Vision and Automobile Driving Fitness in PD.htm

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VOLUME XXI - ISSUE 3/ Fall 2000

Vision and Automobile DrivingFitness in Parkinson's Disease

By Kahn, M.D., Emeritus Clinical, Associate Professor of Ophthalmology, University of Southern California School of Medicine

Visual disturbances are frequently not considered as a clinical symptom in Parkinson’s disease (PD). Laboratory studies in animals and human subjects have, however, shown consistent deficits of various visual functions.

Vaguely described visual complaints are often expressed by PD patients. In the majority of these patients, visual examinations yield normal or near-normal acuities and an absence of ocular disease. Nevertheless, many undergo needless but frequent changes in eyeglasses in attempting to correct their visual difficulties. Information is now becoming available that the complaints of “seeing” may, in part, result from a problem with “looking.”

Until fairly recently it was the accepted notion that Parkinson’s disease is an exclusive motor system disorder. The condition is classically associated with motor signs such as tremor, slowness of movement, rigidity and abnormalities of gait and posture; visual sensory abnormalities were not thought to be included. By now, considerable support based on psychophysical and electrophysical measurements exists attesting to visual dysfunction in a significant number of patients affected by Parkinson’s disease. Animal studies using pharmacological manipulation have indicated an important role for dopamine in the retina. Data obtained from monkeys suffering from a parkinsonian syndrome induced by MPTP strengthen the notion that PD is a clinical syndrome based on specific but distributed lesions of various dopaminergic systems of the human central nervous system, including the visual pathway.

The essential pathological feature of Parkinson’s disease is a loss of dopamine neurons of the substantia nigra and an abnormally low concentration of dopamine in the basal ganglia. In addition to the basal ganglia, low dopamine concentration has been demonstrated in other areas of the central nervous system; however, the retina has not been traditionally included in postmortem studies. A single neuropharmacological study did show, however, reduced DA content in the retina of a patient with PD. In monkeys with MPTP-induced parkinsonism, postmortem examination did demonstrate reduced dopamine content in the retina.

Visual Defects Associated with Parkinson’s DiseaseContrast SensitivityIn 1986 and 1987, investigators in Rotterdam studied contrast sensitivity in parkinsonian patients before and after levodopa treatment. Pretreatment contrast sensitivity function was abnormal in 16 of the 20 eyes. All subjects had visual acuity of 20/30 or better and were free of other neurological disease. The mean age of the patients was 66 years (range, 56-77). After treatment, improvement in the previously impaired contrast sensitivity was observed. None of the abnormal contrast sensitivity changes were related to the stage of Parkinson’s disease. There was no difference in contrast sensitivity function between patients with 20/30 and 20/20 visual acuity. These changes of contrast sensitivity function following treatment suggest that dopamine is a functional transmitter in the visual pathways.

Visual acuity as tested with letters has been demonstrated to be abnormally poor in parkinsonian patients when tested under low light intensity conditions. The standard visual acuity tests assess a patient’s ability to recognize small high-contrast letters. It is well known that this ability can be spared while the ability to see larger low-contrast test targets is degraded. A selective loss of this kind can be orientation-selective, and is seen in Parkinson’s disease.

Paradoxical Movement in PDPatients with severe PD are rigid; they move with extreme difficulty and typically they suffer tremor in several muscles when at rest. Nevertheless, despite these severe motor symptoms, patients with this disease can, on occasion, perform unexpectedly rapid, accurate, and even skilled movements. In some cases these actions appear to be provoked by intense emotion, such as fear or anger. There are, however, other situations in which the patients can move effectively without any obvious cause of strong emotion. There is anecdotal evidence that under certain circumstances PD patients can walk up or down stairs, catch a ball, field a football, jog, or ride a bicycle almost normally. The common feature of all these examples of paradoxical movement is that they seem to be under visual guidance. A test is described in which post-encephalitic patients with Parkinson’s disease had improved walking when transversely oriented stripes were placed along the path in front of the patients. Diagonal stripes were less effective, and stripes that were oriented parallel to the direction in which they were to walk were totally ineffective.

The Role of Eye MovementsThere are several differing types of eye movements involved in effective looking and seeing. One is a very fast eye movement that serves to bring peripheral images of interest to bear on the fovea for closer inspection. The ideal fast movement is one that brings a target of interest from the visual periphery into alignment with the fovea in a single movement. The time interval between the appearance of a target and initiation of a fast movement has been shown to be significantly prolonged in PD. There is also a significantly reduced tendency for parkinsonian patients to make anticipatory fast movements to predictable targets. Both of these types of defective movement of the eyes are more severe in more advanced cases of the condition.

A second type of eye movement is a low, smooth pursuit movement, following the target. PD patients have been shown to have a significant decrease in this type of movement.

A third important type of eye movement is scanning, involving larger changes effected by gross movements of the eyes in a search for known or anticipated targets. Complaints of blurred vision in parkinsonian patients may relate to the demonstrated abnormalities in ocular motor control. For example, it is well known that little or no visual information is acquired during fast eye movements as first described above. In PD, such defective motor function is replaced by fast movements, which results in blurring.

Automobile DrivingFitness in Parkinson’s DiseaseIn a journal article by M. Poser, M.D., of Harvard Medical School, published in 1993, the author reviewed the regulations of the Department of Motor Vehicles of all 50 states with regard to neurologically impaired drivers and applicants for licensure. There was, of course, a great variation on the approach and requirements of the several jurisdictions. The following is a direct quotation of Dr. Poser’s comments with regard to PD:

“Parkinsonism deserves special attention. Although many persons with that condition do not manifest sufficient motor weakness to warrant limiting their driving, slowness of movement (bradykinesia) and rigidity greatly prolong reaction times. As a result, they are unable to respond quickly to changing conditions. On that basis, driving should be forbidden until they can demonstrate improvement on medication. The most accurate assessment is one made not by a physician, but by an experienced driving examiner who conducts a road test under normal traffic conditions. Simulator tests are more realistic for patient testing. In Hoehn and Yahr’s stage 1 of Parkinson’s disease, computer simulator tests show that the accuracy of steering, reaction time, and interpretation of traffic signals are all impaired. The timing of any assessment of driving in Parkinson’s disease may be crucial in relation to disease variability and the ‘on and off ’ phenomenon.”

Practical Application of These FindingsIt would appear that all of us who have been diagnosed as having Parkinson’s disease should indulge in a realistic self-evaluation of the degree to which our driving skills, often already reduced by normal aging, may have been further compromised by our parkinsonism. From a practical standpoint, many or most of us would incur a significant personal and/or occupational hardship if we were to discontinue driving entirely, but I feel that each of us should play “devil’s advocate” and conscientiously interrogate him or herself as to possible self-imposed driving limitations. Situations to be assessed might include:

Night driving: All of the defects in visual function described earlier are exaggerated under conditions of decreased illumination. To a significant degree the avoidance of night driving is seasonally complicated with the yearly onset of daylight savings time, during which one drives to work in daylight and then must drive home in darkness.

Complex driving conditions: Two important examples are freeway driving and making left turns or U-turns in heavily traveled intersections. In both of these situations the driver must make multiple sequential complex decisions in repeated series, and additionally must exert rapid and exact motor responses to effectualize these decisions. Clinical testing has strongly indicated that these are exactly the functions in which parkinsonian patients, to varying degrees and with varying times, show a deficiency.

Age: To a lesser degree than in PD, many of the visual impairments described here are also noted with aging, adding to the degree of visual impairment otherwise present. Additionally, the clouding of the normal lens in the eye is steadily increased in all of us with advancing years and, even if not present to a degree which is diagnosed at cataract, causes problems with glare and often with night driving.

Alcohol: All sensory and motor functions are to some degree demonstrably impaired by even small amounts of alcohol. The parkinsonian individual should avoid adding these additional hazards to his already impaired function by absolute avoidance of alcohol for several hours before driving.

Drugs and medications: It goes with saying that street drugs and driving should not be combined for any driver, let alone those with Parkinson’s disease. The same is generally true for mood-modifying medications, both “uppers” and “downers.” Visual hallucinations have been noted in 5 to 30 percent of patients taking levodopa. The frequency is related to dosage and duration of treatment, as well as to the duration and severity of the disease. Anticholinergic drugs, such as Artane, as well as Eldepryl, have a recognized association with visual hallucinations. Many patients on treatment for parkinsonism are made sleepy at some stage by their medications, and such patients must be aware of the extent of their individual problems in this regard.

On and Off phenomenon: PD patients who experience this problem to a significant degree must guard against the unanticipated changes in their degree of impairment for driving, which may appear without warning.

Fatigue: All drivers are adversely affected by fatigue, and in the parkinsonian patient, at worst, this exaggerates his PD-related impairment, and at best, adds one more adverse element to the driving scene.