectus =
muscles. =20
(a) =20
Recording the extra ocular movements, this should be done =
on a=20
diagram showing any limitation of function. For example: =
B. =
; =20
Disorders of ocular motility include third, fourth, and =
sixth nerve=20
palsies, internuclear ophthalmoplegia, and 1=BD syndrome =
. =20
1. =20
Third Nerve Disorder
a. =20
A third nerve palsy will frequently present as diplopia or=20
ptosis. The patient =
will have=20
a dilated pupil, ptosis on the same side and ophthalmoplegia of =
all=20
muscles except for the lateral rectus on that side and superior=20
oblique. =
b. =20
Sudden onset of a third nerve palsy: Be sure that an aneurysm =
is not=20
present.
c. There are many =
other causers=20
of third nerve palsies, such as brainstem or midbrain =
infarction. These syndromes will give =
other=20
neurologic findings such as ipsilateral third nerve paresis with=20
contralateral hemiparesis (Weber's syndrome), or ipsilateral third =
nerve=20
paresis with contralateral hemitremor expanding mass in the =
temporal lobe=20
because the third nerve caught between the edge of the tentorium =
cerebelli=20
and the uncus of the temporal lobe in Uncal Herniation =
Syndrome. Cavernous sinus lesions =
and=20
superior orbital fissure masses can also cause third nerve =
lesions.
d. Isolated third =
nerve=20
palsies:
Ischemic=20
(from diabetes)
Aneurysmal=20
compression (look for pupil enlargement)
Trauma
Tumor=20
(check for aberrant regeneration)
Infection
Inflammation
Idiopathic
=20
The III=20
Nerve Pathway
&nbs=
p; =
; =20
=20
=
&=
nbsp; &n=
bsp; &nb=
sp; &nbs=
p; =
; =20
(From Bajandas, Kline: Neuro-Ophthalmology)
=20
2. =20
Fourth nerve palsy. =20
The fourth cranial nerve or the trochlear nerve has its =
nucleus in=20
the periaqueductial gray. =20
Fibers of this nerve cross around the periaqueductial gray, =
and are=20
the only cranial nerves to emerge on the dorsal surface of the=20
brainstem. The =
trochlear=20
nerve passes around the brainstem, across the tentorium and goes =
into the=20
dura of the cavernous sinus lateral and inferior to the third =
nerve. It passes through the =
superior=20
orbital fissure and supplies the superior oblique muscles. This nerve has the =
longest course=20
of any cranial nerve in the subarachnoid space. The superior oblique =
muscle is a=20
depressor in adduction. =
It is=20
also a rotator.
a. =
; =20
Dysfunction of the fourth nerve causes the patient to =
complain of=20
vertical diplopia.
b. =
; =20
The most common causes of fourth cranial nerve palsy is=20
trauma. Since this =
is a long=20
and very delicate nerve, it is easily disrupted even by small head =
trauma.
c. =
; =20
Isolated IV palsies
=
;=20
1) =
Trauma
=
;=20
2) =
Ischemic
3) =20
Masses (along the clivus)
The IV Nerve Pathway
&nbs=
p; =20
(from Bajandas, Kline: Neuro-Ophthalmology)
3. =20
The sixth nerve. The sixth nerve or the =
abducens=20
nerve nucleus lies in the dorsal portion of the pons near the =
midline,=20
just underneath the fourth ventricle (see diagram). The sixth nerve =
leaves the=20
brainstem at the pontomedullary junction, it runs in the =
subarachnoid=20
space along the base of the pons where it is closely =
associated with=20
the clivus bone. =
It=20
pierces the dura and runs in the cavernous sinus and enters =
the orbit=20
through the superior orbital =
fissure.
The VI=20
Nerve Pathway
(from Bajandas, Kline: Neuro-Ophthalmology)
a. =20
Pathology:
Isolated=20
sixth nerve palsies have no localizing value. If they are associated =
with other=20
neurologic signs such as fifth nerve palsy, seventh nerve palsy, =
or eighth=20
nerve palsy, they may be of localizing value. Isolated sixth nerve =
palsies are=20
commonly due to small occlusive disease in older individuals, =
trauma in=20
all age groups or underlying tumors. =20
Chronic sixth nerve palsies should be evaluated.
b. =20
Isolated VI nerve palsy:
1) =20
Idiopathic
2) =20
Ischemic
3) =20
Traumatic
4) =20
Inflammation
5) =20
Tumor
6) =20
Cavernous sinus thrombosis
4. =20
Internuclear ophthalmoplegia:
a. =
; =20
The PPRF or parapontine reticular formation is called the =
conjugate=20
gaze center (horizontal =
gaze lies=20
in the pons). =
The PPRF=20
makes internuclear connections to the sixth nerve as well as to =
the third=20
nerve. Its =
connection to the=20
third nerve is called the medial longitudinal fasciculus which =
crosses to=20
the contralateral third nerve. =20
An MLF lesions blocks the information going from the PPRF =
to the=20
third nerve nucleus. =
This=20
results in the internuclear ophthalmoplegias (INO). Since MLF fibers =
originate in one=20
PPRF and cross immediately to the other side, before ascending to =
the=20
third nerve nucleus, an MLF lesion is on the same side as the eye =
with the=20
medial rectus or adduction weakness. =20
The INO is named by the side of the MLF lesion or the side =
of the=20
adduction deficit. =20
Internuclear ophthalmoplegia are frequently seen in =
vascular=20
disease, but also can be seen in demyelinating diseases such as =
Multiple=20
Sclerosis.
b. =
; =20
The clinical picture of a left INO or left MLF lesion: when =
looking=20
to the right there is a failure of adduction of the left eye and =
abducting=20
nystagmus of the right eye. A=20
slowed adducting saccade is another sign of an INO.
=20
=
(from=20
Bajandas, Kline: Neuro-Ophthalmology)
&nbs=
p; =
; =
&=
nbsp; &n=
bsp; &nb=
sp;
=20
5. =20
1=BD syndrome:
a. =
; =20
A lesion of the PPRF
b. =
; =20
Gaze palsy and INO
c. =
; =20
E.G. a RPPRF lesion gives a right
gaze palsy=20
and right INO
e.g. =
A right=20
PPRF gives a right gaze palsy (the one) and =
a right INO=20
(the one-half)
=
C. =20
Other Eye Movements =
;=20
1. =
; =20
Testing for saccades. Saccades are a =
rapid eye=20
movements system which serves to refoviate the eye on an object of =
regard. The =
movement is=20
demonstrated to command by presenting a target, =93Look at my =
finger, look=20
at my nose=94. =
Saccades are=20
fast 200-400 degrees per second. =20
Disorders of the saccades include hypometric =
saccades=20
(multiple small eye movements between two targets), hypermetric =
saccades (saccades that overshoot the endpoint and then go =
back to the=20
desired object), and slow or absent saccades (no fast=20
movement). Saccades =
are=20
generated in the frontal eye fields.
b) =
; =20
Rapid eye movements to get to a new target
c) =
; =20
Starts in the Frontal eye field (contralateral)> to the =
PPRF=20
(burst neurons)> project to abducens, and via MLF to III =
nerve
d) =
; =20
Disorders in saccades: Frontal gaze palsy due to frontal =
lobe=20
injury; dysmetria; saccadic intrusions (square wave jerks); =
opsoclonus=20
(saccadomania)
=20
2. =
; =20
The pursuit system allows the eye to follow a =
target=20
without saccades. =
We are able=20
to maintain acuity during pursuit and pursuit will break down at =
speeds=20
exceeding 30-35 degrees per second. =20
Defective pursuit is seen when pursuit is broken up by =
saccades=20
(saccadic pursuit). =
Pursuit=20
lies in parietal occipital areas.
=20
3. =
; =20
The vestibular ocular reflex (VOR) is a complicated =
pathway=20
which can be affected by many disease processes. We test the reflex in =
two=20
ways. First, in an =
alert=20
patient we can ask them to fixate on a distant target while moving =
them in=20
a swivel chair. The =
eyes=20
should move smoothly side to side. =20
A normal healthy individual should be able to suppress the =
reflex=20
by fixating on his/her thumb while he/she is moved in the swivel=20
chair. The eye =
should remain=20
on the thumb without nystagmus or moving from the target.
=20
4. =
; =20
Dorsal midbrain Syndrome=97Parinaud=92s Syndrome
a) =20
Vertical gaze disorder
1. =20
Complex pathways involving Frontal eye fields, =
parieto-occipital=20
temporal junction, superior colliculus, ri MLF, PPRF and INC
2. =20
Disorders of vertical gaze important: Up gaze paralysis =
(dorsal midbrain=20
syndrome), Down gaze paralysis, progressive supranuclear palsy
b) =20
Characteristic findings in dorsal midbrain syndrome
1. =20
up-gaze paralysis
2. =20
lid-retraction
3. =20
light-near pupillary dissociation
4. =20
convergence retraction nystagmus
5. =
; =20
Nystagmus:
a) =20
Nystagmus is a rhythmic oscillation of the eyes
1. =20
Jerk Nystagmus (initial slow; fast phase). The fast phase names the =
nystagmus; the pathology is the slow drift
2. =20
Pendular nystagmus=97phases opposite in direction but equal =
velocity
b) =20
Nystagmus--what to look for
1. =20
One eye or both
2. =20
Jerk or pendular
3. =20
Horizontal, vertical or both
4. =20
Conjugate or dissociated
5. =20
Primary position or eccentric gaze
6. =20
Change with gaze position
c) =20
Symptoms
1. =20
Oscillopsia, blur, vertigo
d) =20
Nystagmus has basically two parts: a slow phase and a rapid =
recovery phase. The =
slow=20
phase which is the initial phase is considered to be the abnormal=20
movement. The rapid =
phase is=20
corrective. =
Nystagmus,=20
however, it is names by side of the fast or corrective phase. Some nystagmus has =
localizing=20
value.
1) =
; =20
Downbeat nystagmus can be seen with lesions of the =
cervical=20
medullary junction.
2) =
; =20
Upbeat nystagmus (fast phase is up while the eyes =
are in=20
primary position) can be seen with cerebellar or medullary tumors =
such as=20
medulloblastoma.
3) =
; =20
Lateral nystagmus can be due to drugs or structural =
lesions=20
in the cerebellum
6. =20
There are many other abnormal eye movements which are not=20
nystagmus: For example, square wave jerks, flutter, =
opsoclonus.
![](3D"http://umed.med.utah.edu/neuronet/lectures/hm00334a.gif")
![](3D"http://umed.med.utah.edu/neuronet/lectures/bs00438_.gif")