Fwd: Difficulty Seeing in Parkinson

December 31, 2000

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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.

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