Clinical Examination

Viva Practice

Important papers


Operative Techniques



What does the term conjugate gaze mean?
Conjugate gaze refers to the eyes working in unison. A disorder of conjugate gaze means that patients are unable to look in certain directions with both eyes, such as upward, downward or laterally. Patients with conjugate gaze disorders are usually unaware of having any visual defects.They do not have diplopia.

Where are the cortical centres for lateral conjugate gaze?
Centres for lateral conjugate gaze are found in the frontal lobe cortices
and in the occipital lobe cortices. The frontal lobe centres for lateral conjugate gaze lie in the posterior aspect of the frontal lobes. They are quite close to the motor cortex and that is why conjugate deviation of the eyes is seen in a number of paralytic strokes.

What is the function of the frontal lobe centres for lateral conjugate gaze? What happens when if one is destroyed?
The frontal lobe centres for lateral conjugate gaze control voluntary conjugate eye movements to the opposite side. Teleologically, this makes sense: the left half of the brain “sees” space on the right side, therefore the left side of the brain controls movements of the right arm and leg, as well as eye movements to the right side.
If one frontal lobe centre is destroyed, as in a cerebral infarct, the tonic impulses from the opposite frontal lobe cause a deviation of the eyes towards the side of the lesion. The patient looks towards the lesion and away from the paralyzed side
This conjugate deviation occurs only in the acute phase of an infarct. Eventually the patient will recover, but there may be an intermediate stage where they are unable to move the eyes away from the lesion on command, yet able to follow an object to the opposite side. What are the functions of the occipital lobe centres for lateral
gaze? The occipital lobe centres for lateral gaze control the ability of the eyes to follow an object to the opposite
side. Thus, a patient with destruction of the right frontal centre but with an intact right occipital lobe centre
cannot look to the left on command, but may be able to follow an object to the left. If the patient is unable to
follow a moving object, such as a finger, you can assess the occipital lobe centre by having them fixate on an
immobile object while you move their head. Lesions of the occipital centre for lateral conjugate gaze are less common than lesions of the frontal centre for lateral conjugate gaze.

physical diagnosis
Eye positions with destruction of one frontal lobe centre for lateral conjugate gaze. If the frontal lobe centre for conjugate gaze is destroyed, as often occurs with a stroke, the eyes deviate towards the side of the lesion and away from the paralyzed side.

What happens when a frontal lobe centre for lateral conjugate gaze is the site of an epileptogenic focus?
With an epileptogenic focus in the frontal lobe, the patient’s eyes will deviate to the opposite side. (The
patient will look away from the lesion and look at the convulsing limbs). Postictally, the centre is exhausted, and the eyes may deviate towards the epileptogenic focus.

Where are the brainstem centres for lateral conjugate gaze?
What do they do?

The brainstem centres for lateral conjugate gaze are in the pons, very close to the sixth nerve nuclei.The
right frontal centre connects with the left pontine centre, and the left frontal centre with the right pontine
centre.The left pontine centre controls lateral conjugate eye movement to the left, and the right pontine centre
controls lateral conjugate eye movement to the right. Thus, a patient who has a destruction of one pontine centre will look away from the lesion and towards the paralyzed side because of the unopposed action of the opposite pontine centre. Recovery of conjugate gaze after a brainstem lesion is unusual.

If you are assessing an unconscious patient with conjugate lateral deviation of the eyes, how do you determine
whether the lesion is in the cortex or in the brainstem?
The following examinations should help you determine the site of the lesion:
1. Direction of eye deviation. A patient with a concomitant hemiparesis will be looking away from the paralyzed side and towards the lesion if the lesion is in the cortex.
If the lesion is in the pons, the eyes will deviate towards the paralyzed side and away from the lesion.
2. Doll’s eye test.Turn the patient’s head rapidly in the direction of the gaze deviation. If the eyes turn to the opposite side, the lesion is in the hemisphere.
3. Cold calorics. If there is no blood in the ear canal, no perforation of the drum and no possibility of cervical
spine injury, flex the supine patient’s head by 30 degrees to get the horizontal semicircular canal vertical, and irrigate the ear canal on the opposite side from the deviated eyes with 20 mL of cold tap water over 20-30 seconds. If the eyes deviate towards the irrigated side, the lesion is not in the brainstem.
Cold calorics have the effect of temporarily inhibiting the neuronal output of the vestibular system on the irrigated side. If the brainstem is intact, the tonic impulses from the  opposite side cause the eyes to deviate towards the irrigated side.
NB. If coma is due to drug intoxication or hypothermia, Doll’s eye movements and cold calorics may show no response.

Are there other centres for lateral conjugate gaze?
Yes, there are cerebellar centres.
With an acute unilateral cerebellar lesion, the eyes may deviate to the opposite side.
What conditions may result in diminished upward conjugate gaze?
Conditions leading to diminished upward conjugate gaze include the following:
1 old age
2. parkinson’s disease
3. progressive supranuclear palsy
(Steele-Richardson-Olszewski syndrome).

What is progressive supranuclear palsy?
Progressive supranuclear palsy, or Steele-Richardson-Olszewski syndrome, is a disorder with many similarities
to Parkinson’s disease, but with progressive loss of upward and downward conjugate gaze, and later, lateral conjugate gaze. Because of this inability to move the eyes, patients often complain of difficulty in reading.

What is Bell’s phenomenon?
Bell’s phenomenon is the upward and lateral deviation of the eyes that normally occurs when the eyes are closed  Bell’s phenomenon may be present in patients with Parkinson’s disease or progressive supranuclear palsy, even
when there is absent voluntary upward gaze.To observe Bell’s phenomenon, have the patient close the eyes and then lift up one of the lids with your finger.

How common is a loss of downward conjugate gaze?
Loss of downward conjugate gaze is uncommon. It may be seen in the Steele-Richardson-Olszewski syndrome
and in some rare disorders of the midbrain.

What is the medial longitudinal fasciculus and what does it do?
The medial longitudinal fasciculi are paired tracts of nerve fibres coursing through the brainstem. Each connects
the ipsilateral third nerve nucleus with the contralateral pontine centre for lateral conjugate gaze.  Interruption of a medial longitudinal fasciculus prevents adduction of the eye on the side of the lesion.
.A major function of the medial longitudinal fasciculus is to control adduction of the ipsilateral eye (through contraction of the medial rectus).
What happens if one medial longitudinal fasciculus is interrupted?
Interruption of the right medial longitudinal fasciculus will result in failure of voluntary adduction of the right eye when the patient tries to look to the left. In addition, there will be a coarse and short-lived nystagmus of the abducting left eye. In spite of not being able to voluntarily adduct the right eye, the eye will adduct in response to convergence, since convergence is mediated by another pathway.This combination of signs is called the medial longitudinal fasciculus syndrome or internuclear ophthalmoplegia.
What happens if both medial longitudinal fasciculi are interrupted?
If both medial longitudinal fasciculi are interrupted, neither eye can adduct and there will be nystagmus of the leading abducting eye on each side.

What diseases commonly lead to internuclear ophthalmoplegia?
The two diseases most commonly associated with internuclear ophthalmoplegia are multiple sclerosis and Wernicke’s encephalopathy.

What is Wernicke’s encephalopathy?
Wernicke’s encephalopathy is a central nervous system syndrome (DM Thalamus most involved) caused by thiamin deficiency. It occurs on the basis of nutritional deficiency in times of famine, but in the developed world it is usually secondary to alcoholism. The syndrome consists of a variety of ocular movement disorders, one of the common ones being internuclear ophthalmoplegia. Paresis of one or both lateral recti is frequent, and complete ophthalmoplegia may occur. There are a variety of disorders of conjugate gaze and nystagmus in most directions of gaze. In addition, the patients usually suffer from ataxia and a confusional state.

Ocular movements
Saccadic movements- rapid voluntary  movements to search a visual field. Controlled by area 8 of the middle frontal gyrus to initiate contralateral eye deviation.

Pursuit movements- slow involuntary movements to keep the eyes on a moving object. Controlled by the ipsilateral parieto-occiptal cortex with floculonodular input. The pathway originates in the peristriate cortex of the occipital motor area. The fibres then descend and terminate in the ipsilateral horizontal gaze centre in the PPRF. The right occipital lobe therefore controls pursuits to the right and the left occiptal lobe controls  those to the left.


VERTICAL GAZE CENTRE: riMLF( junction of midbrain and thalamus) and Interstitial nucleus of Cajal

Horizontal eye movements are generated from the horizontal gaze centre in the PPRF. From here the output is to the ipsilateral sixth nerve nucleus to abduct the ipsilateral eye. To adduct the contralateral eye, fibres from the PPRF also cross the pons and pass up the medial longitudinal fasciculus (MLF) to the contralateral medial rectus nucleus in the third nerve complex, which also receives independent descending input from the vergence control centres. Anatomical pathway of medial longitudinal bundle.

Stimulation of the PPRF on one side therefore causes a conjugate movement of the eyes to the same side. Loss of normal horizontal eye movements occurs when the PPRF is disrupted as follows.

1.       Lesions of the PPRF give rise to ipsilateral horizontal gaze palsies, sparing the vestibulo-ocular reflex.

2.       Lesions of the MLF are responsible for the clinical syndrome of internuclear ophthalmoplegia (INO), characterized by defective adduction of the ipsilateral eye and ataxic nystagmus of the contralateral abducting eye. Convergence of the two eyes is usually normal.

3.       Lesions affecting both the PPRF  and the MLF on the same side give rise to the ‘one-and-a-half syndrome’, characterized by loss of horizontal movement of the ipsilateral eye and no adduction of the contralateral eye.

Vertical eye movements:

Vertical eye movements are generated from the vertical gaze centre known as the rostral interstitial nucleus of the MLF which lies in the mid-brain just posterior to the red nucleus. From each vertical gaze centre, impulses pass to the subnuclei of the eye muscles controlling vertical gaze in both eyes. Cells mediating upward and downward eye movements are intermingled in the vertical gaze centre, although selective paralysis of up-gaze may occur in spite of this.

Up-gaze palsy is typically caused by lesions involving the posterior commissure and characteristically occurs in Parinaud’s dorsal mid-brain syndrome.

Down –gaze palsy is less common and occurs when both sides of the mid-brain tegmentum posterior to the red nucleus are damaged. Causes include cerebrovascular disease and Parkinson’s disease.

Cerebellar control- The floculonodular lobe and vermis project to the vestibular nucleii to the contralateral 6th and MLF and 3rd and 4th. If the purkinje’s inhibitory input is removed, the medial vestibular nucleus causes eye deviation to opposite side.

Stimulation of superior colliculus and frontal lobe causes eye deviation to opposite side.

Details of the descending projection involved in the volitional control of horizontal saccadic eye movements


Excitatory pathways are shown in orange and the reciprocal inhibitory pathways are shown in blue. The particular pathway shown emanates from the frontal eye field (FEF), which projects through the anterior limb of the internal capsule, decussates to the opposite side at the midbrain-pontine junction, and then innervates the paramedian pontine reticular formation (PPRF). From there, projections directly innervate the lateral rectus (ipsilateral to the PPRF). A second decussation, back to the side of origin of FEF activation, via the MLF, innervates the medial rectus subnucleus of cranial nerve III and then neurons here project to innervate the medial rectus muscle. The right FEF command to trigger a saccade culminates in conjugate eye movements to the left. According to Herring's law, the horizontal yoke pair, the medial and lateral recti, are activated in synchrony.