Optic Nerve Injury Stem Cell Treatment

Stem Cell Treatments for Optic Nerve Injury

Stem Cell Treatmet for Optic Nerve Injuries

Stem Cell Treatment for Optic Nerve Injuries

Optic Nerve Injury Treatments using Stem Cells is now an option...

Via IV and Retrobulbar injections of the patient's own Mesenchymal Stem Cells, we strive to give patients an option where there was none before. The optic nerve is composed of retinal ganglion cell axons and support cells. It leaves the orbit (eye socket) via the optic canal, running postero-medially towards the optic chiasm, where there is a partial decussation (crossing) of fibres from the nasal visual fields of both eyes. The optic nerve is the second of twelve paired cranial nerves but is considered to be part of the central nervous system, as it is derived from an outpouching of the diencephalon during embryonic development. As a consequence, the fibres are covered with myelin produced by oligodendrocytes, rather than Schwann cells, which are found in the peripheral nervous system, and are encased within the meninges.

Damage to the optic nerve typically causes permanent and potentially severe loss of vision, as well as an abnormal pupillary reflex, which is diagnostically important. The type of visual field loss will depend on which portions of the optic nerve were damaged. In general:

  • Damage proximal to the optic chiasm causes loss of vision in the visual field of the same side only.
  • Damage in the chiasm causes loss of vision laterally in both visual fields (bitemporal hemianopia). It may occur in large pituitary adenomata.
  • Damage distal to the chiasm causes loss of vision in one eye but affecting both visual fields: The visual field affected is located on the opposite side of the lesion.

Injury to the optic nerve can be the result of congenital or inheritable problems like Leber's Hereditary Optic Neuropathy, glaucoma, trauma, toxicity, inflammation, ischemia, infection (very rarely), or compression from tumors or aneurysms. By far, the three most common injuries to the optic nerve are from glaucoma, optic neuritis (especially in those younger than 50 years of age), and anterior ischemic optic neuropathy (usually in those older than 50).

  • Glaucoma is a group of diseases involving loss of retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially sparing central vision.
  • Optic neuritis is inflammation of the optic nerve. It is associated with a number of diseases, the most notable one being multiple sclerosis.
  • Anterior Ischemic Optic Neuropathy is a particular type of infarct that affects patients with an anatomical predisposition and cardiovascular risk factors.
  • Optic nerve hypoplasia is the under-development of the optic nerve causing little to no vision in the affected eye.

Our goal is to overcome the limitations that Optic Nerve Injuries have placed on our patients using Autologous Stem Cell Therapies.

Stem Cell Treatments for Optic Nerve Injury and Damage

Streaming NIH Search and Results:

Neuroprotective Effects Of Human Mesenchymal Stem Cells (hMSC) And Platelet Derived Growth Factor (PDGF) On Human Retinal Ganglion Cells (RGCs). Stem Cells. 2017 Oct 17;: Authors: Osborne A, Sanderson J, Martin KR Abstract Optic neuropathies such as glaucoma occur when retinal ganglion cells (RGCs) in the eye are injured. Strong evidence suggests mesenchymal stem cells (MSCs) could be a potential therapy to protect RGCs, however little is known regarding their effect on the human retina. We therefore investigated if human MSCs (hMSCs), or platelet derived growth factor (PDGF) as produced by hMSC, could delay RGC death in a human retinal explant model of optic nerve injury. Our results showed hMSCs and the secreted growth factor PDGF-AB could substantially reduce human RGC loss and apoptosis following axotomy. The neuroprotective pathways AKT, ERK and STAT3 were activated in the retina shortly after treatments with labelling seen in the RGC layer. A dose dependent protective effect of PDGF-AB was observed in human retinal explants but protection was not as substantial as that achieved by culturing hMSCs on the retina surface which resulted in RGC cell counts similar to those immediately post dissection. These results demonstrate that hMSCs and PDGF have strong neuroprotective action on human RGCs and may offer a translatable, therapeutic strategy to reduce degenerative visual loss. This article is protected by copyright. All rights reserved. PMID: 29044808 [PubMed - as supplied by publisher]
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