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:

Related Articles Clemastine rescues myelination defects and promotes functional recovery in hypoxic brain injury. Brain. 2018 01 01;141(1):85-98 Authors: Cree BAC, Niu J, Hoi KK, Zhao C, Caganap SD, Henry RG, Dao DQ, Zollinger DR, Mei F, Shen YA, Franklin RJM, Ullian EM, Xiao L, Chan JR, Fancy SPJ Abstract Hypoxia can injure brain white matter tracts, comprised of axons and myelinating oligodendrocytes, leading to cerebral palsy in neonates and delayed post-hypoxic leukoencephalopathy (DPHL) in adults. In these conditions, white matter injury can be followed by myelin regeneration, but myelination often fails and is a significant contributor to fixed demyelinated lesions, with ensuing permanent neurological injury. Non-myelinating oligodendrocyte precursor cells are often found in lesions in plentiful numbers, but fail to mature, suggesting oligodendrocyte precursor cell differentiation arrest as a critical contributor to failed myelination in hypoxia. We report a case of an adult patient who developed the rare condition DPHL and made a nearly complete recovery in the setting of treatment with clemastine, a widely available antihistamine that in preclinical models promotes oligodendrocyte precursor cell differentiation. This suggested possible therapeutic benefit in the more clinically prevalent hypoxic injury of newborns, and we demonstrate in murine neonatal hypoxic injury that clemastine dramatically promotes oligodendrocyte precursor cell differentiation, myelination, and improves functional recovery. We show that its effect in hypoxia is oligodendroglial specific via an effect on the M1 muscarinic receptor on oligodendrocyte precursor cells. We propose clemastine as a potential therapy for hypoxic brain injuries associated with white matter injury and oligodendrocyte precursor cell maturation arrest. PMID: 29244098 [PubMed - indexed for MEDLINE]
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