Eye Disorders
The advances in the treatment of hypopsia caused by retinal pigment degeneration, macular degeneration and atrophy of the optic nerve.
Retinal abnormality
The retina is a layer of thin hyaline tissue all of the visual information is transferred to the central nervous system by the nerve cells (cones and rods) in the retina in other words, it's extension part of the central nervous system.
The causes of pathological changes: the most common cause is Ischemic retinopathy, outbreak visual loss in single eye should be highly suspected of ischemia retinae. Retinal detachment, macular degeneration, glaucoma and vitreous hemorrhage are causes of retinopathy. The following will mainly explain retinosis.
Retinosis
Retinosis is one of the main causes of chronic decreased visual acuity, in general it includes membrane degeneration and macular degeneration. There are several types which are probably related to other nervous system disease.
Macular degeneration is the main cause of visual loss in elderly people, gradually there is a decrease of central visual acuity, which affects reading, the patient retains the peripheral vision and can still walk.
In young and middle-aged people, the most common disease is a kind of hereditary diseases in the external light layer and the adjacent pigment epithelium, named retinitis pigmentosa. Clinically the contraction of the visual field, central vision relative preservation (tube type field) metamorphopsia (visual distortion), poor adaptation to the dark and night blindness are characteristics of this disease.
Teen-agers retinal degeneration a kind of staged degeneration disease mostly seen in teen-agers which main pathological change is large areas of central retinal lesions it can result in progressive spastic paraplegia or ataxia.
In infants and young children, some Lysosomal diseases called macular degeneration. This is characterized by protein which cannot be degraded and polysaccharide gathering in the brain, optic nerve, macular and retina.
Retinosis is also can seen in oat-cell carcinoma patients, those patients blood serum have antibodies against retinal ganglion cells.
These are a kind of progressive vision loss, night blindness contraction of visual field, fundus pigmentation hereditary, gene mutation and immune injury of eye disease. Commonly seen in heredopathia, modes of inheritance are Autosomal dominant, recessive or X-linked recessive inheritance, most involve both eyes, a single eye being involved and Quadrant are rare. The disease progresses slowly, with an unfavourable prognosis. The younger the age of onset, the more serious, the earlier blindness happens. The older the age of onset, the later blindness happens.
Pathological change:
The main change is degeneration in the stratum neuroepitheliale retinae, especially in the rod cells, than the retina gradually atrophies from the inside to the outside, with gliosis.
Degeneration and hyperplasia occurs in the pigment epithelial cell can find cases of depigmentation or accumulation moving to the entorretina. Glassy degeneration and thickening in the retinal vascular wall, can even entirely shut in the lumen. Different degrees of hardening in the choroidal vessels, results in the blood capillary completely or partially disappearing. The optic nerve may complete atrophy, gliosis in discus opticus which becomes a membrane, connects with the gliosis in the retina.
Clinical manifestation:
1. Night blindness and progressive visual loss.
2. Visual field progressive concentric contraction to tubular visual field.
3. Optic fundus: pale, sallow, retinal vascular narrow, fundus gray cyan contamination, osteoblast pigmentation, obvious in ambitus, atrophy of the retina, can see sclerotic chorioid.
4. Fluorescence fundus angiography: transmitted fluorescence in early stage, arterial filling slowly, macula lutea may have leakage because cystoid macular edema.
5. ERG: extinguished type.
Treatment:
Traditional treatment can not stop degeneration and necrosis in retinal nerve cells and pigment cells. There has been no effective treatment before. In recent years, through more than ten years treatment experience, Wu Stem Cells Medical Center found that stem cells can have a good treatment outcome in Retinosis. Stem cell treatment can effectively slow down or stop the disease progressing. The molecular chaperones from stem cells can clear a part of abnormal accumulation protein, can slow down or stop the disease progress. And immunoregulation from stem cells can resist the antibody which causes damage in the retina and optic nerve, the nerve cell which is differentiated from nerve stem cells can repair part of the damage and the vitium, then can increase the eye sight and expand the visual field of the patient.
Optic Neuropathy (Atrophy)
Optic neuropathy refers to damage to the optic nerve due to any cause. Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptoms are loss of vision, field of vision centripetal narrowed, vision defect, hemianopsia, with colors appearing subtly washed out in the affected eye. On medical examination, the optic nerve head can be visualized by an ophthalmoscope. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye.
Optic neuropathy is often called optic atrophy, to describe the loss of some or most of the fibers of the optic nerve. In short, optic atrophy is the end result of any disease that damages nerve cells anywhere between the retinal ganglion cells and the lateral geniculate body (anterior visual system).
Causes
The optic neuropathy may be caused by any of the following:
• Ischemic optic neuropathy
• Optic neuritis
• Compressive optic neuropathy
• Infiltrative optic neuropathy
• Infiltrative optic neuropathy
• Traumatic optic neuropathy
• Mitochondrial optic neuropathies
• Nutritional optic neuropathies
• Toxic optic neuropathies
• Hereditary optic neuropathies
Treatment
As far as the treatment for optic nerve atrophy is concerned, we should first consider the incentives and then apply the treatment accordingly. For instance, for patients suffering optic nerve atrophy caused by pituitary tumor, they should undergo surgery to cut the tumor out. Optic canal fracture patients should receive treatment to remove the fracture and to release optic canal and the front end of dural sheath's middle part with decompression. Optic nerve inflammation patients should take some measures to resist inflammation and do some immune-regulation work. Once the patient develops optic nerve atrophy, it is almost impossible for him or her to heal. The purpose of early treatment is primarily to protect the remaining optic nerve cells and nerve fibers, and to maintain or even restore part of these cells' function.
However, previous treatment provides no effective way to treat sequela of optic nerve atrophy. There is no way to regenerate the lost optic nerve cells and nerve fibers.
In recent years, using stem cells technology (nerve regeneration technology) we have treated many patients who suffered from optic neuropathy or optic nerve atrophy. Almost all of them have had varying degrees of improvement after receiving treatment.
Neural stem cells are a kind of special cell. With certain positioning and adjusting technology, they will be localized to the accurate lesion part in visual photoreceptor cells, retina and optic nerve. After being positioned in the lesion part, they will differentiate into functional optic neurons, oligodendrocytes and astrocytes, which will increase the number and restoration of optic nerve cells as well as the optic nerve's regulation toward retina and visual photoreceptor cells.
The mesenchymal stem cells can differentiate into photoreceptor cells and immune-adjustment cells. The differentiated cells will first repair patients' autologous cells' synaptic nucleoprotein, and eventually play a positive role in treating lesion in retinal pigment cells and optic nerves.
For patients who suffer from optic nerve injuries or optic nerve atrophy, such a treatment will effectively supplement the missing optic nerve cells and increase the restoration of fibers, and eventually achieve the goal of improving patients' eyesight, field of vision and ability of color discrimination.
Retinal abnormality
The retina is a layer of thin hyaline tissue all of the visual information is transferred to the central nervous system by the nerve cells (cones and rods) in the retina in other words, it's extension part of the central nervous system.
The causes of pathological changes: the most common cause is Ischemic retinopathy, outbreak visual loss in single eye should be highly suspected of ischemia retinae. Retinal detachment, macular degeneration, glaucoma and vitreous hemorrhage are causes of retinopathy. The following will mainly explain retinosis.
Retinosis
Retinosis is one of the main causes of chronic decreased visual acuity, in general it includes membrane degeneration and macular degeneration. There are several types which are probably related to other nervous system disease.
Macular degeneration is the main cause of visual loss in elderly people, gradually there is a decrease of central visual acuity, which affects reading, the patient retains the peripheral vision and can still walk.
In young and middle-aged people, the most common disease is a kind of hereditary diseases in the external light layer and the adjacent pigment epithelium, named retinitis pigmentosa. Clinically the contraction of the visual field, central vision relative preservation (tube type field) metamorphopsia (visual distortion), poor adaptation to the dark and night blindness are characteristics of this disease.
Teen-agers retinal degeneration a kind of staged degeneration disease mostly seen in teen-agers which main pathological change is large areas of central retinal lesions it can result in progressive spastic paraplegia or ataxia.
In infants and young children, some Lysosomal diseases called macular degeneration. This is characterized by protein which cannot be degraded and polysaccharide gathering in the brain, optic nerve, macular and retina.
Retinosis is also can seen in oat-cell carcinoma patients, those patients blood serum have antibodies against retinal ganglion cells.
These are a kind of progressive vision loss, night blindness contraction of visual field, fundus pigmentation hereditary, gene mutation and immune injury of eye disease. Commonly seen in heredopathia, modes of inheritance are Autosomal dominant, recessive or X-linked recessive inheritance, most involve both eyes, a single eye being involved and Quadrant are rare. The disease progresses slowly, with an unfavourable prognosis. The younger the age of onset, the more serious, the earlier blindness happens. The older the age of onset, the later blindness happens.
Pathological change:
The main change is degeneration in the stratum neuroepitheliale retinae, especially in the rod cells, than the retina gradually atrophies from the inside to the outside, with gliosis.
Degeneration and hyperplasia occurs in the pigment epithelial cell can find cases of depigmentation or accumulation moving to the entorretina. Glassy degeneration and thickening in the retinal vascular wall, can even entirely shut in the lumen. Different degrees of hardening in the choroidal vessels, results in the blood capillary completely or partially disappearing. The optic nerve may complete atrophy, gliosis in discus opticus which becomes a membrane, connects with the gliosis in the retina.
Clinical manifestation:
1. Night blindness and progressive visual loss.
2. Visual field progressive concentric contraction to tubular visual field.
3. Optic fundus: pale, sallow, retinal vascular narrow, fundus gray cyan contamination, osteoblast pigmentation, obvious in ambitus, atrophy of the retina, can see sclerotic chorioid.
4. Fluorescence fundus angiography: transmitted fluorescence in early stage, arterial filling slowly, macula lutea may have leakage because cystoid macular edema.
5. ERG: extinguished type.
Treatment:
Traditional treatment can not stop degeneration and necrosis in retinal nerve cells and pigment cells. There has been no effective treatment before. In recent years, through more than ten years treatment experience, Wu Stem Cells Medical Center found that stem cells can have a good treatment outcome in Retinosis. Stem cell treatment can effectively slow down or stop the disease progressing. The molecular chaperones from stem cells can clear a part of abnormal accumulation protein, can slow down or stop the disease progress. And immunoregulation from stem cells can resist the antibody which causes damage in the retina and optic nerve, the nerve cell which is differentiated from nerve stem cells can repair part of the damage and the vitium, then can increase the eye sight and expand the visual field of the patient.
Optic Neuropathy (Atrophy)
Optic neuropathy refers to damage to the optic nerve due to any cause. Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptoms are loss of vision, field of vision centripetal narrowed, vision defect, hemianopsia, with colors appearing subtly washed out in the affected eye. On medical examination, the optic nerve head can be visualized by an ophthalmoscope. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye.
Optic neuropathy is often called optic atrophy, to describe the loss of some or most of the fibers of the optic nerve. In short, optic atrophy is the end result of any disease that damages nerve cells anywhere between the retinal ganglion cells and the lateral geniculate body (anterior visual system).
Causes
The optic neuropathy may be caused by any of the following:
• Ischemic optic neuropathy
• Optic neuritis
• Compressive optic neuropathy
• Infiltrative optic neuropathy
• Infiltrative optic neuropathy
• Traumatic optic neuropathy
• Mitochondrial optic neuropathies
• Nutritional optic neuropathies
• Toxic optic neuropathies
• Hereditary optic neuropathies
Treatment
As far as the treatment for optic nerve atrophy is concerned, we should first consider the incentives and then apply the treatment accordingly. For instance, for patients suffering optic nerve atrophy caused by pituitary tumor, they should undergo surgery to cut the tumor out. Optic canal fracture patients should receive treatment to remove the fracture and to release optic canal and the front end of dural sheath's middle part with decompression. Optic nerve inflammation patients should take some measures to resist inflammation and do some immune-regulation work. Once the patient develops optic nerve atrophy, it is almost impossible for him or her to heal. The purpose of early treatment is primarily to protect the remaining optic nerve cells and nerve fibers, and to maintain or even restore part of these cells' function.
However, previous treatment provides no effective way to treat sequela of optic nerve atrophy. There is no way to regenerate the lost optic nerve cells and nerve fibers.
In recent years, using stem cells technology (nerve regeneration technology) we have treated many patients who suffered from optic neuropathy or optic nerve atrophy. Almost all of them have had varying degrees of improvement after receiving treatment.
Neural stem cells are a kind of special cell. With certain positioning and adjusting technology, they will be localized to the accurate lesion part in visual photoreceptor cells, retina and optic nerve. After being positioned in the lesion part, they will differentiate into functional optic neurons, oligodendrocytes and astrocytes, which will increase the number and restoration of optic nerve cells as well as the optic nerve's regulation toward retina and visual photoreceptor cells.
The mesenchymal stem cells can differentiate into photoreceptor cells and immune-adjustment cells. The differentiated cells will first repair patients' autologous cells' synaptic nucleoprotein, and eventually play a positive role in treating lesion in retinal pigment cells and optic nerves.
For patients who suffer from optic nerve injuries or optic nerve atrophy, such a treatment will effectively supplement the missing optic nerve cells and increase the restoration of fibers, and eventually achieve the goal of improving patients' eyesight, field of vision and ability of color discrimination.
