Vision and PD

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. Click here to return to What is Parkinsons.

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.