Jump to content

Vision restoration therapy: Difference between revisions

Add links
From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
Line 15: Line 15:


===Biology of visual neuroplasticity===
===Biology of visual neuroplasticity===
{{expert}}
[[File:Wiley Human Visual System.gif|thumb|An Illustration of the Visual System.]]
[[File:Wiley Human Visual System.gif|thumb|An Illustration of the Visual System.]]
With visual neuroplasticity, reorganization of the physical structure of the [[brain]] occurs concurrently with reorganization of the [[visual system]] by new connections made by stimulated neurons. Using the imaging technique of [[fMRI]], it was found that brain activity was altered after Vision Restoration Therapy. This associates cerebral reorganization with VRT treatment.<ref name=A0A3 /><ref name=A0A17>Vision Restoration Therapy Shown To Improve Brain Activity In Brain Injured Patients. (2007). Retrieved September 11, 2010 from ScienceDaily, www.sciencedaily.com: http://www.sciencedaily.com/​releases/​2007/​08/​ 070814082950.htm.</ref>
With visual neuroplasticity, reorganization of the physical structure of the [[brain]] occurs concurrently with reorganization of the [[visual system]] by new connections made by stimulated neurons. Using the imaging technique of [[fMRI]], it was found that brain activity was altered after Vision Restoration Therapy. This associates cerebral reorganization with VRT treatment.<ref name=A0A3 /><ref name=A0A17>Vision Restoration Therapy Shown To Improve Brain Activity In Brain Injured Patients. (2007). Retrieved September 11, 2010 from ScienceDaily, www.sciencedaily.com: http://www.sciencedaily.com/​releases/​2007/​08/​ 070814082950.htm.</ref> {{dead-link}}


The [[cerebrum]] is involved with higher brain function, and one component of the cerebrum is the [[primary visual cortex]]. The primary visual cortex is a region in the [[occipital lobe]] that can be altered by neuroplasticity to create new neuronal pathways around damaged areas to help regain lost visual functions. Sensory visual information is sent from the retina of the eye to the [[Lateral geniculate nucleus]] (LGN) in the [[Thalamus]], which relays the visual information to the primary visual cortex by the fibers of the [[optic radiation]]. Lesions or damage to parts of the brain that cause visual field defects usually occur posterior to the [[optic chiasm]].<ref name=A0A2>Farah, M. J. (2000). The Cognitive Neuroscience of Vision. Malden, Massachusetts: Blackwell Publishers Inc.</ref> Although the exact mechanisms that underlie regaining visual field functions through visual neuroplasticity and VRT are not yet fully known, the reorganization of the primary visual cortex is thought to make new connections and pathways in the optic radiation to the LGN to help regain visual field functions. The stimulation of existing neurons near a damaged site in the brain can form new [[synapse]]s with other functional neurons to help take on and compensate for the function lost due to the damaged neurons. This is what is theorized to occur during VRT treatment.<ref name=A0A3 /><ref name=A0A15 /><ref name=A0A2 />
The [[cerebrum]] is involved with higher brain function, and one component of the cerebrum is the [[primary visual cortex]]. The primary visual cortex is a region in the [[occipital lobe]] that can be altered by neuroplasticity to create new neuronal pathways around damaged areas to help regain lost visual functions. Sensory visual information is sent from the retina of the eye to the [[Lateral geniculate nucleus]] (LGN) in the [[Thalamus]], which relays the visual information to the primary visual cortex by the fibers of the [[optic radiation]]. Lesions or damage to parts of the brain that cause visual field defects usually occur posterior to the [[optic chiasm]].<ref name=A0A2>Farah, M. J. (2000). The Cognitive Neuroscience of Vision. Malden, Massachusetts: Blackwell Publishers Inc.</ref> Although the exact mechanisms that underlie regaining visual field functions through visual neuroplasticity and VRT are not yet fully known, the reorganization of the primary visual cortex is thought to make new connections and pathways in the optic radiation to the LGN to help regain visual field functions. The stimulation of existing neurons near a damaged site in the brain can form new [[synapse]]s with other functional neurons to help take on and compensate for the function lost due to the damaged neurons. This is what is theorized to occur during VRT treatment.<ref name=A0A3 /><ref name=A0A15 /><ref name=A0A2 />


Vision Restoration Therapy stimulates the retina of the eye using repetitive points of light that flash on a computer screen. These flashing lights are aimed to stimulate the border of the blind area of a patient’s visual field. The repetitive stimulation is used to help promote visual neuroplasticity and ultimately make new neuronal connections to regain and expand the visual field.<ref name=A0A3 /><ref name=A0A15 />
Vision Restoration Therapy stimulates the retina of the eye using repetitive points of light that flash on a computer screen. These flashing lights are aimed to stimulate the border of the blind area of a patient’s visual field. The repetitive stimulation is used to help promote visual neuroplasticity and ultimately make new neuronal connections to regain and expand the visual field.<ref name=A0A3 /><ref name=A0A15 />{{primary}}


==Process of therapy==
==Process of therapy==

Revision as of 18:40, 5 January 2012

Vision Restoration Therapy (VRT) is a noninvasive, nonsurgical form of Vision therapy provided by NovaVision.[1] This therapy was developed by Bernhard Sabel, Ph.D. The phenomenon underlying the therapy is visual neuroplasticity.[2]

Description of therapy

Vision Restoration Therapy is a computer-based treatment therapy, and is used to help patients with visual field defects regain function by stimulating existing visual neurons to rewire and make new connections.[3] This therapy is cleared by the U.S. Food and Drug Administration (FDA) to treat visual field defects due to stroke, head injury, brain tumors, and brain surgery. Some other defects that can also be treated with VRT include hemianopia, quadrantanopia, scotoma, and diffuse field defect.[2]

Science behind the therapy

Neuroplasticity

There exist two approaches for visual neurolasticity:

The Primary Visual Cortex (red) is shown along with the extrastriate visual cortical areas (orange and yellow) from the rear view. These areas make up the Visual Cortex.

Biology of visual neuroplasticity

An Illustration of the Visual System.

With visual neuroplasticity, reorganization of the physical structure of the brain occurs concurrently with reorganization of the visual system by new connections made by stimulated neurons. Using the imaging technique of fMRI, it was found that brain activity was altered after Vision Restoration Therapy. This associates cerebral reorganization with VRT treatment.[2][5] [dead link‍]

The cerebrum is involved with higher brain function, and one component of the cerebrum is the primary visual cortex. The primary visual cortex is a region in the occipital lobe that can be altered by neuroplasticity to create new neuronal pathways around damaged areas to help regain lost visual functions. Sensory visual information is sent from the retina of the eye to the Lateral geniculate nucleus (LGN) in the Thalamus, which relays the visual information to the primary visual cortex by the fibers of the optic radiation. Lesions or damage to parts of the brain that cause visual field defects usually occur posterior to the optic chiasm.[6] Although the exact mechanisms that underlie regaining visual field functions through visual neuroplasticity and VRT are not yet fully known, the reorganization of the primary visual cortex is thought to make new connections and pathways in the optic radiation to the LGN to help regain visual field functions. The stimulation of existing neurons near a damaged site in the brain can form new synapses with other functional neurons to help take on and compensate for the function lost due to the damaged neurons. This is what is theorized to occur during VRT treatment.[2][4][6]

Vision Restoration Therapy stimulates the retina of the eye using repetitive points of light that flash on a computer screen. These flashing lights are aimed to stimulate the border of the blind area of a patient’s visual field. The repetitive stimulation is used to help promote visual neuroplasticity and ultimately make new neuronal connections to regain and expand the visual field.[2][4]

Process of therapy

Patients undergo therapy in the comforts of their home due to it being a software-based therapy sent to patients as a specialized portable apparatus called NovaVision VRT Device. The therapy requires a prescription from a physician in order to begin. A set of initial evaluation tests are taken using the VRT device to assess the amount of visual impairment and the locations of the borders of the visual field deficit. The therapy provider, NovaVision, then analyzes these data to customize the treatment to target these borders of deficit to help expand the visual field. Usually, patients complete the treatment course in 6 months. The therapy consists of patients using the VRT device for 30 minutes twice a day for 6 days of the week during the 6 month treatment course.[2]

Patients perform this therapy using the VRT device as stated before. The VRT device consists of a chin rest and a specialized computer screen that has High Resolution Perimetry (HRP) incorporated into its software. The built-in HRP helps in assessing and tracking the progress of the patient. The device sends this data directly to the therapy provider for feedback to modify the treatment if necessary.[2] HRP is used to map the visual field of a patient. This allows the therapy providers to have a representation of the patient's visual field.[7] For a general VRT session, the patient’s head is situated at eye level with the VRT device. The therapy begins by projecting a fixation point in the center of the screen. The patient focuses on this fixation point for the entire session. As the patient is focusing on the central fixation point, an individual point appears somewhere on the screen. Only one point is projected at a time alongside the fixation point. The patient must click the mouse every time he or she sees this point while focusing on the fixation point. These responses are collected to calculate stimuli detection rate and response time of the patient. In an effort to see the points on the screen most clearly, the therapy should be conducted in a dimly lit room.[2]

Skepticism

The effectiveness of VRT has been a controversial topic. Beneficial results have been researched and documented by testing small groups of patients. This has led to skepticism by some of the scientific community.[7] Even though VRT has been available for a few years now, optometrists, ophthalmologists, and other eye specialists do not regularly recommend VRT for their patients. The primary cause of this is that eye specialists rarely recommend this therapy to other eye specialists. The skepticism of VRT may be the source of the lack of recommendation.[8]

When VRT was first introduced, the primary skepticism involved the data collection methods that the VRT researchers used to quantify the effective results of using the therapy. The main argument was that the HRP data from the VRT device that was used to measure the progress of the patients was the same data used to show the effectiveness of VRT. These data would not be as reliable as data gathered using some other Perimetry technique.[9] Skeptics turned to studies that assessed VRT effectiveness using Tubinger Automatic Perimetry and Scanning laser ophthalmoscopy (SLO), which showed that no beneficial results in improving the visual field were associated with VRT use.[9] Skepticism also arose about the quality of life questionnaire surveys that patients took after VRT treatment. The possibility of the placebo effect could be present in the answering of these questionnaires.[9] Patients could have stated that their qualities of life did improve just because they had finished the therapy, even if no improvements actually occurred. Others questioned the neuroplastic mechanism behind VRT, stating that no salvageable tissue remains in the occipital lobe with vision deficits such as hemianopia. Neuroplasticity cannot make new connections according to this claim, which debunks VRT in its entirety.[9][10] It was proclaimed that eye movements were the cause of visual rehabilitation instead of self regeneration of the brain and visual neuroplasticity.[9]

Pilot studies

Pilot studies have looked into the effects of Vision Restoration Therapy in treating visual field defects that have resulted from anterior ischemic optic neuropathy and glaucoma. Although these are pilot studies and require more data, it seems promising that VRT can help restore some visual functions of patients with anterior ischemic optic neuropathy.[11]

References

  1. ^ Caplan, L. R., Firlik, A., Newman, N. J., Pless, M., Romano, J. G., & Schatz, N. (2005). Vision restoration therapy. [Letter]. British Journal of Ophthalmology, 89(9), 1229-1229. doi: 10.1136/bjo.2005.069773
  2. ^ a b c d e f g h Frequently Asked Questions: Vision Restoration Therapy: Vision Rehab after Stroke or TBI. (2007). Retrieved November 12, 2010 from NovaVision, www.novavision.com: http://www.novavision.com
  3. ^ Romano, J. G., Schulz, P., Kenkel, S., & Todd, D. P. (2008). Visual field changes after a rehabilitation intervention: Vision restoration therapy. [Article]. Journal of the Neurological Sciences, 273(1-2), 70-74. doi: 10.1016/j.jns.2008.06.026
  4. ^ a b c Sabel, B. A. (2008). Plasticity and restoration of vision after visual system damage: An update. [Article]. Restorative Neurology and Neuroscience, 26(4-5), 243-247.
  5. ^ Vision Restoration Therapy Shown To Improve Brain Activity In Brain Injured Patients. (2007). Retrieved September 11, 2010 from ScienceDaily, www.sciencedaily.com: http://www.sciencedaily.com/​releases/​2007/​08/​ 070814082950.htm.
  6. ^ a b Farah, M. J. (2000). The Cognitive Neuroscience of Vision. Malden, Massachusetts: Blackwell Publishers Inc.
  7. ^ a b Mueller, I., Mast, H., & Sabel, B. A. (2007). Recovery of visual field defects: A large clinical observational study using vision restoration therapy. [Article]. Restorative Neurology and Neuroscience, 25(5-6), 563-572.
  8. ^ Dr. Mona Patel, Doctor of Optometry at the Ochsner Clinic LLC in Marrero,LA. Interview date October 25, 2010.
  9. ^ a b c d e Horton, J. C. (2005). Disappointing results from Nova Vision's visual restoration therapy. [Editorial Material]. British Journal of Ophthalmology, 89(1), 1-2. doi: 10.1136/bjo.2004.058214
  10. ^ Disappointing results from Nova Vision’s visual restoration therapy
  11. ^ Jung, C. S., Bruce, B., Newman, N. J., & Biousse, V. (2008). Visual function in anterior ischemic optic neuropathy: Effect of Vision Restoration Therapy - A pilot study. [Article]. Journal of the Neurological Sciences, 268(1-2), 145-149. doi: 10.1016/j.jns.2007.12.001
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Vision_restoration_therapy&oldid=469759835"