Supranuclear oculomotor disorders

Conjugate eye movements

Conjugate eye movements are binocular movements in which the eyes move synchronously and symmetrically in the same direction. There are 3 main types of movements: saccadic, smooth searching, non-optical reflex. Saccadic and searching movements are controlled at the brainstem and brainstem levels. Supranuclear disorders cause gaze paresis characterized by the absence of diplopia and normal vestibulo-ocular reflexes (e.g., oculocephalic movements and thermal stimulation).

Saccadic movements

Saccadic (jerky, intermittent) movements are based on the rapid placement of an object on the fovea or the movement of the eyes from one object to another. This can be done voluntarily or reflexively, which is initiated by the appearance of an object on the periphery of the visual field. Voluntary saccades are similar to the artillery system in the speed of localization of a moving object.

The horizontal saccade pathway begins in the premotor cortex (frontal eye fields). From there, fibers pass to the contralateral horizontal eye movement center in the brainstem paramedian reticular formation, so that each frontal lobe initiates contralateral saccades. Irritant lesions may cause contralateral eye deviation.

Smooth search movements

During search movements, fixation is maintained on an object localized by the saccadic system. The stimulus is the movement of the image near the fovea. The movements are slow and smooth.

The pathway begins in the peristriate cortex of the occipital lobe. The fibers terminate in the ipsilateral horizontal eye movement center in the SMRF. Accordingly, each occipital lobe controls search on the ipsilateral side.

Non-optical reflexes

The function of non-optical (vestibular) reflexes is to maintain the position of the eye when the position of the head and body changes.

The pathway begins with the labyrinths and proprioceptors of the cervical muscles, transmitting information about head and neck movements. Afferent fibers form synapses in the vestibular nuclei and pass to the center of horizontal eye movements in the SMRF.

Paresis of horizontal gaze

Clinical anatomy

Horizontal eye movements are generated by the horizontal movement center in the SPRF. Fibers connect it to the ipsilateral nucleus of cranial nerve VI, which abducts the ipsilateral eye. To adduct the contralateral eye, fibers from the SPRF cross the midline at the level of the brainstem and, as part of the contralateral medial longitudinal fasciculus, reach the medial straight nucleus in the contralateral complex of cranial nerve III (which also receives independent descending input from vergence control centers), so stimulation of the SPRF on one side causes consensual eye movements in the same direction. It is important to remember that upon leaving the SPRF, the MLP immediately crosses the midline and ascends to the opposite side. Loss of normal horizontal eye movements occurs when these pathways are destroyed.

Symptoms

• Lesions of the SPRF cause ipsilateral horizontal gaze paresis (inability to look in the direction of the lesion).
• The lesion of the internuclear ophthalmoplegia is responsible for the clinical syndrome of internuclear ophthalmoplegia. Left-sided

Causes of internuclear ophthalmoplegia

• demyelination
• vascular disorders
• brainstem and fourth ventricle tumors
• injury
• encephalitis
• hydrocephalus
• progressive supranuclear palsy
• medicines
• distant effects of carcinoma

Internuclear ophthalmoplegia is characterized by the following:

• When looking to the right, there is insufficient adduction of the left eye and ataxic nystagmus of the right eye.
• The gaze to the left is normal.
• Convergence is intact in isolated lesions.
• Vertical nystagmus when attempting to look up.

Combined damage to the SPRF and MPP on one side causes the "one and a half syndrome". Left-sided damage is characterized by the following:

• Ipsilateral gaze paresis.
• Ipsilateral internuclear ophthalmoplegia.
• The only remaining movement is abduction of the contralateral eye, accompanied by ataxic nystagmus.

Vertical gaze paresis

Clinical anatomy

Vertical eye movements are generated by a vertical gaze center known as the rostral interstitial nucleus of the MOP, which lies dorsal to the red nucleus in the midbrain. From the vertical gaze center, impulses pass to the extraocular muscle nuclei that control vertical movements of both eyes. The cells that mediate up and down eye movements are intermingled in the vertical gaze center, but when it is stimulated, selective paralysis of up and down gaze is possible.

Parinaud's dorsal midbrain syndrome

Symptoms

• Supranuclear paresis of upward gaze.
• Correct position of the eyes in the primary position.
• Normal downward gaze.
• Dilated pupils with dissociation of reactions to light and approach.
• Eyelid retraction (Collier's sign).
• Convergence paralysis.
• Convergence-retraction nystagmus.

Reasons

• in children - stenosis of the aqueduct of Sylvius, meningitis;
• in young people - demyelination, trauma and arteriovenous malformations;
• in the elderly - vascular lesions of the midbrain, space-occupying lesions of the periaqueductal gray matter and aneurysms of the posterior cranial fossa.

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Progressive supranuclear palsy

Progressive supranuclear palsy (Sleele-Kiciiardson-Olszewski syndrome) is a severe degenerative disease that develops in old age and is characterized by:

• Supranuclear gaze palsy, in which downward movements are initially impaired.
• Later, as the disease progresses, upward movements become impaired.
• Later, horizontal movements are impaired, and eventually complete gaze paresis develops.
• Pseudobulbar paresis.
• Extrapyramidal rigidity, ataxic gait and dementia.