Dear Listfriends,
Dr. Abraham Lieberman, Director of the National Parkinson Foundation,
has written an article on vision problems with PD. You can read the
article at the NPF website, under "Ask Doctor Lieberman" at:

http://www.parkinson.org/index.htm

For those of you who do not have access to the Internet, the article is
below.
Best,
Kathrynne
---------------------

Seeing in People with Parkinson disease
        by Abraham Lieberman MD

    Some Parkinson people have difficulty seeing.  The common symptoms
are
difficulty reading, visual blurring, difficulty keeping the eyes open,
and
hallucinations.  Hallucinations: seeing objects or
people no one else sees result not from a condition in the eye but a
problem in the brain. Hallucinations were discussed previously

     Many Problems “Seeing” are Related to Aging Not Parkinson Disease
Parkinson is a disease of aging, and many of the problems “seeing”
relate
to aging not Parkinson.  A Parkinson person with problems “seeing”
should
consult an ophthalmologist: a medical doctor who can diagnose and treat
all
eye conditions.  Subsequent visits can be with an optometrist: a
licensed
professional who can diagnosis and treat specific conditions.

     The ophthalmologist will check your visual acuity  on an eye chart
both for distance (far) vision and near (reading) vision.  A common
condition is presbyopia: where the length of your lens changes
with age and in order to read  you’re forced to hold the paper further
and
further away.
       Another problem is cataracts where your lens becomes cloudy and
you
think you’re looking through “water.”
       A quick way of checking if the problem is with your lens is to
look
through a “pin-hole”: if the images become sharper the likelihood is
that
it’s your lens.
        The ophthalmologist may, depending on your symptoms, check your
color
vision and/or your ability to distinguish among different shades of
color
or gray (called contrast sensitivity).
     The visual  acuity tests the function of your lens.  Color vision
and/or contrast sensitivity tests your retina and optic
nerves.
      If you think of your eye as a camera, the pupil is the opening or
aperture or shutter.  The lens is the lens.  The retina  is the film.
The
optic nerves transmit the image from the retina to your brain.
        Another common condition is glaucoma.  Glaucoma  results from an
accumulation of fluid behind the eye.  The fluid presses on the optic
nerves and can, in time, lead to blindness. Acute glaucoma
is often accompanied by pain.  Chronic glaucoma is usually silent.  The
ophthalmologist will check the pressure in your eye to determine whether
you have glaucoma
.
Problems “Seeing” and Anti-Parkinson Drugs
        Certain Parkinson drugs, the anti-cholinergic drugs such as
Artane,
Akineton, and Cogentin, certain anti-depressant drugs such as the
tri-cyclic drugs that have anti-cholinergic properties ( examples
are Elavil, Norpramin, and Sinequan) and certain drugs used to treat
over-active bladders that have anti-cholinergic properties (examples
are
Ditropan and Detrol)  can increase eye pressure-- especially in
people with a certain type of glaucoma called narrow angle glaucoma.
If
you have Parkinson disease and glaucoma and you’re taking an
anti-cholinergic drug you should check with your eye doctor.
        The eye doctor with an ophthalmoscope will look at the back of
your eye,
the retina.  The retina is the only place in the body where the arteries
(as distinct from the veins) can be examined. Looking at
the arteries of the eye is a “window” into all the arteries elsewhere.
Such information is especially helpful in people with conditions such as
diabetes and high blood pressure, conditions  that affect the
arteries.  Other retinal conditions  that can be diagnosed with an
ophthalmoscope include macular degeneration.

How Parkinson Disease Can Effect the Eyes
        Parkinson disease does not affect  the lens or the optic nerve.
The
following, however,  may be affected in Parkinson disease or by the
drugs
used to treat Parkinson disease.
    1. The Eye-lids
        Early in Parkinson disease, before treatment, the lids and the
muscles
that control them become rigid and slow.  This results in retraction of
the
lids causing the person to “stare” or look “startled.”  This is more
marked
in a Parkinson-like condition called Progressive Supra-nuclear Palsy
(abbreviated PSP).
        In addition, in Parkinson disease,  the frequency of  eyes
blinking
 is decreased.  This is one of the earliest Parkinson symptoms.
        Sometimes the eyelids go into spasm, they close forcibly and
involuntarily, and stay closed for hours:  a condition called
blepharospasm.   Blepharospasm, or forced eye-lid closure is a dystonia.
Dystonia and blepharospasm usually occur separately from Parkinson
disease.
 They can, however, occur as part of Parkinson disease.  Dystonia and
blepharospasm can be improved, worsened, or unaffected by
Parkinson drugs.  Blepharospasm is best treated by injections of
Myo-Bloc
or Botox, drugs that weaken the lids sufficiently to stop them from
closing
involuntarily– while allowing them to close voluntarily.
        2. The Pupils
        The pupils or “camera shutters” are unaffected in Parkinson
disease.
However, some of the drugs used in treating Parkinson disease, the
anti-cholinergic drugs, dilate or widen the pupil causing
visual blurring.  The blurring may be pronounced when you read– or in
the
dark. If we compare the eye to a camera, the smaller the opening of the
eye
or the camera the sharper the image on the retina.  The
wider the opening of the eye or the camera the fussier the image. The
anti-cholinergic drugs include Artane, Akineton, and Cogentin.  They
include the tricyclic anti-depression drugs such as Elavil,
Norpramin, and Sinequan. They include drugs to control over-active
bladders
drugs such as Ditropan and Detrol.
        The anti-cholinergic drugs were the first anti-Parkinson drugs.
In the
late 19th Century Parisian women, to enhance their beauty, to have
“bed-room eyes”  put belladonna drops, an anti cholinergic
agent, in their eyes– widening their pupils.  Belladonna also dried
their
saliva.  When one of them asked Dr. J Charcot, a French neurologist (and
Sigmund Freud’s teacher) about this– he conceived the idea of
using belladonna to dry the saliva of his Parkinson patients who had too
much saliva and drooled.  Not only did belladonna dry their saliva-- it
decreased their tremor.  Anti-cholinergics, as can be seen, have a
wide range of effects:  on the pupil, the salivary gland, the bladder,
and
the brain.
        3. The Eye Muscles
         There are 6 eye muscles in each eye.  Two muscles, the lateral
and medial
rectus, move the eye ball laterally from side-to-side.  The lateral
rectus
is controlled by a nerve that originates in the
brainstem, that part of the nervous system between the brain and the
spinal
cord.  This nerve is called  Cranial Nerve 6.  The medial rectus is
controlled by a nerve that originates in a part of the brainstem near
the substantia nigra, where the process of Parkinson begins.  This nerve
is
called Cranial Nerve 3. Two muscles, the superior and inferior rectus,
move
the eye ball up-and-down. These muscles are controlled
by Cranial nerve 3.   Cranial Nerve 3 also carries the fibers that
narrow
the pupil.  When these fibers are blocked by anti-cholinergic drugs, the
pupil dilates or widens.
        Two muscles, the superior and inferior oblique, rotate the eye
ball.  The
superior oblique is controlled by a nerve that starts in a part of the
brainstem near the substantia nigra, where Parkinson
starts.  The nerve is called Cranial Nerve 4.  The inferior oblique is
controlled by Cranial Nerve 3.
       Given the origin of two of the Cranial Nerves, numbers 3 and 4,
near
the substantia nigra  it’s surprising, happily, that eye movement
difficulty, and problems seeing, aren’t as frequent in Parkinson disease
as
in
PSP.
        The six muscles of  the right eye are “yoked” and work-in-tandem
with the
six muscles of the left eye.  And the three Cranial Nerves 3,4, 6 of the
right eye are “yoked” with the three Cranial Nerves of the
left eye.  Thus when in looking  to your right,  your right lateral
rectus
moves your right eye-ball toward your right ear, while your left medial
rectus muscle moves your left eye-ball toward your nose.  Because
your right lateral rectus and your left medial rectus are “yoked”, an
image
falls on a comparable spot on your right and left retina  and you see
the
images seen by the right and left eye as one.   If the muscles
and Cranial Nerves weren’t yoked, didn’t work-in-tandem, then instead of
one image you might see, depending on the degree to which they weren’t
“yoked” a blurred image, 1 ½ image, or,  two images.
Seeing “double” usually occurs not with  malfunction of the muscles, but
with malfunction of one or more Cranial Nerves.  Such malfunction  can
result from pressure on a Cranial Nerve inside the skull, or
by a stroke of the Cranial Nerve, such as may occur in diabetes.   The
Cranial Nerves have their own blood supply, so like the brain they are
subject to strokes.
        The eye muscles aren’t affected, as far as we can tell, by the
rigidity
and slowness of movement that affect other muscles in Parkinson
disease.
Nonetheless, it’s possible, that some of the difficulty
“seeing”, especially in reading,  may result from subtle difficulties in
the eye muscles.
      A common difficulty, convergence insufficiency, in which both eyes
must simultaneously approach each other– as in holding an object (such
as a
book) up close and reading it may result, in part, from such a
difficulty.
Some of these problems can be corrected by using prisms.
        4. Parkinson Disease and Progressive Supra Nuclear Palsy (PSP)
        Although the nerves to the eyes aren’t affected in Parkinson
disease,  the
“command” centers that control the nerves,  centers located in the
brainstem are affected, and markedly so, in PSP
    To a lesser extent, they’re affected in Parkinson disease.  In PSP,
a
person loses the ability to look-up or down, and later to look from
side-to-side.   The eyes in PSP  are “frozen.”  A person with PSP
can see because his retina and optic nerves are working.  But he can’t
track or follow unless he shifts his head from side-to-side to follow
horizontal movements.  Or bobs his head up-and-down to follow vertical
movements.  In some Parkinson people there’s a mild inability to look-up
or
down.
        The earliest PSP eye symptoms are tested by asking a person to
follow a
stripped moving cloth.  In following the stripes  a person, any person,
develops side-to-side eye movements, called Opticokinetic
Nystagmus.  Opticokinetic Nystagmus has a fast or “jerk-like” phase
followed by a slow phase.  In PSP, but not in Parkinson disease,
Opticokinetic Nystagmus disappear.
        5.  Eye Movements, the Brainstem, and Parkinson Disease
        The fast and slow movements of Opticokinetic Nystagmus and other
types of fast and  slow eye movements originate in the brainstem.  They
are
studied with an Electro Nystagmogram (ENG).  Each eyeball has an
electrical
potential.  Four electrodes, identical to the electrodes of an
electroencephalogram, an EEG, are placed over each eye, one  at the
right
and left corners of the eye socket,  one at the top and one at the
bottom
of the eye socket.  The electrodes than track the eye
movements:  their speed (fast or slow), their amplitude, and their
direction.
       Three types of eye movements, detected on the ENG, may be
relevant
to Parkinson disease.
        (i) The “fast movement” that bring images in the periphery to
bear on the
fovea, the most
sensitive part of the retina.   Normally such a “fast movement” brings
the
image from the periphery into focus on the fovea in a single move.  In
Parkinson disease,  the time from when the image is seen, to
when the “fast movement” starts, is delayed compared to people without
Parkinson.  This is the eye movement equivalent of  bradykinesia, the
slowness of movement that characterizes Parkinson.
        Normally, if we anticipate seeing an image, we start the “fast
movement.”
Often, the person
with Parkinson disease, when he anticipates seeing an image, can’t start
the “fast movement.” This is the eye movement equivalent of freezing.
As
Parkinson advances, eye movement “bradykinesia” and eye movement
“freezing”
become more pronounced.  These delays in movement can’t be appreciated
without an ENG.  They may be responsible, in part, for the difficulty
seeing in Parkinson disease, the difficulty
that can’t be diagnosed on a routine examination.
    (ii)  The “low amplitude smooth pursuit movement,” the movement that
tracks a predictably moving target, such as a  plane traveling at a
given
speed, or a golf or tennis ball traveling at a given
speed.  The “low amplitude smooth pursuit movement” is slowed in
Parkinson
disease and may explain why some Parkinson people complain of
difficulty
seeing or following moving objects.  The ”low
amplitude smooth pursuit movement”  may be important in driving, in
playing
golf, in playing tennis.
    (iii)  The “scanning eye movement.”  The “scanning eye movement” is
used in looking through a field of objects while searching for a
specific
object.  This “scanning” may be slowed in Parkinson
disease resulting in an ability to distinguished  among objects of
similar
colors, shapes, or sizes.  This could result, in part, for the symptom
of
“blurred vision.”
    6. Eye Movements and Walking
        Parkinson people who are unable to walk  can on occasion,
suddenly and
unexpectedly, walk or run.  This is called  “kinesia paradoxica”  and is
the opposite of  the sudden inability to walk, called
“akinesia paradoxica.” or freezing.  Occasionally,  “kinesia paradoxica”
may be provoked by fear or anger as a Parkinson person “breaks free” of
his frozen state.  Occasionally, a Parkinson person will
“break free” of his frozen state by catching a ball, jogging, or walking
up-stairs.  Catching a ball, jogging, or walking up-stairs are guided by
vision.   Similarly,  a Parkinson person can “break free” of his frozen
state by stepping over a horizontal line,  or by walking across a floor
painted with horizontal stripes, stripes at right or acute angles to his
direction of walking.  Stripes parallel to his direction of walking are
ineffective.  Catching a ball, jogging, walking-up stairs, or stepping
over
a horizontal line provokes eye movements.  These eye movements, through
an
as yet unknown mechanism, activate walking.
    7. The Retina
    The main feature of Parkinson disease is a decreased number of
dopamine
cells in he substantia nigra and a decreased dopamine content in the
basal
ganglia.  One study showed a decreased dopamine
content in the retina.  The reason only one study showed this is that
usually the retina’s not studied in Parkinson disease.  In monkeys with
MPTP caused Parkinson, autopsy examinations reveal a decreased
dopamine content in the retina. And subsequent studies indicate an
important role in vision for dopamine in the retina.  These studies also
suggest that the dopamine deficiency in Parkinson disease extends
outside the brain to the retina.
    In 1986, doctors in Holland studied contrast sensitivity in
Parkinson
people before and after levodopa. Before treatment,  contrast
sensitivity
was defective  in 16 of 20 people.  All the people had
visual acuity of at least 20/30.  The average age was 66 years.  After
levodopa treatment, contrast sensitivity was improved in all.  These
changes in contrast sensitivity following levodopa suggest
dopamine is an important chemical in the retina and the entire visual
system.
         Visual acuity tests your ability to recognize  high-contrast
letters:
black letters, of varying size, on a white background under conditions
of
normal lighting.   Lens problems such as presbyopia or
cataracts are common causes of decreased visual acuity when tested with
black letters on a white background under conditions of normal
lighting.
But among Parkinson people with normal lenses, visual acuity may be
normal
when tested with black letters on a white background.  But decreased
when
tested with letters of different shades of gray, on a gray background.
Or
visual acuity may be decreased when tested under conditions of low
lighting.   Such problems may arise from a decreased dopamine
content in the retina.  This may make driving at night difficult.
        The above phenomena may explain, in part,  many of the problems
Parkinson
people have in “seeing”, problems not detected by ordinary testing, and
problems that, when not explained, are frustrating and bewildering to
the
Parkinson patient, their family, and friends.




--
Kathrynne Holden, MS, RD
Author: "Eat well, stay well with Parkinson's disease"
"Constipation and Parkinson's" --  audiocassette & guidebook
"Guidelines for Medical Nutrition Therapy for Parkinson's
disease" & Risk Assessment Tools
"Risk for malnutrition and bone fracture in Parkinson's
disease," J Nutr Elderly. V18:3;1999.
http://www.nutritionucanlivewith.com/