- Written by Super User
- Published: 14 July 2019
- Hits: 1418
https://doi.org/10.30702/Ophthalmology.2019/09.094253
Moyseyenko N. M.
Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine
Abstract. Ultrastructural changes in the retina during traumatic optic neuropathy (TON) treatment were studied. Our previous studies experimentally confirmed that after the damage to the orbital part of the optic nerve, within the background of high-dose corticosteroid monotherapy, not only the structure of the cranial part of the optic nerve restores but also its functional activity improves, by the example of zoonotic reactions to light. It was detected that phosphene electrostimulation (PES) of the contralateral side, due to retino-hypothalamic bonds, changes the architectonic nature of the suprachioscular nucleus of the hypothalamus, which, in turn, leads to the increase in the production of endogenous corticosteroids. In our opinion, this mechanism could be an alternative to the comprehensive treatment of TON. Decrease in the doses of corticosteroid infusions would reduce their toxicity, stimulate production of endogenous hormones and provide the necessary neuroprotective effect.
The purpose of the study was to investigate the changes in the retinal ultrastructure in traumatic optical neuropathy in response to neuroprotective therapy.
Methods. Ninety rabbits were treated with methylprednisolone 30 mg/kg only or with methylprednisolone 15 mg/kg in combination with phosphene stimulation with a current strength of 800 mA on the side of the lesion and 300 mA contralaterally.
Results. According to our research, traumatic damage to the orbital part of the optic nerve causes colliquative necrosis of ganglion cells and retinal nerve fibre layer oedema. Corticosteroid megadose monotherapy has resulted in a partial restoration of morphological parameters of the ipsilateral retina. Combination therapy with phosphene electrostimulation was characterized by the decrease in the retinal thickness, reduction of cytokaryometric indices and regeneration processes in bipolar and ganglionic neurons.
Conclusion. Thus, combination therapy of TON with the use of phosphene electrostimulation may be an alternative to conventional treatment, since it allows reducing the dose of corticosteroid infusions and provides the necessary neuroprotective effect.
Keywords: traumatic optical neuropathy, retina, neuroprotective therapy, phosphene electrostimulation.
REFERENCES
- Cook MW, Levin LA, Joseph MP, Pinczower EF. Traumatic optic neuropathy. A meta-analysis. Arch Otolaryngol Head Neck Surg. 1996 Apr;122(4):389–92.
- Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology. 1999 Jul;106(7): 1268–77.
- Liu D, Li L, Augustus L. Prostaglandin release by spinal cord injury mediates production of hydroxyl radical, malondialdehyde and cell death: a site of the neuroprotective action of methylprednisolone. J Neurochem. 2001 May;77(4):1036–47.
- Ben Simon GJ, Hovda DA, Harris NG, Gomez-Pinilla F, Goldberg RA. Traumatic brain injury induced neuroprotection of retinal ganglion cells to optic nerve crush. J Neurotrauma. 2006 Jul;23(7):1072–82.
- Bikbova G, Oshitari T, Baba T, Yamamoto S. Neurotrophic factors for retinal ganglion cell neuropathy - with a special reference to diabetic neuropathy in the retina. Curr Diabetes Rev. 2014 May;10(3):166–76.
- Weber AJ, Harman CD, Viswanathan S. Effects of optic nerve injury, glaucoma, and neuroprotection on the survival, structure, and function of ganglion cells in the mammalian retina. J Physiol. 2008 Sep;586(18):4393–400. https://doi.org/10.1113/jphysiol.2008
- Feng L, Puyang Z, Chen H, Liang P, Troy JB, Liu X. Overexpression of Brain-Derived Neurotrophic Factor Protects Large Retinal Ganglion Cells After Optic Nerve Crush in Mice. eNeuro. 2017 Jan 17;4(1):ENEURO.0331-16.2016. https://doi.org/10.1523/ENEURO.0331-16.2016
- Anderson RL, Panje WR, Gross CE. Optic nerve blindness following blunt forehead trauma. Ophthalmology. 1982 May;89(5):445–55.
- Spoor TC, Hartel WC, Lensink DB, Wilkinson MJ. Treatment of traumatic optic neuropathy with corticosteroids-correction. Am J Ophthalmol. 1991 Apr;111(4):526.
- Kitthaweesin K, Yospaiboon Y. Dexamethasone and methylprednisolone in treatment of indirect traumatic optic neuropathy. J Med Assoc Thai. 2001 May;84(5):628–34.
- Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD000196.
- Liu D, Li L, Augustus L. Prostaglandin release by spinal cord injury mediates production of hydroxyl radical, malondialdehyde and cell death: a site of the neuroprotective action of methylprednisolone. J Neurochem. 2001 May;77(4):1036–47.
- Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004 Oct;364 (9442):1321–8. https://doi.org/10.1016/S0140-6736(04)17188-2
- Moyseyenko N. [Activation of regenerative processes optic nerve in traumatic injury under high doses of corticosteroids]. Ukrainian Neurosurgical Journal. 2016;1:40–3. (in Ukrainian). https://doi.org/10.25305/unj.61883
- Moyseyenko NN. The role of neurohumoral dysfunction in pathogenesis of the traumatic optic neuropathy. World Of Medicine And Biology. 2017;3(61):138–42. https://doi.org/10.26724/2079-8334-2017-3-61-138-142
- Fischer D, Harvey AR, Pernet V, Lemmon VP, Park KK. Optic nerve regeneration in mammals: Regenerated or spared axons? Exp Neurol. 2017 Oct;296:83–88. https://doi.org/10.1016/j.expneurol.2017.07.008
- Benowitz LI, He Z, Goldberg J. Reaching the brain: Advances in optic nerve regeneration. Exp Neurol. 2017 Jan;287(Pt 3):365–73. https://doi.org/10.1016/j.expneurol.2015.12.015
- Fischer D, Leibinger M. Promoting optic nerve regeneration. Prog Retin Eye Res. 2012 Nov;31(6):688–701.
- Sánchez-Migallón MC, Valiente-Soriano FJ, Salinas-Navarro M, Nadal-Nicolás FM, Jiménez-López M, Vidal-Sanz M. Nerve fibre layer degeneration and retinal ganglion cell loss long term after optic nerve crush or transection in adult mice. Exp Eye Res. 2018 May;170: 40–50. https://doi.org/10.1016/j.exer.2018.02.010
Received: 29 Oct 2018
Published: April 2019