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

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DIAGNOSIS OF NYSTAGMUS AND SACCADIC INTRUSIONS

The Nature and Visual Consequences of Abnormal Eye Movements that Prevent Steady Fixation

Clinical and Laboratory Methods for Evaluating Nystagmus and Saccadic Intrusions

A Pathophysiological Approach to the Diagnosis of Nystagmus

Nystagmus due to Vestibular Imbalance Periodic Alternating Nystagmus Seesaw and Hemi-seesaw Nystagmus

Nystagmus Occurring When the Eyes Are in Eccentric Gaze

Nystagmus Occurring in Association with Disease of the Visual System

Convergent-Divergent Forms of Nystagmus Congenital Forms of Nystagmus

Lid Nystagmus Saccadic Intrusions

TREATMENTS FOR NYSTAGMUS AND SACCADIC INTRUSIONS

Rational Basis for Therapy of Abnormal Eye Movements

Pharmacological Treatments ofAbnormal Eye Movements

Optical Treatments of Abnormal Eye Movements

Procedures to Weaken the Extraocular Muscles

Application of Somatosensory or Auditory Stimuli to Suppress Nystagmus

SKEW DEVIATION AND THE OCULAR

TILT REACTION(OTR)

Clinical Features of Skew Deviation and

OTR

Topologic Diagnosis of Skew Deviation and the OTR

DISEASE OF THE VESTIBULAR

PERIPHERY Vertigo and Dizziness

Clinical Features of Acute Peripheral Vestibulopathy

Acute Vertigo Recurrent Vertigo

Posturally-Induced Vertigo Treatment of Vertigo OSCILLOPSIA

Oscillopsia due to an Abnormal VOR Oscillopsia due to Paresis of Extraocular

Muscles

Oscillopsia due to Nystagmus and other Abnormal Eye Movements

OCULAR MOTOR SYNDROMES CAUSED BY LESIONSIN THE MEDULLA

Medullary Lesions Impairing GazeHolding Effects of Disease involving the Inferior

Olivary Nucleus

Effects of Disease Restricted to the Vestibular Nuclei

Wallenberg's Syndrome (Lateral Medullary Infarction)

OCULAR MOTOR SYNDROMESCAUSED BY DISEASE OF THE CEREBELLUM

Three Principal Cerebellar Syndromes Other Disorders of Eye Movements

Attributed to Cerebellar Disease

Developmental Anomalies of the Hindbrain and Cerebellum

Ocular Motor Findings in the Hereditary Ataxias

Cerebellar Infarction Cerebellar Mass Lesions

OCULAR MOTOR SYNDROMES CAUSED BY DISEASE OF THE PONS

Lesions of the Abducens Nucleus

Lesions of the Paramedian Pontine

Reticular Formation (PPRF)

Lesions of the Medial Longitudinal Fasciculus: Internuclear Ophthalmoplegia (INO)

Combined Unilateral Conjugate Gaze Palsy and INO: "One-and-a-half Syndrome" and Other Variants

Selective Cell Vulnerability in the Pons OCULAR MOTOR SYNDROMES CAUSED

BY LESIONS OF THE

MESENCEPHALON

Modern Concepts of Vertical Gaze Palsies Lesions of the riMLF and Vertical Saccadic

Palsy

Lesions of the Interstitial Nucleus of Cajal (INC)

Effects of Lesions of the Posterior Commissure and Nucleus of the Posterior Commissure

Clinical Manifestations of Other Mesencephalic Lesions

Selective Cell Vulnerability in the Mesencephalon

OCULAR MOTOR SYNDROMESCAUSED BY LESIONS IN THE SUPERIOR COLLICULUS

OCULAR MOTOR SYNDROMESCAUSED BY LESIONS IN THE DIENCEPHALON

Effects of Thalamic Lesions on Eye Movements

Effects of Pulvinar Lesions on Eye Movements

OCULAR MOTOR ABNORMALITIES AND DISEASE OF THE BASALGANGLIA Parkinson's Disease and Conditions Causing

Parkinsonism Huntington's Disease (HD)

Other Diseases of Basal Ganglia

OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN THE CEREBRAL HEMISPHERES

Disturbances of Gaze With Acute Hemispheric Lesions

Enduring Disturbances of Gaze Caused by Unilateral Hemispheric Lesions

Effects of Focal Hemispheric Lesions on Gaze

Ocular Motor Apraxia

Eye Movements During Epileptic Seizures ABNORMALITIES OF EYE MOVEMENTS

IN PATIENTS WITH DEMENTIA Alzheimer's Disease Creutzfeldt-Jakob Disease

AIDS and Dementia

EYE MOVEMENT DISORDERS IN

PSYCHIATRIC ILLNESSES

EYE MOVEMENTSIN STUPOR AND COMA Resting Position of the Eyes in Unconscious

Patients

Spontaneous Eye Movements in Unconscious Patients

Reflex Eye Movements in Unconscious Patients

OCULAR MOTOR DYSFUNCTION AND MULTIPLE SCLEROSIS

OCULAR MOTOR MANIFESTATIONS OF METABOLIC AND DEFICIENCY DISORDERS

EFFECTS OF DRUGS ON EYE MOVEMENTS

In this chapter, we describe the clinical features of central disorders of ocular motility, presenting video clips of the

more common conditions. In each case, we draw on the anatomic and physiologic

principles developed in previous chapters

to provide a pathophysiological explanation for the disorder. The reader should

be aware that, at the bedside, these pathophysiologic hypotheses may fall short of

explaining clinicalfindings. When they do so, we hope that they may encourage a reevaluation of the assumptions that are used in clinical diagnosis. The advantage

some prior interest, born of theory, is already awakened in the mind." First, we will discuss abnormal eye movements that occur during attempted fixation— nystagmus and saccadic intrusions. Then we will discuss disease of the vestibular periphery, skew deviation, vertigo, and oscillopsia. The rest of this chapter deals with

the topological diagnosis of eye movements caused by disease of the brain, starting at the medulla and progressing rostrally to cerebral cortex, with special mention given to certain multifocal disorders and the effects of drugs.

DIAGNOSIS OF NYSTAGMUS AND SACCADIC INTRUSIONS

The Nature and Visual

Consequences of Abnormal Eye

Movements That Prevent

Steady Fixation

A common clinical problem is the diagnosis of abnormal eye movements—often oscillations—that disrupt steady fixation. Such movements may interfere with vision. Recall the visual requirements of eye movements: To see an object best, its image must be held steadily over the foveal region of the retina. Excessive motion of images on the retina causes vision to decline and may lead to the illusion of motion of the seen world (oscillopsia). Furthermore, if the image of the object is moved away from the fovea to peripheral retina, it will be seen less clearly. Abnormal eye movements that prevent steady fixation are of two main types: pathological nystagmus* and saccadic intrusions. The essential difference between nystagmus and saccadic intrusions lies in the initial eye movement that takes the line of sight away from the object of regard. For nystagmus, it is a slow drift (or "slow-phase") as opposed to an inappropriate saccadic movement that intrudes on steady fixation. After the initial movement, corrective or other abnormal eye movements may follow. Thus, a definition of nystagmus is repetitive, to- and-fro movement of the eyes that is initiated by slow phases. Nystagmus may consist mainly of sinusoidal slow-phase oscillations (pendular nystagmus) or, more

*The word nystagmus derives from a comparison with nodding of the head (slow downward drift and sudden upward jerk) during drowsiness.

commonly, of an alternation of slow drift and corrective quick phase (jerk nystagmus). Although nystagmus is often described by the direction of its quick phases (e.g., downbeat nystagmus), it is the slow phase that reflects the underlying disorder. Saccadic intrusions are rapid movements that take the eye away from the target and comprise a spectrum ranging from single saccades to sustained saccadic oscillations.

Not all nystagmus is pathological. Normally, physiological nystagmus acts to preserve clear vision during self-rotation when the vestibulo-ocular and optokinetic responses prevent excessive slip of images on the retina and quick phases reset the eyes into their working range. Thus, both vestibular and optokinetic nystagmus act to hold retinal images steady. The opposite is true of pathologic nystagmus, which causes excessive drift of images of station-

ary objects on the retina and so degrades vision.3923

Clinical and Laboratory Methods

for Evaluating Nystagmus and

Saccadic Intrusions

HISTORY-TAKING IN PATIENTS WITH ABNORMAL EYE MOVEMENTS THAT

DISRUPT FIXATION

The diagnosis of nystagmus and saccadic intrusions is often possible on the basis of a careful history and systematic examination. Inquire about the duration of the nystagmus, whether it is accompanied by other neurologic symptoms, and whether it interferes with vision and causes oscillopsia. Determine if nystagmus or associated visual symptoms are worse when

worse on right gaze). Ask about "jumping eyes," strabismus, or eye operations since childhood. Document current medications. If the patient habitually tilts or turns the head, determine whether these findings are evident on old photographs.

EXAMINATION OF ABNORMAL

EYE MOVEMENTS THAT

DISRUPT FIXATION

Before examining eye movements, check the visual system (including color vision) looking for signs of optic nerve demyelination or malformation or ocular albinism, which often suggests the diagnosis. Then examine the stability of fixation with the eyes close to central position, viewing near or far targets, and at eccentric gaze angles. For each eye, note the planes in which the nystagmus occurs (horizontal, vertical, torsional, mixed). Compare the oscillations of each eye and note whether the direction or amplitude differs and whether there is an asynchrony (i.e., a phase shift between the two eyes), which may lead to movements that sometimes are in opposite directions. When the size of the oscillations differs in each eye, it is referred to as dissociated nystagmus. When the direction of the oscillations in each eye differs, it is called disconjugate nystagmus or disjunctive nystagmus. It is often useful to make a note of the direction and amplitude of nystagmus for each of the cardinal gaze positions. If the patient has a head turn or tilt, the eyes should be observed in various directions of gaze when the head is in that position as well as when the head is held straight. During fixation, occlude each eye in turn to check for latent nystagmus. Some nystagmus is intermittent and requires sustained observation over 2 to 3 minutes. Low amplitude nystagmus may only be detected while viewing the patient's retina with an ophthalmoscope.1526 (Note that the direction of horizontal or vertical nystagmus is inverted when viewed through the ophthalmoscope.)

Always examine the effect on nystagmus of removing fixation; nystagmus due to peripheral vestibular imbalance may only be apparent under these circumstances. Removal of fixation can be achieved by eyelid closure; nystagmus is then detected by recording eye movements, by observing movement of the corneal bulge, or by palpating the globes. Because lid closure itself may affect nystagmus, it is better to examine the effects of removing fixation

with the eyes open; two clinical methods are available. The first is to observe the nystagmus behind Frenzel goggles, which prevent fixation of objects and also provide the examiner with a magnified, illuminated view of the patient's eyes. The second technique consists of transiently covering the fixating eye during ophthalmoscopy in an otherwise dark room and noting the effects on retinal motion in the eye being viewed. Evaluation of nystagmus is incomplete without a systematic examination of each functional class of eye movements—vestibular, smooth-pursuit, saccades, and vergence (see Appendix A); selective defects may indicate the nature of the underlying disorder.

At the bedside, a complete description of nystagmus, separating it into horizontal, vertical, and torsional components, depends upon the coordinate system in which the observer couches his or her observations. This, in turn, may be influenced by the vantage point of the observer relative to the direction in which the patient is looking, i.e., the patient's line of sight, and also by the position of the eye of the patient in the orbit. Consider a patient with the head still who has a spontaneous jerk nystagmus that appears horizontal in the straight-ahead position of gaze, i.e., the eyes are rotating around the rostralcaudal (yaw) axis relative to the head. If the patient looks far up, and if the eyes continue to rotate around the same (yaw) axis relative to the head (which is typical for a nystagmus of vestibular origin), then the nystagmus would appear to have a developed a torsional component if the line of sight of the observer is moved upward to coincide with that of the eye of the patient. In this case, the observer, by moving the vantage point to match the axis along which the patient is looking, will be describing the nystagmus in an eye-fixed coordinate system. However, the nystagmus may still be rotating the eye around the same head-fixed (yaw) axis even though the nystagmus has acquired a torsional component. The nystagmus has appeared to change direction when described in an eye-fixed but not when described in a head-fixed coordinate system. If on upward gaze the nystagmus still appears

"horizontal" to the observer, when viewed in an eye-fixed coordinate system, the axis of rotation around which the eye was rotating, relative to the head, must have changed.T

Similar considerations apply to a central position vertical nystagmus, such as "downbeat" nystagmus, in which the eyes are rotating around the interaural (pitch) axis. If the patient looks far to the right, and if the nystagmus continues to rotate the eyes around the same (pitch) axis relative to head, then the nystagmus would appear to have a developed a torsional component if the nystagmus is described in an eye-fixed coordinate system. Again, the nystagmus may still be rotating the eye around the same head-fixed (pitch) axis, even though the nystagmus has acquired a torsional component. The nystagmus has appeared to change direction when described in an eye-fixed but not when described in a head-fixed coordinate system. However, if on lateral gaze the nystagmus still appears "vertical" to the observer, when viewed in an eye-fixed coordinate system, the axis of rotation around which the eye was rotating, relative to the head, must have moved. Of course, once cognizant of these frame-of-reference issues, the observer can perform the necessary mental transformation to determine the axis of rotation of nystagmus no matter what the direction of gaze of the patient or what the position of the examiner relative to the patient's line of sight. These distinctions about which axis the eye rotates when the eyes move eccentrically may be important in determine the etiology of nystagmus, since the axis of rotation of nystagmus of vestibular origin (peripheral or central) usually remains constant, no matter what the direction of gaze, in a head-fixed coordinate system, whereas other forms of central nystagmus may change their axis of rotation with the position of gaze.

tNote that when the eyes are directed straight ahead, the eye and head frames of reference coincide. One must examine the eyes in an eccentric rotation to determine the effect of eye position on the axis of rotation, and hence in what framework a particular nystagmus is organized.

MEASUREMENT OF ABNORMAL EYE MOVEMENTSTHAT DISRUPT FIXATION

It is often helpful to measure the abnormal eye movements because analysis of their dynamic properties will usually identify the nature of the oscillation. First, measurements will differentiate between nystagmus and saccadic intrusions, which may be difficult to do on a clinical basis. Second, characterization of the nystagmus waveform—especially the slow phase (Fig. 10-1)—often provides a pathophysiological "signature" of the underlying disorder. Conventionally, nystagmus is measured in terms of its amplitude and frequency and their product—intensity. However, the visual symptoms due to nystagmus usually correlate best with the speed of the slow phase and the displacement from the

fovea of the image of the object of re-

gard.235'827'836

Although many different methods for

recording eye movements are now available (Appendix B),236-396'437 the best ap-

proach for patients with nystagmus is the magnetic search coil technique (see Fig. 1-1, Chap. 1). This method is preferable because many patients with ocular oscillations cannot accurately point their eyes at visual targets to allow a reliable calibration; however, the contact lens that the patient wears can be precalibrated on a protractor device. Furthermore, this is the only technique that allows precise measurement of horizontal, vertical, and torsional oscillations over an extended range of amplitudes and frequencies. Although originally introduced as a research tool, the technique is now widely used to evaluate clinical disorders of eye movements; we have studied over 500 patients with this method.

A Pathophysiological Approach to the Diagnosis of Nystagmus

Although nystagmus can be classified using descriptive features, our approach will be to identify the pathophysiology of the underlying disorder and therefore the etiology of the oscillation. In health, three