Strabismus, nystagmus, and driving

Strabismus

Deviation of one eye from parallelism with the other can be caused by paralysis of an ocular muscle or cranial nerve (paralytic strabismus) or by other abnormalities of the visual axes secondary to an intrinsic imbalance of ocular muscle tone (nonparalytic strabismus), which is usually congenital in origin.

If strabismus is accompanied by severe amblyopia, the patient should be considered a one-eyed driver for driving purposes.

Persons with strabismus usually have reduced or absent stereopsis, but have usually adapted to this defect and rarely suffer from diplopia or visual fatigue.

They sometimes have an altered visual field, with deviations of over 20 degrees.

Phorias and convergence problems usually give rise to diverse abnormalities of fusion and stereopsis. Affected individuals often complain of visual fatigue and sleepiness when driving long distances.

Nystagmus

Involuntary, rapid, and repetitive movements of the eyes in a horizontal, vertical, or rotary direction.

It is physiologic if the movement is detected during extreme lateral gaze, optokinetic if the movement induced by repetitive visual stimuli, and vestibular if the movement is triggered by caloric testing.

Pathologic nystagmus can be caused by a defect in afferent sensory inflow to the nervous system or by a defect in the efferent mechanism (motor imbalance).

Acquired nystagmus is usually a symptom of pathologic processes affecting the central nervous system, and until its cause and course are established, driving is not permitted.

Nystagmus is also observed in cases of drug intoxications by phenytoin, barbiturates, alcohol, and in patients with neurological disease due to tumors, vascular diseases and encephalitis.

Nystagmuses cannot be concealed and are increased by covering one eye.

They can cause a manifest or latent reduction in visual acuity, torticollis and altered binocular vision.

Tips

• If a patient with strabismus starts with diplopia, it must be considered that he is decompensated, and we should warn him that, until the diagnosis is confirmed and he adjusts to the situation, he may not drive.
• With diplopia or nystagmus, if the visual capacity levels legally established for each group are not reached, the patient may not drive.
• In adapted convergence problems, fatigue and somnolence occur with long-distance driving, so short, known distance should be recommended, or shifting driving with the companion.
• Adults who have been able to adapt fulfill an activity very similar to people with normal binocular vision. At this time, medical assessment and judgment are not easy, but we have to make an effort for it.
• We know that all ocular motility disorders, though very well adapted, can decompensate in situations of anxiety, stress, somnolence, copious meals, alcohol and drugs. The physicians should inform of this risk when our patient is a driver.
• Some drugs such as sulfonamides, piperazine, and quinine can cause ocular motility disorders, and we should warn about it.
• The physician should be attentive to the possible masking and simulation by the patient during the examination, making him understand that a wrong assessment can mean a preventable worsening that may have an impact for his health.
• We should convey them our interest to protect them and others when driving, and explain in each case the problem to reduce it and that they can drive without risks.
• It is important that the physicians ask the specialist for a report that shows the data on the therapeutics, control of the disease, stability of the condition over time, recovery or adaptation to the new situation, and advise the patient with it at his recognition center for an appropriate evaluation of the license or extension, always indicating him that it is for his safety and that of others.