optic atrophy
Introduction
Introduction Optic atrophy is not the name of a disease, but refers to a formation change caused by any disease causing retinal ganglion cells and axons to occur, resulting in a thinning of the optic nerve. It is a general term for pathology. Axillary cell axonal degeneration occurring between the retina and the lateral geniculate body. Optic atrophy is the ultimate result of optic nerve lesions, manifested as degeneration and disappearance of optic nerve fibers, conduction dysfunction, visual field changes, vision loss and loss. Generally divided into two categories of primary and secondary.
Cause
Cause
It can be caused by a variety of reasons, such as ischemia, inflammation, compression, trauma and demyelinating diseases.
1. Secondary optic nerve atrophy caused by intracranial hypertension
2. Intracranial inflammation, more common in tuberculous meningitis or optic arachnoiditis
3. Retinopathy
(1) vascular, central retinal artery or vein obstruction, arteriosclerosis of the optic nerve itself, normal nutritional vascular disorders, bleeding (digestive tract and uterus, etc.).
(2) inflammation.
(3) After glaucoma.
(4) Retinitis pigmentosa.
(5) Refsum disease.
(6) Black Mongolian familial dementia.
4. Optic neuritis and optic neuropathy
(1) vascular, such as ischemic optic neuropathy.
(2) Demyelinating disease.
(3) Vitamin deficiency.
(4) Poisoning due to lead or other metals.
(5) Herpes zoster.
(6) syphilis.
5. Caused by oppression
Tumors, including meningiomas, craniopharyngioma, pituitary adenomas, aneurysms (anterior communicating aneurysms).
Skeletal diseases, including Paget's disease, deformity osteitis, and cranial stenosis.
Ankle tumor.
6. Trauma
7. Metabolic diseases such as diabetes, gangliosides, etc.
8. Hereditary diseases
Leber disease, cerebellar ataxia, peripheral neuropathy such as Chareot-Marie-Tooth disease.
9. Nutritional optic atrophy
10. Miscellaneous
In children, the reasons are more complicated as follows:
Chromosomal abnormality
Meow syndrome, the long arm of chromosome 18 is missing.
2. Lipid diseases
Tay-sachs disease, Sandhoffs disease, lactosyl (neuro) sphingosine poisoning, NIEMANN-Pieck disease, --lipoproteinemia (Bassen-kornzwig syndrome).
3. Mucopolysaccharidosis
Hurlers mucopolysaccharidosis, with cystineuria.
4. Mineral metabolism defects and their metabolism
Menkes disease, juvenile diabetes, pancreatic cystic fibrosis, systemic gangliospasm, Zellwage's disease, Albers-Schönberg disease.
5. Hereditary retinitis pigmentosa
Ushers syndrome, Kesrns-Sayer syndrome, Alstrom syndrome.
6. Gray matter
Battens disease, infant axonal malnutrition, Hallervorden-Spatz disease.
7. Cerebellar ataxia
Behr optic atrophy, Marie ataxia, hereditary motor or sensory polyneuropathy, Charcot-Marie-Tooth disease, olive-pons cerebellar degeneration.
8. Primary white matter lesions
Abnormal white matter degeneration, Krabbers disease, Cavernous white matter degeneration (Canaran), Sudan white matter degeneration, Merzbacher-pelizaeus disease, Cockayne syndrome.
9. Demyelinating disease
Adrenal white matter degeneration, multiple sclerosis.
10. Familial optic atrophy
Leber disease, infantile optic atrophy (recessive, dominant).
11. Increased intracranial pressure
False brain tumors, intracranial hemorrhage, skull stenosis, and aqueduct blocked hydrocephalus.
Examine
an examination
Related inspection
Eye and temporal area CT examination pupillary reflex
1. Visual evoked potential (VEP) examination
It can be seen that the P100 peak latency is delayed or/and the amplitude is significantly reduced. VEP can objectively evaluate visual function and is of great significance for the diagnosis, disease monitoring and efficacy evaluation of OA.
2. Central field of view quantitative threshold check procedure using common computer automatic perimetry
Visible centripetal narrowing, sometimes can prompt the cause of the disease, such as bilateral hemianopia should exclude the intracranial visual cross-occupying lesions, large center or paracentral dark spots should exclude Leber hereditary optic neuropathy. This test can be used for visual function assessment and is of great significance for the diagnosis, disease monitoring and efficacy evaluation of OA.
3. CT or MRI examination of the skull or eyes
Visible and invasive optic neuropathy patients, visible intracranial or intraorbital space-occupying lesions oppression optic nerve, optic neuromyelitis, multiple sclerosis and other patients with central nervous system white matter demyelinating lesions. This test can exclude or confirm oppressive and invasive optic neuropathy and demyelinating lesions in the etiology of OA.
4. Using genetic testing technology
Detection of mitochondrial DNA or nuclear genes by blood, other body fluids or cells shows that there is a mutation in the corresponding gene locus in patients with OA caused by hereditary optic neuropathy, which can exclude or confirm hereditary optic neuropathy in the etiology diagnosis of OA.
Diagnosis
Differential diagnosis
1. Acute phase and anterior ischemic optic neuropathy, optic disc vasculitis, optic nerve papillitis, no obvious changes in the fundus and posterior optic neuritis.
2. The atrophic period should first exclude intracranial compression lesions and be differentiated from other genetic types of optic atrophy.
3. The disease needs to be differentiated from demyelinating diseases such as multiple sclerosis and optic neuromyelitis.
