Ординатура / Офтальмология / Английские материалы / The Neurology of Eye Movements_Leigh, Zee_2006

cal features with other disorders of mitochondrial DNA (discussed in Chap. 9).

Pelizaeus-Merzbacher disease is an X- linked recessive dysmyelinating disease.540 Affected children may have ocular motor apraxia and cerebellar signs including saccadic dysmetria and pendular nystagmus (see VIDEO: "Pelizaeus-Merzbacher disease").1008'1393 The peroxisomal assembly disorders, such as the neonatal form of adrenoleukodystrophy, also may be associated with pendular nystagmus,790 as is another congenital disorder affecting myelin, Cockayne's syndrome.280

Vitamin E deficiency may cause a progressive neurologic condition characterized by areflexia, cerebellar ataxia, and loss of joint position sense.242 Ocular motor involvement includes progressive gaze restriction, sometimes with strabismus. Vitamin E deficiency occurs in childhood, when it may be due to abetalipoproteinemia (Bassen-Kornzweigdisease).1510 It is also reported in adults with bowel disease that interferes with fat absorption182 or as an inherited ataxia on chromosome 8ql3, the site of the alpha-tocopherol transfer protein gene.1052-1514 Vitamin E deficiency

is characterized by a dissociated ophthalmoplegia, and by nystagmus in which ad-

duction is fast but with a limited range and abduction is slow but with a full range.1510

These findings presumably reflect a mixture of central and peripheral pathology.

Wilson's disease, hepatolenticular degeneration, is an autosomal recessive, inherited disorder of copper metabolism. The defect is in a copper-transporting ATPase with the gene at q14.3 on chromosome 13. A CT typically shows hypodense areas, and PET scanning indicates a decreased rate of glucose metabolism in the globus pallidum and putamen.597 The classicclinical picture is a movement disorder with dysarthria, psychiatric symptoms and associated liver disease. Ocular motor disorders in Wilson's disease include a distractibility of gaze, with inability to voluntarily fix upon an object unless other, competing, visual stimuli are removed (e.g., fixation of a solitary light in an otherwise dark room).850 Slow vertical saccades have also been reported in one patient with Wilson's disease.770 A lid-opening apraxia has been noted.750 Using the magnetic search coil technique, we have measured the eye movements of a 19-year-old man who showed marked distractibilityof gaze but whose saccades were of normal velocity. The eye movements of Wilson's disease, therefore, show some similarities to those described in Huntington's disease and Alzheimer's disease. The distractibility in both conditions may be due to involvement of the inhibitory pathways from the basal ganglia to the superior colliculus, as discussed in Chap. 3.

EFFECTS OF DRUGS ON

EYEMOVEMENTS

Many drugs affect eye movements; Table 10-21 summarizes reports of effects of certain individual agents. Drugs taken in combination (e.g., anticonvulsants) can cause defects in ocular motility with relatively nontoxic blood levels.1371 For example, patients taking a combination of phenytoin and carbamazepine may complain of oscillopsia, which is due to sponta-

neous nystagmus, an inappropriate VOR, or diplopia.1134 Many drugs affect central vestibular and cerebellar connections and

cause ataxia and gaze-evoked nystagmus.1126

Although all classes of eye movements may be affected by therapeutic doses of various drugs, smooth pursuit, eccentric gaze holding, and convergence are particularly susceptible. So, for example, diazepam, methadone, phenytoin, barbiturates, chloral hydrate, and alcohol all impair smooth-pursuit tracking. However, some drugs have specific effects on ocular motility and thus have provided insights into both the function of the ocular motor system and the mode of drug action. For example, diazepam (a benzodiazepine) reduces saccadic peak velocity but does not impair accuracy, whereas methadone shows the converse effect. Diazepam reduces the gain of the VOR; in experimen-

tal animals the time constant is prolonged, but in humans it is reduced.1058

In toxic doses, all eye movements may be impaired by neuroactive drugs, particularly when consciousness is impaired. Phenytoin may cause a complete ophthalmoplegia in an awake patient, and therapeutic levels may cause ophthalmoplegia in patients in stupor.1171 Phenytoin and diazepam can lead to opsoclonus.345 The tricyclic antidepressants may cause complete, or internuclear, ophthalmoplegia in stuporous -patients. Lithium intoxication causes a variety of abnormalities, including fixation instability and downbeat nystagmus.462 In one patient, who prior to death showed marked impairment of all types of horizontal eye movements and downbeat nystagmus, neuronal loss was mainly confined to the nucleus prepositus hypoglossi and adjacent medial vestibular nuclei.295 Thus, the pathophysiology was similar to that produced by experimental lesions of these nuclei in monkeys:230 The neural integrator (gaze-holding network) was disrupted. The propensity of lithium to damage this area of the medulla has been attributed to the proximity to the choroid plexus of the fourth ventricle (and hence high local levels of lithium).295 Cerebellar damage may also occur after lithium intoxication.1232

Phenytoin

Carbamazepine

Phenobarbital and other barbiturates

Phenothiazines

Impaired smooth pursuit and VOR suppression136

Gaze-evoked nystagmus616-1143

Downbeat nystagmus121

Periodic alternating nystagmus228 Partial or total gaze palsy475

Convergence spasm563

Decreased velocity of saccades10143'1361 Impaired smooth pursuit334 Gaze-evoked nystagmus1134'1308'1408 Oculogyric crisis117

Downbeat nystagmus250

Partial or total gaze palsy978'1016

Reduced peak saccadic velocity1224'1361 Gaze-evoked nystagmus1129

Impaired smooth pursuit1224 Impaired vergence1475 Decreased VOR gain331 Internuclear ophthalmoplegia97 Perverted caloric responses1288

Vertical nystagmus855

Partial or total gaze palsy97'414

Oculogyric crisis830

Internuclear ophthalmoplegia291

In addition to drugs, certain toxins are

reported to affect eye movements. Some, such as chlordecone1359 and thallium,893

cause saccadic oscillations. Intoxication with hydrocarbons is reported to cause vestibulopathy,634'1056 and exposure to trichloroethylene and other solvents may affect pursuit, visual suppression of the

VOR, and saccades.974 Prolonged toluene abuse, especially in glue-sniffing addic-

tion, may lead to a variety of ocular motor disturbances, including pendular and downbeat nystagmus891'901 and saccadic oscillations.953

Tobacco and nicotine have a number of ocular motor effects. They cause upbeat nystagmus,1285'1286 impaired pursuit,1287 decrease in saccade latency,1162 and increased square-wave jerks during pursuit,1363 but with normal performance on

the antisaccade test.1163 Cocaine also can

affect eye movements. The most dramatic abnormality is opsoclonus.378'417'1225 A va-

riety of drugs are ototoxic, notably the aminoglycoside antibiotics. These are discussed under the section on Oscillopsia.

Finally, systematic study of the effects of new drugs on eye movements is likely to provide insights into the pharmacological substrate of the ocular motor system and lead to the development of novel treatments for abnormal eye movements that prevent clear vision.

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