Oculomotor Apraxia Definition

Oculomotor apraxia describes an eye movement disorder characterized by loss of or severely diminished volitional saccades with retention of the fast phases of vestibular nystagmus. Reflexive saccades stimulated by objects of interest in the peripheral visual field may be disordered or normal.

Congenital oculomotor apraxia (Cogan's syndrome) manifests in newborn infants. During the first 3 months of life, affected infants are unable to look toward objects held out to them, and may be mistakenly thought of as blind. In the following months of development, instead of normal changes in gaze position, a compensating strategy evolves. Thrusting movements of the head in the direction of interest are used to bring the eyes into alignment with the object of interest. Since VOR movements largely negate the movement of the eyes with head turn, the child must turn the head well beyond the point of interest, allowing the limits of duction movements to finally position the eyes as desired. In the second phase, with the eyes having taken up fixation, visual pursuit and VOR inputs serve to keep the eye fixed on the object, while the head is then able to return to the midposition. Congenital oculomotor apraxia gradually disappears during the first two decades of life. In adulthood, many of these patients require only a small head movement to serve as a "trigger" that initiates a refixation saccade.

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Congenital oculomotor apraxia affects only horizontal eye movements. Rare acquired forms of oculomotor apraxia develop in the setting of severe cerebral disease, and these cases have impairment of both horizontal and vertical saccadic movements.

It is not known where the damage responsible for oculomotor apraxia is located. The PPRF can be excluded as the site of the lesion, since vestibular stimuli elicit fast phases of nystagmus in such patients.

Gaze-Evoked Nystagmus Definition

Gaze-evoked nystagmus is the result of a gaze-holding deficit. The eyes can indeed be moved into an eccentric position by saccades or by the VOR. However, they cannot be held in the eccentric position. Instead, they drift back toward the midline and must be redirected repeatedly toward the object of regard. This gaze-evoked nystagmus can be so pronounced that the eyes return all the way to the midline during the slow phase of the nystagmus. The drift is at first quick but then slows gradually as the eyes approach the midline.

The structures responsible for fixation maintenance are widely dispersed in the brainstem (particularly in the nucleus prepositus hypoglossi) and in the cerebellum. Thus, gaze-evoked nystagmus tells the examiner very little about the location of a lesion.

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Gaze-evoked nystagmus should cause the physician to ask whether tranquilizer or antiseizure medications are being used. Only when drug effects have been ruled out should the workup proceed in a search for disease in the cerebellum and/or brainstem.

Endpoint nystagmus refers to a minor gaze-holding deficit that should not be regarded as clinically important. Endpoint nystagmus appears only beyond a gaze eccentricity of about 35°.

Saccadic Dysmetria Definition

Refixation saccades are considered dysmetric when they consistently over- or undershoot their intended target. This leads to small corrective saccades before the target is properly centered in the visual field. Saccades that fall short of the mark are said to by hypometric, while those that move past the target and then double back are hypermetric.

Testing for dysmetria is best done with the method illustrated in ■ Fig. 11.3.

Hypometric saccades are not necessarily pathological; they can be the product of inattention or poor cooperation. Hypermetric saccades on the contrary are always pathological and strongly suggest the presence of a lesion in the cerebellar vermis.

Dysmetria caused by Wallenberg syndrome (infarction of the lateral medulla) on the left side will produce the following findings: saccadic movements to the left are hyper-metric, whereas those to the right are hypometric. Upward saccades veer to the left, and downward saccades veer to the left. This so-called saccadic lateropulsion can be understood as the result of an ipsilesional impulse added to each saccade (■ Fig. 11.6).

Apraxia Definition

Fig. 11.6. Saccadic lateropulsion to the left following a left side infarct of the lateral medulla (Wallenberg syndrome). The intended target of the movement is reached only with the help of several corrective, hypometric saccades. a Hypermetria to the left with corrective hypometric saccades to the right. b Hypometria to the right. c Leftward diversion (lateropulsion) of upward saccade followed by hypometric corrective saccades up and to the right. d Leftward diversion of downward saccade followed by hypomet-ric corrective saccades down and to the right

Fig. 11.6. Saccadic lateropulsion to the left following a left side infarct of the lateral medulla (Wallenberg syndrome). The intended target of the movement is reached only with the help of several corrective, hypometric saccades. a Hypermetria to the left with corrective hypometric saccades to the right. b Hypometria to the right. c Leftward diversion (lateropulsion) of upward saccade followed by hypometric corrective saccades up and to the right. d Leftward diversion of downward saccade followed by hypomet-ric corrective saccades down and to the right

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  • Sinit
    How to help babies with oculomotor apraxia?
    8 years ago
  • keith
    What is ocular apraxia?
    3 years ago

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