Eye movement disorder

Introduction to eye movement disorders The eye movement, the trochlear, and the nerves have the function of controlling the movement of the extraocular muscles of the eyeball. They are often called the motor nerves of the eye. When the above nerves or nerve nuclei are damaged alone or in combination, eye movements may not occur or double vision. The extraocular muscles are all paralyzed and the eyeballs are fixed. Extraocular muscle injury, infection, or extraocular muscle paralysis caused by myopathy, eye movement can also occur, clinically known as eye movement disorders. Here, it mainly describes the ocular dyskinesia that occurs when the oculomotor nerve or nerve nucleus is damaged. The ocular dyskinesia has important clinical significance for the diagnosis of skull base lesions, brain stem lesions and cranial neuropathy. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: strabismus

Causes of eye movement disorders

(1) Causes of the disease

The causes of eye movement disorders are mainly the following:

1. Aneurysm: An aneurysm of the skull base artery or internal carotid artery, which can cause eye movement and/or nerve palsy. The internal carotid aneurysm in the cavernous sinus can cause eye movement, trochle, abduction and trigeminal nerve. Eye palsy, called cavernous sinus syndrome, posterior cerebral artery, superior cerebellar artery, aneurysm of posterior communicating artery, can cause oculomotor nerve palsy, but generally does not cause sacral nerve paralysis alone.

The mechanism of cranial nerve palsy may be: 1 acute expansion of saccular aneurysm, compression or pulling nerve; 2 venous congestion leading to nerve edema; 3 bleeding causes arachnoid adhesion and other reasons.

2. Infection: Inflammation within or after sputum can cause paralysis of the motor nerves of the eye and produce the following syndromes:

(1) sacral apex syndrome: patients with otitis media and chronic mastoiditis, inflammation can cause the syndrome when the intracranial development destroys the sacral apex, clinically manifested as bilateral strabismus, invading the semilunar ganglion can cause facial numbness Or pain.

(2) Neuritis: For patients with sinusitis, numbness, trochle, and paralysis of the nerves may occur.

(3) supracondylar syndrome and apex syndrome: patients with pituitary tumor, tympanitis, sinusitis, stunned, stunned, paralyzed, and trigeminal ocular paralysis That is, supracondylar syndrome, if there is visual impairment, it is called apex syndrome.

(4) cavernous sinus syndrome: sinusitis, facial infection, otitis media, mastoiditis, inflammation around the tonsils, patients with orbital abscess, may be followed by thrombotic cavernous sinusitis or cavernous sinus thrombosis.

Clinical manifestations: sacral tissue, edema of upper and lower jaw, edema of bulbar conjunctiva, prominent eyeball, paralysis of movement in all directions, dilated pupils, loss of light reflex or forehead pain, numbness, accompanied by high fever and chills, bilateral cavernous sinus Connected by the sinus, if one side of the cavernous sinus thrombosis often affects the contralateral side within a few days, bilateral symptoms appear and can spread to adjacent tissues leading to meningitis, brain abscess and other diseases.

(5) Other infections: various meningitis such as tuberculosis, suppurative, viral, fungal meningitis, can affect eye movement, block, spread nerve, make it paralyzed; eyelid cellulitis can cause eye muscle paralysis; brain Inflammation can cause nuclear eye muscle paralysis; herpes zoster, chickenpox, mumps can also cause eye muscle paralysis.

3. Head trauma: Eyelid fractures and intra-orbital hemorrhage can lead to extraocular muscle spasm. The upper and lower oblique muscles are most vulnerable. The fracture of the apex can cause eye movement, blockage, nerve palsy and trigeminal nerve branch damage. Both the oculomotor nerve and the parasympathetic nerve are severely damaged. At this time, the sympathetic and parasympathetic functions are impaired, which may lead to normal pupil size, but the photoreaction disappears. One side of the intracranial hematoma leads to the cerebral hiatus, and the ipsilateral eye appears. Neurological paralysis and contralateral hemiplegia, resulting in intraocular muscle spasm after ciliary ganglion injury.

4. Intracranial primary and secondary tumors of brain tumors: Both can cause paralysis of eye movements. Tumors that originate in the brainstem are common causes of eye movement, trochle, and nerve palsy. Midbrain tumors are easy to cause motion. Eyes, trochlear nerve palsy, pons tumors easily cause paralysis of the nerves, tumors in the cerebral hemisphere can cause ipsilateral oculomotor nerve paralysis and contralateral hemiplegia due to the sacral hiatus, mainly due to the intrusion into the underlying mass to push the brain stem down, Pulling the oculomotor nerve may also be caused by the posterior cerebral artery, the upper cerebellar artery with the brain stem moving down and pressing the oculomotor nerve. The sacral nerve is too long to be pressed on the humeral rock tip due to its formation in the skull. , or pulled at any part of the stroke, resulting in bilateral positioning nerve paralysis, pituitary tumors, pineal tumors, etc. can cause eye movement, trochle, nerve expansion and trigeminal nerve palsy due to tumor enlargement.

5. Cerebral arteriosclerotic vascular disease: Patients with cerebral arteriosclerosis and hypertension often have eye muscle paralysis, which may be due to brain stem hemorrhage, subarachnoid hemorrhage or vascular obstruction that supplies nerve trunk or nerve nucleus. It can also be caused by hardened blood vessels such as the posterior cerebral artery, oppression of the superior cerebellar artery, oculomotor nerve paralysis, internal auditory artery and cerebellar anterior inferior arteriosclerosis caused by nerve palsy.

6. Myasthenia gravis: Myasthenia gravis is a common cause of ophthalmoplegia. The striated muscles of the various muscles or limbs that are innervated by the medulla may be affected, but the extraocular muscles are more common.

7. Others: For example, diabetic ophthalmoplegia is caused by oculomotor nerves, and nerve palsy is more common. Because the sacral fibers are located in the peripheral part above the oculomotor nerve, it is not susceptible to ischemic damage, and generally no pupillary changes occur. Different from dilated pupils caused by aneurysm; ocular paralytic migraine, ophthalmoplegia (eye movement, paralysis and diplopia) at the time of onset or after attack; extraocular muscle dystrophy Eyelid drooping can also occur, and gradually develop into all extraocular tendons.

Eye movement disorder prevention

Usually pay attention to living habits, diet also needs a certain amount of nutrition. Diabetic ophthalmoplegia must actively control blood sugar treatment. Brain stem and brain neuropathy caused by vitamin B1 deficiency can be treated with a large amount of vitamin B1, and the symptoms can quickly disappear. Note that you can usually eat more animal liver. Appropriate supplementation of calcium cod liver oil can play a preventive role. Pay attention to the early prevention of active medical examination.

Eye movement disorder complications Complications

Both the ocular motor nerve and the trigeminal ocular branch pass through the lateral wall of the cavernous sinus and the supraorbital fissure into the eyelid to control the eye movement and the forehead and periocular skin sensation. Therefore, when the lesion occurs in this part, the ocular motor nerve and the trigeminal nerve branch are damaged together. Clinically known as supracondylar syndrome or cavernous sinus syndrome, the latter may have symptoms of obstruction of ocular venous return in the early stage.

Symptoms of eye movement disorders Common symptoms Playing the piano finger (toe) sign vestibular reflex disappears after circulation ischemic eyeball floating phenomenon disappears light reaction double vision supracondylar syndrome eyeball squint muscle paralysis sag

Eye movement disorders that occur when the motor or nerve nucleus is damaged can be divided into the following three categories:

1. Peripheral damage to the oculomotor nerve damage occurs when the ptosis, the eyeball down the external strabismus, the eyeball can not go up, the inner and the lower direction, and there is double vision, pupil dilated, light and adjustment reflex disappear, clinically common In the midbrain lesions, skull base artery tumors, arteriovenous malformations, nasopharyngeal carcinoma, cerebral hiatus hernia, diabetic neuropathy, alcoholism, painful ophthalmoplegia and so on.

When the trochlear nerve is damaged, the movement of the eyeball is downward and abduction is weakened. When the eyeball moves downward, the double vision is aggravated, and the damage of the trochlear nerve is rare.

When the nerve damage occurs, intraocular strabismus occurs, the eyeball can not be abducted, and diplopia appears when gazing outward. The nerve damage is seen in the pons lesion, the skull base metastasis, and the intracranial pressure is increased.

Because the eye movement nerve and the trigeminal nerve branch pass through the outer wall of the cavernous sinus and the supraorbital fissure into the eyelid to control the eye movement and the forehead, the skin around the eye, so the eye movement nerve and the trigeminal eye branch are damaged when the lesion occurs in this part. It is clinically known as supracondylar syndrome or cavernous sinus syndrome, and the latter may have symptoms of obstruction of ocular venous return in the early stage.

2. The nuclear lesions are often accompanied by the symptoms of adjacent tissue damage. The nucleus of the oculomotor nerve is often associated with medial longitudinal bundle damage, and there are intraocular and extraocular tendons and both-eye dyskinesia; the nucleus lesions often merge with the facial nerve and the trigeminal nucleus. Medial longitudinal bundle damage, presence of augmentation, trigeminal nerve, facial nerve palsy, and binocular dyskinesia; the trochlear nerve is rarely damaged alone, if the nuclear lesion, it will damage more adjacent tissues such as pyramidal tract, sensory pathway, Cross-sectional paralysis can occur, such as Weber syndrome in the midbrain, Foville syndrome in the pons, etc., so the main features of nuclear lesions are:

(1) Nuclear paralysis of the motor of the eye is bilateral, but asymmetrical.

(2) Selective damage to part of the eye muscles, separation of ophthalmoplegia.

(3) The pupil is reduced, and the photoreaction disappears and the response is regulated.

(4) Damage to the tissue surrounding the nucleus of the eye movement is often accompanied by a long bundle sign.

3. The normal movement of the nucleus of the eyeball is the joint movement of the bilateral eyeballs. It is regulated by the joint movement of the brain and the brainstem. When the above pathway is damaged, the two-eye dyskinesia occurs. The eyes cannot go up, down, or Side rotation, called gaze numbness; if the eyes can not be turned sideways, it is called Fei-Ge two numbness, that is, one side of the eyeball rectus tendon, the contralateral external rectus tendon.

One side of the pons occlusion center is damaged, the double eye can not gaze to the side of the lesion, but to the contralateral side; one side of the cerebral cortex gaze central damage (located in the posterior part of the frontal and middle back) produces the opposite symptoms, such as irritative lesions such as Jackson epilepsy The eyes are biased to the opposite side of the lesion, watching the twitching limbs, so the cerebral palliative lesions of the pons and the cortical gaze central irritative lesions produce the same symptoms of gaze paralysis, and vice versa.

Destructive lesions of the upper ventricle can produce the Parinaud syndrome of both eyes with the same vertical dyskinesia. The eyes can not move upward in the same direction to produce "sunset phenomenon", often accompanied by the disappearance of pupillary photoreaction, more common in pineal tumors; upper irritative lesions It is manifested as an eye-catching crisis, which can be caused by Parkinson's syndrome and metoclopramide (metoclopramide) after cerebral inflammation.

Examination of eye movement disorders

1. Blood routine, blood electrolytes.

2. Blood sugar, immune items, cerebrospinal fluid examination, if abnormal, there is a differential diagnosis.

3. CT, MRI.

4. EEG.

5. Skull base film, paranasal sinus film.

6. ENT examination.

Diagnosis and differentiation of eye movement disorders

diagnosis

Diagnosis can be made based on medical history, clinical manifestations, and examination.

Differential diagnosis

1. The cause identification is mainly based on the diagnostic criteria for different intracranial or extracranial diseases that can cause damage to the motor or nerve nucleus of the eyeball or extraocular muscle paralysis.

2. The location diagnosis and differentiation of the eye movement nerve or nerve nucleus injury is identified according to the different characteristics of the ocular dyskinesia and the combined symptoms.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.