Neuro-ophthalmology

Published on 08/03/2015 by admin

Filed under Opthalmology

Last modified 08/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 5147 times

19 Neuro-ophthalmology

OCULAR MOVEMENT

Signals that control ocular movement are initiated in the cerebral hemispheres in a manner analogous to other motor neuronal pathways. They are then transmitted to the gaze centres and ocular motor nuclei in the midbrain and pons and leave the brain in the third, fourth and sixth cranial nerves. Supranuclear neuronal pathways conduct impulses to the gaze centres internuclear pathways coordinate the gaze centres with the ocular motor nuclei and the infranuclear pathways are the individual ocular motor nerves. A great deal is known about the organization of horizontal gaze control in the pons but less is known about the midbrain mechanisms subserving vertical and torsional ocular movements. Still less is known about the cortical areas involved in ocular motor control but in recent years considerable advances have been made. Horizontal and vertical conjugate eye movements (i.e. movements of both eyes as a yoked pair and mediated through supranuclear neuronal pathways) can be divided into saccadic, pursuit and vestibular movements, each of which has its own velocity and control characteristics. Torsional mechanisms are active during conjugate eye movements to prevent unwanted torsional movements genuine torsional movements are seen mostly as ocular counter-rolling during head tilt. These movements are conjugate in the sense that as one eye intorts the other extorts but the associated vertical movements are disconjugate as the intorting eye elevates and the extorting eye depresses.

SUPRANUCLEAR GAZE CONTROL

Saccadic movements are rapid and relocate fixation of gaze, either reflexly or voluntarily. They are initiated in the contralateral premotor frontal cortex and, once initiated, the movement is irrevocable and ocular position cannot again be modified until the saccade has been completed. A saccade occurs after a latent period of about 200 ms following initiation and has a high velocity of up to 700°/sec. Saccades are tested clinically by instructing the patient to look first at one stationary target and then at another, or to look right and left or up and down with no target present (see Fig. 19.4).

Pursuit movements are slower and are concerned with keeping the target at the fovea. They appear to be generated in the ipsilateral occipital cortex but little is known about the supranuclear pathway. Pursuit movements have a latency of about 125 ms from initiation and a maximum velocity of less than 50°/sec. The movement is smooth and modified continuously according to the speed of the target if the pursuit movement lags behind the target position a corrective saccade is inserted to keep up. Pursuit movements are tested by asking the patient to follow a slowly moving target. It is of great importance that the target is clearly visible and that it is not moved too fast (see Fig. 19.5).

Vestibular ocular movements are initiated in the semicircular canals by head movements. They serve to maintain gaze direction in space independently of head, neck and body movements and have similar characteristics to pursuit movements, except that they can reach much higher velocities. The vestibular ocular reflexes (VOR) keep the horizon steady as we walk (our head bobs up and down, the eyes moving in the opposite direction to that of the head). In some circumstances this reflex has to be suppressed as it would be impossible otherwise to follow a target in space while the head is moving (e.g. to read on a train). In most situations we make a combination of eye movements directed to the target, head movements that are similarly directed, and vestibular ocular movements that compensate for any movements of the head that are not determined by the motion of the target.

Vestibular ocular movements may be tested by a ‘doll’s head’ manoeuvre, in which the patient is asked to fixate on a target while the examiner rotates the patient’s head (see Fig. 19.6). The doll’s head manoeuvre tests both the left and right labyrinths and may be normal even if one labyrinth is totally nonfunctioning. To test each labyrinth separately, caloric stimulation can be employed which induces nystagmus by syringing the external auditory meatus with cold or warm water. Recently a bedside test has been described, based on the observation that the initial component of a rapid head rotation depends upon the integrity of the labyrinth towards which the head is turned (see Fig. 19.8).

Vergence movements are disconjugate and, although a centre for convergence has been identified with reasonable certainty, it is still not known whether a centre for divergence as such exists. Vergence is tested by asking the subject to follow an approaching target. Each type of conjugate movement should be examined in both the horizontal and vertical axis. Precise recording of ocular movement by electro-oculographic or infrared techniques has contributed enormously to the understanding of the physiology of ocular movements but careful examination of ocular motility can supply all the information needed to make a clinical diagnosis. Clinically dysfunction of the horizontal and vertical gaze systems is frequently dissociated. It is helpful to examine each type of movement in turn, in each axis, to decide whether the problem involves either the horizontal or the vertical gaze control or both systems. Most diseases disrupt saccadic and pursuit movements initially with doll’s head movements being preserved until relatively late in the course of the disease. An exception is vestibular failure (such as that following the use of ototoxic drugs, e.g. streptomycin) where the vestibular ocular reflex is selectively lost.

During examination of ocular movements it is important to note whether the patient can hold a steady gaze in the primary or eccentric positions (stability of fixation) and also the presence and type of nystagmus, or spontaneous movements, in any position of gaze.

image

Fig. 19.8 Only one functioning labyrinth is required for the tests described in Fig. 19.6 to be normal. Caloric testing can be used to examine each labyrinth separately. Caloric reflexes are produced by stimulating the semicircular canals and vestibular nuclei with warm or cold water and can provide useful information on the integrity of these pathways in the brainstem; this is especially useful in the neurological assessment of brainstem damage in an unconscious patient. In a conscious patient cold water in the external auditory meatus generates a nystagmus of both eyes with a fast phase to the opposite side but in unconscious patients the saccadic phase is lost and a tonic deviation to the same side is seen. This indicates an intact pons but the results must be interpreted with caution after acute drug overdoses when false-negative responses may be seen. Calorics can be adapted to test vertical gaze (and therefore the integrity of the midbrain) by syringing both ears.

ANATOMY OF THE OCULAR MOTOR PATHWAYS

CONJUGATE GAZE PALSIES

HORIZONTAL SUPRANUCLEAR PALSY

A horizontal gaze palsy results in an inability to make a conjugate ocular movement to one side and may result from a supranuclear or pontine lesion. These can be distinguished from each other by using ‘doll’s head’ or caloric stimuli; the ability to stimulate lateral gaze with these tests depends on the integrity of the pontine pathways and is preserved in the presence of a supranuclear lesion.

image

Fig. 19.20 A CT scan of the patient seen in Fig. 19.18, showing a large infarct in the internal capsule due to the occlusion of middle cerebral artery branches, corresponding to lesion 1 in Fig. 19.21. If the patient survives the acute ocular deviation recovers rapidly. Horizontal gaze becomes full and saccades return to normal. This is probably due to a restoration of control mechanisms by the superior colliculus.

VERTICAL GAZE PALSY

Vertical gaze palsies are caused by lesions in the area of the upper midbrain and are less common. They produce a characteristic triad of signs known as Parinaud’s syndrome or the dorsal midbrain syndrome: loss of vertical gaze and the pupillary light reflex with preservation of the near reflex and the bizarre movement abnormality known as convergence retraction nystagmus. Vertical gaze is controlled from a centre in the posterior commissure which integrates vertical gaze; there is a downgaze centre caudal to the thalamus but isolated lesions of this area are exceptionally rare. Most vertical gaze palsies affect both upgaze and downgaze although small or early lesions in the region of the posterior commissure tend to affect upgaze preferentially; early lesions affect saccades only with preservation of pursuit and oculocephalic (doll’s head) movements. Lesions compressing the midbrain may also obstruct the aqueduct producing hydrocephalus and often papilloedema; lateral extension may involve the optic radiations and posterior extension produces ataxia from cerebellar compression. Although tumours of the pineal gland are the most common cause of Parinaud’s syndrome, atherosclerosis, embolism, vasculitis, demyelination or arteriovenous malformations may occasionally be the causal factor.