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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.

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. this makes sense: the left half of the brain “sees” space on the right side. but there may be an intermediate stage where they are unable to move the eyes away from the lesion on command. 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. Lesions of the occipital centre for lateral conjugate gaze are less common than lesions of the frontal centre for lateral conjugate gaze.LATERAL CONJUGATE GAZE 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 patient looks towards the lesion and away from the paralyzed side This conjugate deviation occurs only in the acute phase of an infarct. you can assess the occipital lobe centre by having them fixate on an immobile object while you move their head. as in a cerebral infarct. but may be able to follow an object to the left. such as a finger. as well as eye movements to the right side. 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. Eventually the patient will recover. If the patient is unable to follow a moving object. The frontal lobe centres for lateral conjugate gaze lie in the posterior aspect of the frontal lobes. 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. If one frontal lobe centre is destroyed. the tonic impulses from the opposite frontal lobe cause a deviation of the eyes towards the side of the lesion. Teleologically. yet able to follow an object to the opposite side. therefore the left side of the brain controls movements of the right arm and leg. physical diagnosis .

Where are the brainstem centres for lateral conjugate gaze? What do they do? The brainstem centres for lateral conjugate gaze are in the pons. and the right pontine centre controls lateral conjugate eye movement to the right. If you are assessing an unconscious patient with conjugate lateral deviation of the eyes. as often occurs with a stroke. the eyes deviate towards the side of the lesion and away from the paralyzed side. Thus. and the left frontal centre with the right pontine centre. and the eyes may deviate towards the epileptogenic focus. Direction of eye deviation. the centre is exhausted. If the frontal lobe centre for conjugate gaze is destroyed. 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. Postictally. the patient’s eyes will deviate to the opposite side. 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. 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 right frontal centre connects with the left pontine centre.The left pontine centre controls lateral conjugate eye movement to the left. . very close to the sixth nerve nuclei. Recovery of conjugate gaze after a brainstem lesion is unusual. 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 eyes will deviate towards the paralyzed side and away from the lesion. (The patient will look away from the lesion and look at the convulsing limbs).Eye positions with destruction of one frontal lobe centre for lateral conjugate gaze.

Turn the patient’s head rapidly in the direction of the gaze deviation. is a disorder with many similarities . What is progressive supranuclear palsy? Progressive supranuclear palsy. parkinson’s disease 3. no perforation of the drum and no possibility of cervical spine injury. the lesion is in the hemisphere. With an acute unilateral cerebellar lesion. Cold calorics. or Steele-Richardson-Olszewski syndrome. the lesion is not in the brainstem. Doll’s eye test. If the brainstem is intact. If the eyes deviate towards the irrigated side. progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome). Doll’s eye movements and cold calorics may show no response. the tonic impulses from the opposite side cause the eyes to deviate towards the irrigated side. Cold calorics have the effect of temporarily inhibiting the neuronal output of the vestibular system on the irrigated side. the eyes may deviate to the opposite side. If there is no blood in the ear canal. 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 coma is due to drug intoxication or hypothermia. VERTICAL CONJUGATE GAZE What conditions may result in diminished upward conjugate gaze? Conditions leading to diminished upward conjugate gaze include the following: 1 old age 2.2. NB. If the eyes turn to the opposite side. 3. flex the supine patient’s head by 30 degrees to get the horizontal semicircular canal vertical. there are cerebellar centres. Are there other centres for lateral conjugate gaze? Yes.

have the patient close the eyes and then lift up one of the lids with your finger. It may be seen in the Steele-Richardson-Olszewski syndrome and in some rare disorders of the midbrain. Because of this inability to move the eyes.To observe Bell’s phenomenon. even when there is absent voluntary upward gaze. 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.A major function of the medial longitudinal fasciculus is to control adduction of the ipsilateral eye (through contraction of the medial rectus). Interruption of a medial longitudinal fasciculus prevents adduction of the eye on the side of the lesion. 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. How common is a loss of downward conjugate gaze? Loss of downward conjugate gaze is uncommon. but with progressive loss of upward and downward conjugate gaze. In spite of not being able to voluntarily adduct the right eye. since convergence is mediated by another pathway. Each connects the ipsilateral third nerve nucleus with the contralateral pontine centre for lateral conjugate gaze. MEDIAL LONGITUDINAL FASCICULUS SYNDROME (INTERNUCLEAR OPHTHALMOPLEGIA) 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. and later. . there will be a coarse and short-lived nystagmus of the abducting left eye.to Parkinson’s disease. patients often complain of difficulty in reading. In addition.This combination of signs is called the medial longitudinal fasciculus syndrome or internuclear ophthalmoplegia. lateral conjugate gaze. the eye will adduct in response to convergence. .

In addition. Pursuit movements. PPRF AND 6TH NERVE NUCLEII VERTICAL GAZE CENTRE: riMLF( junction of midbrain and thalamus) and Interstitial nucleus of Cajal . What is Wernicke’s encephalopathy? Wernicke’s encephalopathy is a central nervous system syndrome (DM Thalamus most involved) caused by thiamin deficiency. Paresis of one or both lateral recti is frequent. Ocular movements Saccadic movements.What happens if both medial longitudinal fasciculi are interrupted? If both medial longitudinal fasciculi are interrupted. and complete ophthalmoplegia may occur. the patients usually suffer from ataxia and a confusional state. It occurs on the basis of nutritional deficiency in times of famine. The fibres then descend and terminate in the ipsilateral horizontal gaze centre in the PPRF. HORIZONTAL GAZE CENTRE. Controlled by the ipsilateral parieto-occiptal cortex with floculonodular input. What diseases commonly lead to internuclear ophthalmoplegia? The two diseases most commonly associated with internuclear ophthalmoplegia are multiple sclerosis and Wernicke’s encephalopathy.slow involuntary movements to keep the eyes on a moving object. There are a variety of disorders of conjugate gaze and nystagmus in most directions of gaze.rapid voluntary movements to search a visual field. one of the common ones being internuclear ophthalmoplegia. The syndrome consists of a variety of ocular movement disorders. The pathway originates in the peristriate cortex of the occipital motor area. neither eye can adduct and there will be nystagmus of the leading abducting eye on each side. Controlled by area 8 of the middle frontal gyrus to initiate contralateral eye deviation. but in the developed world it is usually secondary to alcoholism. The right occipital lobe therefore controls pursuits to the right and the left occiptal lobe controls those to the left.

characterized by defective adduction of the ipsilateral eye and ataxic nystagmus of the contralateral abducting 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.Horizontal eye movements are generated from the horizontal gaze centre in the PPRF. 3. although selective paralysis of up-gaze may occur in spite of this. sparing the vestibulo-ocular reflex. To adduct the contralateral eye. which also receives independent descending input from the vergence control centres. Loss of normal horizontal eye movements occurs when the PPRF is disrupted as follows. Lesions affecting both the PPRF and the MLF on the same side give rise to the ‘one-and-a-half syndrome’. Anatomical pathway of medial longitudinal bundle. 1. 2. Stimulation of the PPRF on one side therefore causes a conjugate movement of the eyes to the same side. Lesions of the MLF are responsible for the clinical syndrome of internuclear ophthalmoplegia (INO). . impulses pass to the subnuclei of the eye muscles controlling vertical gaze in both eyes. 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. characterized by loss of horizontal movement of the ipsilateral eye and no adduction of the contralateral eye. Up-gaze palsy is typically caused by lesions involving the posterior commissure and characteristically occurs in Parinaud’s dorsal mid-brain syndrome. Convergence of the two eyes is usually normal. Cells mediating upward and downward eye movements are intermingled in the vertical gaze centre. From here the output is to the ipsilateral sixth nerve nucleus to abduct the ipsilateral eye. Lesions of the PPRF give rise to ipsilateral horizontal gaze palsies. From each vertical gaze centre.

If the purkinje’s inhibitory input is removed. back to the side of origin of FEF activation. projections directly innervate the lateral rectus (ipsilateral to the PPRF). the horizontal yoke pair. Stimulation of superior colliculus and frontal lobe causes eye deviation to opposite side. the medial vestibular nucleus causes eye deviation to opposite side. Cerebellar control. the medial and lateral recti. According to Herring's law. via the MLF.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. and then innervates the paramedian pontine reticular formation (PPRF). decussates to the opposite side at the midbrain-pontine junction. innervates the medial rectus subnucleus of cranial nerve III and then neurons here project to innervate the medial rectus muscle.The floculonodular lobe and vermis project to the vestibular nucleii to the contralateral 6th and MLF and 3rd and 4th. which projects through the anterior limb of the internal capsule. The right FEF command to trigger a saccade culminates in conjugate eye movements to the left. From there. . 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. are activated in synchrony. A second decussation. The particular pathway shown emanates from the frontal eye field (FEF).

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