Compressive optic neuropathy

Introduction to oppressive optic neuropathy Compressive optic neuropathy (compressiveopticneuropathy) is caused by direct compression or infiltration of intraorbital or intracranial tumors or metastatic cancer. It is sometimes misdiagnosed clinically and should be vigilant. In the eye, including optic glioma, meningioma, hemangioma, lymphangioma, teratoma and malignant tumors. In the intracranial area, the saddle area is more common, such as pituitary adenoma, craniopharyngioma, etc., other front wings, middle part of the sphenoid wing, saddle nodules, sphenoid ridge and olfactory meningioma are also missing. An internal aneurysm in which the internal carotid artery is bent, hardened, or occurs in the terminal branch of the internal carotid artery or the anterior cerebral artery or anterior communicating artery may gradually compress the unilateral optic nerve. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: optic atrophy

Causes of optic neuropathy

In the eye including optic glioma, meningioma, hemangioma, lymphangioma, teratoma and malignant tumor (cancer, lymphoma, sarcoma, multiple myeloma), etc., in the intracranial saddle area occupying lesions More common, such as pituitary adenoma, craniopharyngioma, etc., other anterior wing, middle part of sphenoid wing, saddle nodule, sphenoid ridge and olfactory meningioma are also missing, internal carotid artery bending, hardening or occurring The aneurysm of the carotid artery terminal or anterior cerebral artery or anterior communicating artery can also gradually compress the unilateral optic nerve, metastatic cancer such as nasopharyngeal carcinoma, lymphoid reticuloma (He Jiejin's disease) and frontal glioma And astrocytoma, hamartoma, tuberculoma, syphilis gelatinous, cryptococcosis, sarcoidosis, cancerous meningeal lesions can cause, pituitary apoplexy can cause sudden disappearance of monocular vision, sinus cyst, polyp oppression, In particular, the sphenoid sinus and posterior ethmoid sinus are more concealed. Thyroid lesions cause hypertrophy of the eye muscles, post-sacral edema and skeletal deformities can oppress the optic nerve.

Compressive optic neuropathy prevention

There is no effective preventive measure for this disease. Early diagnosis and early treatment are the key to the prevention and treatment of this disease.

Compressive optic neuropathy complications Complications optic atrophy

Occasionally, the ipsilateral hemianopia is due to the involvement of the ipsilateral optic tract, and the paracentral arch is still visible, and the vertical nasal side and temporal hemianopia are observed.

Symptoms of oppressive optic neuropathy Common symptoms Visual acuity often hazy blurry blackness mechanical compression optic corneal reflex disappearing optic atrophy single eye suddenly appears... visual field defect eye pain posterior optic neuritis hemianopia

Unilateral progressive and painless occult vision loss is the main clinical feature. The visual acuity is often foggy and fuzzy. The temporary erythema can occur immediately when looking at a certain position. Due to direct compression of the optic nerve or blood vessels, Loss of vision is often found by chance. Aneurysms can cause eye pain. There is no change in the early fundus. It can be found in a year or more. The color of the optic disc is pale. Finally, the optic nerve is pale and can be cup-shaped. It can be located near the optic disc. Less associated with optic disc edema, rare central retinal vein thrombosis, due to intracranial tumors (especially the frontal lobe olfactory sulcus meningioma) can oppress the optic nerve atrophy caused by the optic nerve, late due to intracranial hypertension can be optic disc edema, clinical It is often called Foster kennedy syndrome. The visual field examination is of great significance. The dark spot in the center can be seen early, and it can be quickly expanded to the peripheral part. It can maintain one stage of vision and retain the peripheral edge. Finally, the visual acuity disappears. Some cases are due to Different compression sites can cause segmental visual field defects, which are early features, inward expansion, and finally affect central vision, above the lateral iliac crest The field defect is often mild, which is caused by the involvement of the cross-nasal fibers. Because the subnasal fibers are squatting forward, close to the front end of the optic tract, and the central point of the ipsilateral dark spot exists. If this sign appears, it can be considered as a compression optic neuropathy. , has a diagnostic significance, occasionally cross-lateral ipsilateral hemianopia, due to ipsilateral visual beam involvement, but also can be seen in the central arch, vertical nasal and temporal hemianopia.

Pituitary dysfunction is a common lesion in the sellar region, especially pituitary adenoma, craniopharyngioma and other common symptoms, amenorrhea, impotence, smooth skin, pubic hair disappear, etc., but no endocrine in meningioma and aneurysm .

Examination of optic neuropathy

1. Blood examination of erythrocyte sedimentation rate and blood routine examination to exclude the necessary laboratory tests for other systemic diseases.

2. The brachial artery biopsy is suspected to be arteritic AION. If necessary, a radial artery biopsy should be performed. The typical histological change is granulomatous inflammation of the vessel wall.

3. Fundus fluorescein angiography has a certain diagnostic value for ischemic optic neuropathy. In the early stage of angiography, some parts of the optic disc show weak fluorescence, while other parts of the optic disc show normal fluorescence.

4. Systemic examination: CT scan of the head, blood test.

Diagnosis and differentiation of optic neuropathy

diagnosis

It is difficult to diagnose clinical symptoms and signs alone, and there is no difference between optic neuritis and retrobulbar optic neuritis due to inflammation. Neuroradiology is of great value for sputum and cranial space-occupying lesions, eyelids, flat slices or Multi-layer cross-section, optic nerve hole and other films have considerable value. The late development of head CT and MRI is more epoch-making significance. It can be diagnosed for changes in intraorbital and intracranial space-occupying diseases. For patients with suspected arterial disease, neck should be performed. Arterial angiography, misunderstanding CT can diagnose all lesions in the skull, small meningioma diameter of 1cm, all tests can be negative, should be followed up by ultrasound exploration for the tip of the pressure lesions can have characteristic findings, contrast sensitivity test It has certain value for oppressive optic neuropathy. Sometimes, although the visual acuity is normal, there may be abnormal changes, even earlier than the visual field and color vision test. When other tests find abnormalities, the test shows that the spatial frequencies are generally declining. Electrophysiological examination is helpful for diagnosis and can be qualitative, but positioning is difficult. It is more normal for vision and optic disc, only visual blur is more meaningful. In particular, the contrast between the eyes can be clearly diagnosed. In middle-aged people, if the monocular is progressive optic atrophy, the history is short, and the visual field defect progresses vertically, and the glaucoma, vascular disease or myeloma can be excluded, the meninges should be considered. The presence of tumors, the loss of bilateral vision and no myelitis should consider intracranial compression lesions, it is worth noting that, similar to posterior optic neuritis, and visual volatility, should consider the presence of craniopharyngioma and aneurysm Possibly, the former can be improved temporarily due to the treatment of cysts, and the latter may have instability changes.

In short, for unexplained unilateral or bilateral progressive vision loss, no improvement in treatment or temporary improvement in visual acuity, clinical diagnosis of optic neuritis, retrobulbar optic neuritis or optic atrophy, etc., should consider intracranial space Sexual lesions, the possibility of oppression of the optic nerve. Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

It must be differentiated from optic neuritis and retrobulbar optic neuritis caused by inflammation.

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