Gaze palsy

Introduction The normal movement of the eyeball is the joint movement of the bilateral eyeballs, which is regulated by the joint movement center of the brain and the brainstem. When the above-mentioned pathway is damaged, the two-eye co-movement disorder occurs, and the eyes cannot rotate upward, downward, or sideways, which is called gaze. paralysis. It is caused by aneurysm, various infections, head trauma, brain tumor, cerebral arteriosclerotic vascular disease, myasthenia gravis and the like. Others such as diabetic ophthalmoplegia, ophthalmoplegia, migraine, and extraocular muscle malnutrition can also be caused.

Cause

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. The posterior cerebral artery, the superior cerebellar artery, and the aneurysm of the posterior communicating artery can cause oculomotor nerve paralysis, but generally do not cause the numbness of the trochlear nerve.

The mechanism of cranial nerve palsy may be:

(1) The saccular aneurysm is acutely dilated, oppressing or pulling the nerve.

(2) venous congestion leads to nerve edema. ;

(1) Tibial Rock Tip Syndrome: In patients with otitis media and chronic mastoiditis, inflammation can cause this syndrome when the intracranial development destroys the humeral tip. Clinical manifestations of binocular strabismus, invading the half-moon ganglion can cause facial numbness or pain.

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

(3) supracondylar syndrome and apex syndrome: patients with pituitary tumor, tympanitis, sinusitis, paralysis of the eye, the trochlear, the nerve and the trigeminal nerve branch may occur when the disease invades the sacral fissure and the optic nerve hole. 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, orbital abscess, may be followed by thrombotic cavernous sinusitis or cavernous sinus thrombosis.

The clinical manifestations are: intraorbital tissue, edema of the upper and lower jaws, edema of the conjunctiva, prominent eyeballs, paralysis in all directions, dilated pupils, loss of light reflection or forehead pain, numbness, accompanied by high fever and chills. The bilateral cavernous sinus is connected by the sinus sinus. If the cavernous sinus thrombosis on one side can often affect the contralateral side within a few days, bilateral symptoms appear and can spread to adjacent tissues, leading to diseases such as meningitis and brain abscess.

(5) Other infections: various meningitis such as tuberculous, suppurative, viral, fungal meningitis, can affect eye movement, trochlear, nerve expansion, 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; apical fractures can cause eye movements, trochle, nerve palsy and trigeminal nerve branch damage, because Both the oculomotor nerve and the parasympathetic nerve are severely damaged. At this time, the sympathetic and parasympathetic nerve functions are all impaired, which may lead to normal pupil size and disappearance of photoreaction. One side of the intracranial hematoma caused by the cerebral hiatus hernia, ipsilateral oculomotor nerve paralysis and contralateral hemiplegia; ciliary ganglion injury leads to intraocular tendon.

4. Brain tumors: Both intracranial and secondary tumors can cause paralysis of eye movements. Tumors that originate in the brainstem are a common cause of eye movements, trochules, and paralysis. Midbrain tumors are prone to cause eye movements, trochlear nerve paralysis, and pons tumors are prone to cause paralysis of the nerves. Tumors in the cerebral hemisphere can cause ipsilateral oculomotor palsy and contralateral hemiplegia due to the sacral hiatus, mainly due to the intrusion of the posterior mass to push the brain stem down, pulling the oculomotor nerve, or possibly due to the posterior cerebral artery and cerebellum. The upper artery is accompanied by a downward movement of the brain stem to compress the oculomotor nerve. Because of its long formation in the skull, the nerve is most likely to be compressed on the humeral tip, or pulled at any part of its stroke, resulting in bilateral nerve palsy with no localization value. Pituitary tumors, pineal tumors, etc. can cause eye movements, trochle, nerves 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 the hardening of blood vessels such as the posterior cerebral artery and the superior cerebellar artery to make the eye movement, the trochlear nerve paralysis, and the internal auditory artery and the cerebellar anterior inferior arteries cause scleral nerve paralysis.

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 more common with oculomotor nerves and nerve numbness. Because the sacral fibers are located in the peripheral part above the oculomotor nerve, they are not susceptible to ischemic damage, and generally no pupil changes occur. Different from dilated pupils caused by aneurysm; ocular paralysis migraine, ophthalmoplegia (eye movement, nerve palsy 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.

an examination

Related inspection

Vision screening optic nerve examination

Diagnostic examination

Laboratory tests: Select the necessary selective tests based on the likely cause.

1. Blood routine, blood electrolytes.

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

Other auxiliary examinations: the following inspection items have abnormal diagnostic significance

1. CT, MRI.

2. EEG.

3. Skull base film, paranasal sinus film.

4. Otolaryngology examination.

Differential diagnosis

Eyes gazing upward: epilepsy-like hypoglycemia manifests as a shallow coma, with moist skin, blemishes, sputum, gaze upwards, double pupils, light reflexes, stiff neck, thick lungs, and strong heart sounds.

Neonatal gaze on both eyes: neonatal seizures can be manifested as binocular gaze, loss of consciousness, limb convulsions, lip blemishes, etc., can be divided into febrile seizures and no heat convulsions, febrile seizures may be caused by intracranial infections, no Heat convulsions may be caused by hypoxic ischemic encephalopathy and intracranial hemorrhage, hypocalcemia, etc. caused by hypocalcemia, generally no sequelae, others may have sequelae: including epilepsy, cerebral palsy.

Gaze sign: thyroid-related eye disease is divided into 0 to 6 levels: 0: no signs, asymptomatic; level 1: only signs (upper palpebral retraction, gaze sign); level 2: soft tissue involvement; level 3: eyeball protrusion; 4 Grade: extraocular muscle involvement; grade 5: corneal involvement; grade 6: visual loss of hyperthyroidism symptoms may also have cleft palate broadening and gaze signs.

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.