Conjugate paralysis

Damage caused by an abnormality in the tissues due to trauma or illness can disrupt the transmission of signals from the brain to the eye. Almost all conjugated gaze paralysis comes from a lesion somewhere in the brain stem , usually in the midbrain or bridge . These lesions can be caused by a stroke or diseases, such as Kerber-Salus-Elschnig syndrome, progressive supranuclear paresis of the gaze , olivopontocerebellar syndrome, or Nimann-Peak disease, type C. ^[four]

Conjugate paralysis can be classified as paralysis affecting the horizontal gaze or vertical gaze.

Horizontal gaze paralysis

Horizontal gaze paralysis affects the movement of the gaze of both eyes relative to the midline of the body. Paralysis of the horizontal gaze is usually caused by damage to the brain stem and connecting nerves, usually in the bridge . ^[five]

Vertical gaze paralysis

Paralysis of the vertical gaze affects the movement of one or both eyes either in the direction of up, or up and down, less often only down. It is very rare to paralyze the movement of only one eye in only one direction, although by definition it is not paralysis of the conjugated gaze, because, by definition, paralysis of the conjugated gaze affects the movement of both eyes. Vertical gaze paralysis is often caused by damage to the brain due to a stroke or tumor . In the case where only a downward view suffers, the cause, as a rule, is progressive supranuclear palsy. ^[6]

The location of the lesion determines the type of paralysis. Non-selective paralysis of the horizontal gaze is caused by a lesion in the abducent nucleus. This is where the cranial nerve VI loses its path to the lateral rectus muscle, which controls the horizontal movement of the eye from the midline of the body. The cranial nerve VI also has interneurons connected to the medial rectus muscle, which controls the horizontal movement of the eyes away from the midline of the body. ^[7] Since the lateral rectus muscle controls movement from the center of the body, lesions in the abduction nucleus tear apart the control of movement away from the center, preventing the right eye from moving to the right and the left eye from moving to the left. Nerve VI has the largest subarachnoid distance to the target tissue, which makes it susceptible to damage. ^[8] Damage to anywhere in the abduction nucleus, cranial nerve VI, neurons, or interneurons can affect the movement of the eyes toward the lesion. Damage to both sides of the abduction nucleus can lead to a complete loss of horizontal eye movement. ^[five]

Another type of gaze palsy is horizontal saccadic paralysis. Saccades are very fast involuntary eye movements. ^[9] Paramedian bridge reticular formations (PPRF), as well as the bridge, are responsible for saccades, transmitting signals to the abduction nuclei. ^[10] Lesions in PPRF slow down saccadic horizontal eye movement or, in the case of very serious injuries, their absence. ^[5] This is because the control paths of saccadic movements are destroyed by the defeat and only slow movements controlled by various motor paths are possible, but they are ineffective.

Lesions in the midbrain can interfere with efferent motor signals before they enter the bridge. It can also lead to a slowdown of horizontal saccadic movements and the inability of the eye to find the target during saccades. This damage usually occurs in the oculomotor core of the midbrain. ^[11] As with horizontal saccadic paralysis, saccades stop or slow down from a path violation, only in this case the signal is broken before it reaches PPRF.

One and a half syndrome is associated with damage to paramedian reticular formations and the medial longitudinal bundle. ^[12] These combined damages cause a complete defective look at the same side and “half” of the look at the opposite side. ^[5] As seen in horizontal saccadic paralysis, impaired vision on the opposite side is caused by the destruction of the paths coming from the PPRF, while the “half” is the deterioration of the signal passing through the medial longitudinal bundles, which is unable to achieve its goal. Syndrome one and a half, as a rule, is associated with a horizontal gaze.

Although less often than horizontal, the syndrome of one and a half from damage to the para-median bridge reticular formations and the medial longitudinal bundle can affect the vertical gaze. This can lead to a deterioration of the vertical gaze, allowing only one eye to move vertically. ^[five]

Symptoms of conjugated gaze paralysis include impaired gaze in various directions and different types of eye movement, depending on the type of gaze paralysis. Signs of a person with paralysis may be frequent head movements instead of eyes. ^[13] For example, a person with horizontal saccadic paralysis can turn his head around while watching the events of the film or lift up high instead of holding his head still and moving his eyes only, which, as a rule, goes unnoticed. Someone with non-selective paralysis of a horizontal gaze can slowly turn their heads back and forth while reading a book instead of slowly scanning their eyes across the page.

The patient can be diagnosed with conjugated gaze paralysis by a physician who has performed a series of tests to examine the possibilities of patient eye movement. In most cases, gaze paralysis may simply be an inability to move both eyes in the same direction. However, sometimes the patient pretends to have nystagmus in both eyes as evidence of paralysis of the conjugated gaze. ^[14] Nystagmus back and “jerk” forward of the eye while trying to keep your gaze in one direction. ^[15]

There is no cure for conjugated gaze paralysis itself, so gaze paralysis should most likely be treated only surgically. ^[3] As indicated in the reason section, gaze paralysis may be associated with a lesion caused by a stroke or other condition. Some conditions such as progressive supranuclear palsy are incurable, ^[16] and treatment includes only therapy to restore some functions that do not include gaze control. Other conditions, such as Neeman-Peak type C disease, are limited to drug therapy. ^[17] Victims of stroke with conjugate paralysis can be treated with intravenous therapy if the patient is sufficiently early in shape, or with surgical procedures in other cases. ^[18]

The prognosis of lesions of the visual nerve pathways, which causes paralysis of the conjugated gaze, varies greatly. Depending on the nature of the lesion, recovery may occur quickly or never. For example, optic neuritis caused by inflammation can be healed in just a few weeks, while patients with ischemic optic neuropathy cannot be healed. ^{[19] [20]}

Progressive Scoliosis horizontal gaze paralysis (HGPPS) is a very rare form of conjugated gaze paralysis, appearing in only a few dozen families around the world. HGPPS prevents the horizontal movement of both eyes, as a result of which people with this problem have to move their heads to see moving objects. In addition to impaired gaze movement, HGPPS is associated with progressive scoliosis, although eye symptoms usually appear before scoliosis. HGPPS is caused by a mutation in the Robo3 gene , which leads to the intersection of motor and sensory signals, preventing horizontal eye movement. In addition to mutations, damage to the midbrain and bridge are common. This may also include the complete absence of formations in the bridge, a tubercle on the face ( English facial colliculus ), which is responsible for some facial movements. ^[21] The reason for progressive scoliosis in HGPPS and why HGPPS does not affect the vertical gaze is incomprehensible. Progressive scoliosis is usually treated with surgery. ^[13]