I decided to write this article after reading quite sad notification dedicated to a patient whose cornea was restored after longstanding blindness. In spite of operation successfulness, researchers observing the patient during 7 months after the operation, concluded that due to long-term visual deprivation the vision restoration may never be complete.
Being flurried with this unpromising news I
decided to investigate whether any solutions may exist. Now I would like to
share my findings with you.
Finding No.1: the issue does really exist.
One would
think that the newly developed surgical techniques, such as corneal and limbal
stem-cell transplantation, intraocular lens and artificial cornea implantation
would have to solve the issue of complete visual perception restoration for the
targeted patients. However what have turned out in fact? Studies of patients
who underwent the restorative eyesight surgery after years of blindness do not
give encouraging results. For example, Dr. Fine et al. studied the patient MM,
who lost one eye at the age of 3,5 and was blinded in the other one after
chemical and thermal damage to cornea [1]. This patient underwent the corneal
and limbal stem-cell transplantation surgery when he was 43 years old. The
surgery was successful and the patient gained acuity of 0,02 [2]. He could
easily recognize simple shapes, identify colors and discriminate the direction
of both simple and complex plaid motion [1].
In spite the patient regained the important vision functions; he still
had low acuity performance even upon 2 years after surgery as well as difficulties
with three-dimensional form, face, and gender recognition and interpretation
[1]. Even 7 years after the operation,
he still had poor spatial resolution and limited visual abilities [3].
With this
regard it is worth to mention about the “critical period theory”. The critical
period is a period of visual development when the visual stimuli are necessary
for the visual function development. This theory was extended by researchers
Dr. Lewis and Dr. Maurer, who noted that different visual functions have
different sensitive periods of development [4]. Thus, in case the visual
deprivation starts at 6 months of age, it prevents the development of normal
acuity, but does not affect the sensitivity to the global direction of motion,
which develops during the period near birth.
Accordingly, Dr. Fine et al.
supposed that MM had dissimilarities in visual function restoration because the
ability to interpret three-dimensional
forms and faces develops after early development, while the ability to
interpret motions is formed earlier in childhood [1]. Regarding the acuity it
was concluded that long standing visual loss deteriorated the spatial
resolution of the patient’s relevant visual cortex area.
Another observation
Dr. Ostrovsky et al. did while studying two congenitally blind children
suffering from dense bilateral cataract [5]. The children gained partial vision
restoration at the age of 7 and 13 due to intraocular lens implantation. As the
result, after operation children had acuity of 0,2 and 0,25 and both could
perform simple shape recognition. Nevertheless they still had poor but improved
with time (during 10-18 months) recognition of overlapping simple shapes,
i.e. perceptual organization of the
visual scene.
Thus, the theory about critical / sensitive
periods may explain the partial visual function recovery after restorative
eyesight surgery in patients who lost sight in the childhood. Nevertheless, how
the similar issue may be explained when the vision loss happens in the
adulthood?
Dr. Sikl et
al. studied the subject who lost his vision at the age of 17 because of the
explosion [6]. The patient’s cornea was damaged in both eyes. At the age of 71
he underwent an artificial cornea implantation. As the result, the patient
gained acuity of 0,33. Upon 6 and 8 months post surgery he performed a good
object recognition: 92% recognition of canonical form objects versus 20-30%
demonstrated by early-blindness patients postoperatively. Also the patient
differentiated face from non-face stimuli and successfully fulfilled simple
tasks of visual space perception. At the
same time he still had difficulties with complex 3-dimentional visual scenes
recognition, gender and two faces shown simultaneously differentiation, as well
as limited ability to integrate partial information. A neuropsychological
examination did not reveal any cognitive deficits and the patient’s performance
matched his age.
As far as is known, the sensory substitution
(e.g. spatial detection of sound, Braille reading) helps greatly to sightless
individuals in their daily life. However, does this result of cross modal
plasticity always have an advantageous impact?
Unfortunately,
it does not. Dr. Dormal et al. investigated a patient whose vision severely
deteriorated in childhood (during the age of 2,5-13 years) because of dense
bilateral cataracts [7]. After artificial cornea implantation at the age of 47,
the subject’s acuity improved from 0,04 up to 0,2 (1,5 months post surgery) and
up to 0,7 (7 months post surgery). The researchers noted the contrast
sensitivity and face individuation improvements (which though were still below
the normal range). The activity of the visual cortex before and after the
restorative eyesight surgery was monitored via functional magnetic resonance
imaging (fMRI). The researchers noted that before the surgery visual cortex of
the patient actively responded to audio stimuli. After the surgery the visual
cortex still responded to audio input which overlapped with visual responses.
Though the activation of visual cortex with sound was decreased post surgery,
it still was recorded even 7 months after the surgery. In other words, the
audio signals still competed with visual ones for being analyzed by visual
cortex. In the researcher’s opinion it may explain why the patient’s visual
performance still was below the normal level after the sight-restorative
surgery.
According
to all above mentioned,
it seems that if
the longstanding eyesight loss happens due to damage of anterior eye tissues,
surgical restoration of the tissues is not enough to regain the visual
functions to the full extent. Sounds quite pessimistic, isn’t it?
It may
well be not so sad if to come to understanding that the visual function loss is
not restricted solely to the local tissue damage [8].
Finding No.2: applying
of alternating current may partially return visual perception to sightless.
Formerly I have already written
about this therapeutic approach. Treatment with rtACS leads to improvement of
patients’ visual tasks performance. The success of rtACS was ascertained,
particularly, by clinical observational study, where patients with optic nerve
damage exhibited significant improvements in both visual field (by 9,3%) and acuity
(by 0.02) after the treatment [9]. An explanation of such phenomenon was
proposed by Dr. Sabel et al. within “residual vision activation theory” [10].
According to the theory, the visual system pathway usually is not damaged totally. There still exist some survived residual structures. Nevertheless they can’t provide proper transfer of visual information because the neuronal cell loss leads to neuronal network disorganization, i.e. to loss of network synchrony. Stimulation with rtACS forces the disorganized neuronal network to fire simultaneously. That restores the network synchrony of both survived cells within damaged region and cells of upstream visual pathway. Repetition of rtACS stimulation stabilizes the network firing synchrony. The mechanism involved is similar to one underlying the process of normal learning.
According to the theory, the visual system pathway usually is not damaged totally. There still exist some survived residual structures. Nevertheless they can’t provide proper transfer of visual information because the neuronal cell loss leads to neuronal network disorganization, i.e. to loss of network synchrony. Stimulation with rtACS forces the disorganized neuronal network to fire simultaneously. That restores the network synchrony of both survived cells within damaged region and cells of upstream visual pathway. Repetition of rtACS stimulation stabilizes the network firing synchrony. The mechanism involved is similar to one underlying the process of normal learning.
Notably that even patients considered to be
“legally blind,” almost always have some degree of residual vision and
therefore some restoration potential [10].
According to Dr. Sabel, the subject’s age, as well as age, type and location of the damage throughout visual system pathway do not influence the degree of visual restoration (it refers to injuries of nerve tissues, that is retina, optic nerve, brain regions). The only known parameter that matters for restoration, though, is the size and topography of areas of residual vision (ARVs). Vision restoration may be induced in most visual field impairments (scotoma, tunnel vision, hemianopia, acuity loss), irrespective of their etiology (e.g. stroke, neurotrauma, glaucoma, amblyopia, age-related macular degeneration). However, vision restoration is rarely complete and does not take place in all patients.
According to Dr. Sabel, the subject’s age, as well as age, type and location of the damage throughout visual system pathway do not influence the degree of visual restoration (it refers to injuries of nerve tissues, that is retina, optic nerve, brain regions). The only known parameter that matters for restoration, though, is the size and topography of areas of residual vision (ARVs). Vision restoration may be induced in most visual field impairments (scotoma, tunnel vision, hemianopia, acuity loss), irrespective of their etiology (e.g. stroke, neurotrauma, glaucoma, amblyopia, age-related macular degeneration). However, vision restoration is rarely complete and does not take place in all patients.
Sum of Findings No.1 and No.2: should we expect a light at the end of
the tunnel?
Comparing of all
abovementioned facts brought me to one presumption. Whereas noninvasive stimulation
of visual system tissues with alternating current may improve visual perception
even in patients whose blindness is caused by damage to the nervous tissues of
the visual pathway. Probably, such approach could also help to the patients whose
nerve tissues are not affected but because of the long term visual input absence
the visual function restoration doesn’t happen completely. Definitely this is
what should be investigated, but what if rtACS is what could help in
rehabilitation of the patients after surgical vision restoration and allow them
to regain the visual function to the full extent?
References:
1. Fine I, Wade AR, Brewer AA, May
MG, Goodman DF, Boynton GM, Wandell BA, MacLeod DIA (2003). Long-term deprivation
affects visual perception and cortex. Nat Neurosci 6: 915–916. DOI:10.1038/nn1102
2. Saenz M., Lewis L. B., Huth A.G., Fine
I., Koch C.(2008). Visual motion area MT+/V5 responds to
auditory motion in human sight-recovery subjects. J Neurosci. 28(20):
5141–5148. doi:10.1523/JNEUROSCI.0803-08.2008.
3.
Heimler B et al. Revisiting the adaptive and maladaptive effects of crossmodal
plasticity. Neuroscience (2014), http:// dx.doi.org/10.1016/j.neuroscience.2014.08.003
4.
Lewis T. L., Maurer D. (2005). Multiple Sensitive Periods in Human Visual
Development: Evidence from Visually Deprived Children. 2005 Wiley Periodicals, Inc., DOI:
10.1002/dev.20055.
5. Ostrovsky, Y., Meyers, E.,
Ganesh, S., Mathur, U., and Sinha, P. (2009). Visual parsing after recovery from
blindness. Psychol. Sci. 20, 1484–1491. doi: 10.1111/j.1467-9280.2009.02471.x
6. Šikl R, Šimeček M,
Porubanová-Norquist M, Bezdíček O, Kremláček J, Stodůlka P, Fine I, Ostrovsky
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Dormal G, Lepore F, Harissi-Dagher M, Albouy G, Bertone A, Rossion B, Collignon
O (2014). Tracking the evolution of crossmodal plasticity and visual functions
before and after sight-restoration. Journal of Neurophysiology, 113, 1727-1742.
doi: 10.1152/jn.00420.2014
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C., Fedorov A., Hinrichs H., Sabel B.A.(2014).Brain functional connectivity
network breakdown and restoration in blindness. Neurology 6, 542–551.doi:10.1212/ WNL.0000000000000672
9. Fedorov A, Jobke S, Bersnev
V, Chibisova A., Chibisova Y., Gall C.,
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10. Sabel
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