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Vision therapy: ocular motor training in mild traumatic brain injury

Jason J S Barton MD PhD FRCPC (1)


Paul Ranalli MD FRCPC (2)

1) Departments of Medicine (Neurology), Ophthalmology and Visual Sciences,


Psychology, University of British Columbia, Vancouver, Canada
2) Departments of Medicine (Neurology), Ophthalmology and Visual Sciences, Oto-
laryngology, University of Toronto, Toronto, Canada (pjranalli@aol.com)

Address correspondence to:

Jason J S Barton
Section K, Neuro-ophthalmology
VGH Eye Care Centre
2550 Willow Street
Vancouver, British Columbia
Canada V5Z 3N9
604 875 4339 (phone)
604 875 4302 (fax)
jasonbarton@shaw.ca

Key words: midline shift; post-trauma vision syndrome; eye exercise; attention
word count: abstract - 151; article – 4396 (limit 4500)
references – 99 (limit 100)

This article has been accepted for publication and undergone full peer review but has not
been through the copyediting, typesetting, pagination and proofreading process which may
lead to differences between this version and the Version of Record. Please cite this article as
doi: 10.1002/ana.25820

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Vision therapy in mTBI

ABSTRACT

Vision therapy in the form of ocular motor training is increasingly used to treat visual
complaints, particularly in the setting of persistent symptoms after mild traumatic brain
injury (mTBI). In this review we discuss the rationale behind this intervention and the
evidence for its efficacy. While the efficacy of exercises for primary convergence
insufficiency is plausible and supported by data, there is not yet strong evidence of
benefit for the post-traumatic variant. It is not established that abnormalities in fixation,
pursuit and saccades in mTBI are the cause of post-concussive symptoms, or that these
abnormalities arise from ocular motor damage rather than being secondary effects of
cognitive problems with attention or executive control. The few studies to date have
significant methodological weaknesses. More substantial evidence is required before
vision therapy can be accepted as a useful tool in the rehabilitation of patients with brain
trauma.

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Vision therapy in mTBI

‘Vision therapy’ has been defined as “a sequence of neurosensory and neuromuscular


activities…to develop, rehabilitate and enhance visual skills and processing” 1 . A
significant component of current vision therapy is devoted to treating vergence,
accommodative, and eye movement anomalies, which often involves sessions of “ocular
motor training” 2 . The most established indication for vision therapy is primary
convergence insufficiency. Study of this application began with small randomized trials
of vergence training 3, 4 . A larger study of 60 older adults who were randomly assigned to
a control group or 24 weeks of treatment then showed more improvement on objective
and subjective measures with combined office and home training 5 . The Convergence
Insufficiency Treatment Trial consisted of a series of reports of placebo-controlled multi-
center randomized studies in children 6-9 and young adults 10 . These showed that vergence
measures and symptoms improved more after 12 weeks of office-based therapy than with
home-based exercises, prisms, or an office-based placebo 11 .

Vision therapy has also been promoted for a wide range of neurologic and other
developmental conditions 12, 13 , though with little evidence yet for most 13 . Here we focus
on the most rapidly growing use of vision therapy, for persistent visual and non-visual
symptoms that are attributed by some to a visual disorder caused by mild traumatic brain
injury (mTBI). The rationale behind this is a deceptively simple calculus, which runs
something like this:
1. Visual symptoms are common after head trauma.
2. Ocular motor function can be abnormal after head trauma.
3. Ocular motor dysfunction can affect vision.
4. Improving ocular motor function can reduce visual symptoms from head
trauma.
However, simple arguments often turn out to hide important complexities. In this
review we visit these four points to examine the logic and evidence behind each of these
four statements.

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Vision therapy in mTBI

1. Visual symptoms in traumatic brain injury.

Visual complaints are not uncommon after head trauma 14, 15 . Some reflect damage to
the optic nerve or other components of the retino-striate relay. These are identified by
their visual field defects 15 , clinical signs, or neuroimaging, just as with other pathology.
Such damage occurs mainly after severe injuries 16, 17 : a recent meta-analysis found that
only 6% of mTBI patients had visual field defects and none had a decline in visual acuity
18 .

Nevertheless, less specific visual symptoms form part of the range of persistent
complaints of mTBI patients. This is reflected in items relating to blurry vision, diplopia
and dizziness on instruments like the Rivermead Post-concussion Symptoms
Questionnaire 19 , as well as symptoms of eye strain, light sensitivity, and difficulty
reading 20 . Factor and classification analyses suggest that the large variety of post-
concussive symptoms can be grouped into separate domains such as cognition, mood,
pain, and dizziness/visual complaints, which vary in their prevalence and association with
each other and can follow diverging trajectories in recovery 21-25 .

Beyond symptoms like blur and diplopia, there are proposals that visual or ocular
motor dysfunction may be at the root of a larger range of symptoms. Post-trauma vision
syndrome 26, 27 is one such construct (Table). The term is somewhat problematic. It is not
a symptomatic descriptor, since some of the listed symptoms are not visual. As a
mechanistic explanation, it is not clear that its hypothesized account of impaired visual
processing 27 is the cause of all of these complaints. Brain trauma can have diffuse,
multiple effects, including impacts on ocular motor, vestibular, cognitive, psychological
and musculoskeletal systems, which could generate some of these symptoms too.
Problems that have their counterparts in other modalities – e.g. both light and sound

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Vision therapy in mTBI

intolerance, or poor concentration when reading or in conversation – are particularly


likely to reflect problems handling stimuli at a broader level than just vision.
Midline shift syndrome is another proposed visual consequence of trauma. It refers to
a deviation of the subjective estimate of midline. It is hypothesized to represent a
mismatch between visual and proprioceptive information about the body’s centre of mass
28 , but why a mismatch should lead to a biased error is not clear. This is reported to occur
with strokes, brain trauma, or even aging. Strokes tend to cause focal lesions whose
locations determine their behavioural effects, but the location of the damage that causes
midline shift has not yet been stated. Nevertheless, shifts in midline are not unknown in
patients with unilateral lesions: right parietal lesions can cause an egocentric hemi-
neglect, with ipsilateral deviation of the estimate of ‘straight ahead’ in the dark 29 .
Subjects with unilateral vestibular lesions can show past-pointing towards the side of the
lesion with eyes closed 30 . It is less clear why a similar spatial shift should results from a
diffuse problem like mTBI, which by most definitions excludes focal lesions on imaging
31 .

2. Ocular motor dysfunction in traumatic brain injury

There is evidence of ocular motor dysfunction after head trauma, particularly if the
latter is severe. An early eye-tracker study of 28 patients with brain trauma requiring
craniotomy found various abnormalities in 75%, including impaired vergence, delayed
and inaccurate saccades, and reduced pursuit 32 . Clinical signs of convergence
insufficiency were found in 40% of subjects who had been in coma after trauma, and
attributed to midbrain damage 33 . Convergence insufficiency and nerve palsies were the
most common ocular motor problems in a series of 60 patients, most with severe head
injuries 34 . Convergence and accommodation problems are also frequent with brain
trauma in the military setting, including blast injuries 15, 35, 36.

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Vision therapy in mTBI

What about mTBI specifically? Ocular motor nerve palsies are rare, occurring in only
0.3% 37 . Some reported that convergence insufficiency is present in up to half of patients
38, 39 but others found it to be minimal 40 . A meta-analysis concluded that convergence
insufficiency occurs in 37% of mTBI patients 18 . Detailed studies have showed that
dynamic vergence measures are reduced 41 , and vergence instability may be reflected in
greater horizontal dysconjugacy during naturalistic viewing 42 .

Pursuit of a predictably moving target is reduced in some studies 43-45 but others
found little change 46, 47 . More complex protocols showed an impaired ability to follow
the predicted trajectory of a target after it disappears 48, 49 . Some reported that pursuit gain
is not reduced but more inconsistent, a defect accentuated by a concurrent working
memory task 50, 51 . These support assertions that tracking deficits in mTBI are due to
attentional and executive dysfunction rather than ocular motor impairment 44 .

Studies of saccades in mTBI have produced mixed results. Some found slower,
hypometric or delayed saccades 47, 52 . Others did not find any deficits in the accuracy or
timing of visually guided saccades, antisaccades or memory-guided saccades 40, 53 . A key
report showed that both post-injury status and task complexity are important determining
factors 45 . This compared 36 mTBI patients with persistent post-concussive symptoms to
36 without. Simple visually guided saccades were not impaired on any metric and the
velocities of all types of saccades were normal. Rather, those with post-concussive
symptoms had more errors with antisaccades and memory-guided saccades, fewer self-
paced saccades, and minor problems with timing memory-guided saccades. They
concluded that ocular motor measures indexed cognitive problems with decision-making,
attention, sequence programming, and response inhibition. This accords with reviews and
meta-analyses showing that mTBI minimally affects visually guided saccades but impairs
saccades with more cognitive demands, namely antisaccades and memory-guided
saccades 54, 55 . In a related vein, a study using a simultaneous working memory task found
that in mTBI saccades are only impaired under conditions of high cognitive load 56 .

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Vision therapy in mTBI

Despite these nuances, there is a suggestion that ocular motor deficits may be an
objective biomarker of mTBI 55, 57 . The claim is that eye movements are vulnerable to
trauma because they use widely distributed pathways that are susceptible to brain injury
55, 57 . However, most studies of pursuit and saccades show that their basic properties are
unaffected by mTBI, and that problems only become apparent under greater cognitive
demands. If so, the value of eye movements in mTBI may derive more from their probing
of cognitive operations frequently impacted by head injury. This becomes relevant to
vision therapy when we ask what it is that is being trained. It also underscores the need to
exclude confounding effects of co-morbid conditions or psychoactive drugs that can
secondarily alter eye movements 58-60 . Ocular motor studies in schizophrenia typically
consider or control for medication effects 59, 61, 62 , but less so the mTBI literature.

3. The link between visual symptoms and ocular motor signs.

Do ocular motor signs cause symptoms in daily life? Problems with convergence or
accommodation can cause blur or binocular horizontal diplopia when the patient is
reading but not when viewing distant objects. Convergence insufficiency has also been
blamed for more vague symptoms provoked by near work, including headaches, eye
strain, and reading complaints such as moving print, losing one’s place on the line, lack
of concentration and poor comprehension 63, 64 . Such symptoms do occur with atraumatic
convergence insufficiency 65 , but given the potentially diffuse nature of mTBI, one needs
to be cautious that cognitive problems with attention, concentration, and working
memory are not contributing to these less specific complaints.
A causal link between impaired pursuit or saccades and post-traumatic symptoms is
more dubious. For one, patients with impaired pursuit or saccades from cerebellar
dysfunction generally do not have similar complaints. Conversely, ocular motor tests may
provoke headache or dizziness in mTBI patients even though pursuit and saccades appear

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Vision therapy in mTBI

normal clinically 66 . The possibility that cognitive problems cause both ocular motor
changes as well as visual complaints like impaired reading means that the latter two may
be correlated but not necessarily that one causes the other. Thus retrospective reviews
that find that patients with visual symptoms often have abnormal eye movements 67

provide correlative observations but logically cannot establish causal links.

4. Vision therapy (ocular motor training): the evidence

Regardless of the variable certainty about the link between different eye movements
and the diverse symptoms of mTBI, an important issue is the empirical evidence for
amelioration of symptoms by vision therapy.

i. Training of vergence eye movements

While there is good evidence that exercise therapy can help primary convergence
insufficiency6-10 , there is less data about its effect on the post-traumatic variant. One
retrospective review claimed resolution or improvement of convergence insufficiency in
all of 43 patients treated a mean of 31 weeks after injury, but did not provide data on the
80 who declined or did not complete treatment 39 . There is one prospective study of 19
patients with various forms of brain damage, 15 with trauma of undefined severity 63 .

Thirteen of the 19 completed 12 weeks of home computer vergence therapy and


improved in objective measures and symptom scores, though not back to normal. The
authors acknowledged the limitations of small sample size and the lack of a placebo arm.
A study to be discussed in more detail below included vergence exercises as part of a
larger training program in 12 mTBI subjects 2 . This used a crossover design comparing 6
weeks of ocular motor versus placebo training. Vergence was trained with both prisms
and moving targets. Training was reported to improve laboratory measures of vergence,

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Vision therapy in mTBI

the near point of convergence, scores on the Convergence Insufficiency Symptom Scale,
and performance on the Visual Search and Attention Test. In a 6–month follow- up of
eight subjects, vergence and accommodation measures remained good, but scores on the
Convergence Insufficiency Symptom Scale relapsed to baseline 68 . However, in separate
ANOVAs for the two crossover groups, vergence improvements were seen only in the
five who started with the placebo, whereas the only effect in the four who started with
treatment was a positive placebo effect on near point of convergence.
Overall, there are points lending support for treating post-traumatic convergence
insufficiency. It likely occurs with mTBI. It can cause symptoms such as blur or diplopia
when reading. There is evidence that training improves primary convergence
insufficiency. However, what is missing is proof that treatment works for the post-
traumatic variant, a need that has motivated a recent pilot study 69 .

ii. Accommodative therapy

Accommodation and convergence are closely linked functions. They occur together
as parts of the near triad, and dysfunction of either can degrade vision at near. Patients
with convergence problems often but not invariably have accommodative insufficiency:
for example, 74% of children in the Convergence Insufficiency Treatment Trial also had
accommodation dysfunction 70 . Accommodative problems occur with mTBI 71 , with a
meta-analysis suggesting a prevalence of about 40% 18 . For these reasons, current vision
therapy protocols often include accommodative training 70, 72, 73.

Compared to vergence therapy, less is known about accommodative training. An


earlier review concluded that there were no studies with sufficiently sound experimental
design prior to 2009 74 . Subsequently, a sub-analysis of the Convergence Insufficiency
Treatment Trial looked at 164 children with associated accommodative insufficiency and
found that both home and office therapy were superior to placebo in their effects on

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Vision therapy in mTBI

accommodation 70 . As others noted 73 , though, there are little data on treating


accommodative insufficiency in mTBI. A retrospective study included accommodative
therapy with ocular motor training but did not describe the effects on accommodation 72 .

The 2013/14 Ciuffreda group’s studies below reported that their non-targeted treatment
protocol in 12 subjects improved accommodative amplitude, facility and velocity, but not
gain 73 . The general concerns about this study will be described below.

ii. Training of conjugate (version) eye movements

The use of training to improve other eye movements after brain damage began with
two studies 30 years ago. The first studied ten patients shortly after head trauma 75 .

Although no diagnostic criteria were given, most likely had severe injuries, since the
timeline started when subjects “regained consciousness”. Subjects were without
brainstem or cerebellar disorders, had intact visual fields, and were not on medication for
at least four days. Six of the ten trained on saccades, optokinetic nystagmus and vergence
for 7 to 15 weeks, four served as controls. Before training their saccades were delayed,
slower and less accurate. Latency normalized and saccadic gain improved over 7 months
in all ten, though faster with training. Optokinetic gain also improved in all, with some
trained subjects showing faster improvement, particularly at higher target velocities. A
second study followed nine patients with traumatic lesions of one hemisphere, five of
whom had 3 to 10 weeks of pursuit training 76 . All began with an ipsi-directional defect
in smooth pursuit, and the gain of pursuit or the optokinetic slow phase improved faster
with training.
These early works have some key points. On the positive side, they had untrained
brain-injured subjects as controls: as important as the training effects were their
observations of natural recovery in these controls. On the negative side, subjects were not
randomized. They had severe brain injuries, limiting the relevance to mTBI. Finally,

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Vision therapy in mTBI

there was no comment about the effect on symptoms or daily life, as these studies were
aimed at showing plasticity, not therapeutic efficacy.
Symptoms formed part of the inclusion criteria in another study 77 . Patients were
diagnosed with mTBI by a neurologist or neuropsychologist, by unstated criteria, and
included if they had some visual complaint. Eighteen subjects were treated and 32 not: it
is not stated if assignment was random. The form and duration of rehabilitation were
individualized. All had a detailed clinical evaluation but the findings were not reported.
The outcome variable was the latency or amplitude of the visual evoked potential (VEP),
which normalized in a third of treated but in none of the untreated individuals. Effects on
visual symptoms were not described.
The results of a pilot study of two patients, one with trauma and one with a left
occipital stroke 78 , were likely included in a later uncontrolled report of 9 subjects with
trauma and 5 with strokes causing hemifield defects 79 . Criteria for and severity of injury
were not given. Subjects had two 6-week periods of training of fixation, saccades, pursuit
and a ‘simulated reading’ task, with or without auditory feedback. They improved on a
subjective questionnaire about reading and made fewer saccades on a simulated reading
test. However, there was no change in eye movements or comprehension during actual
reading.
Two years later this group retrospectively reviewed 33 subjects with brain trauma, on
average about 3 years after injury, as well as 7 subjects with strokes 72 . Diagnostic criteria
for and severity of traumatic brain injury were not defined. They reported various
problems with vergence, accommodation and versions, and trained everyone on all three.
Reading problems, eyestrain and headache were the most common symptoms, and
convergence insufficiency the most frequent finding. They claimed success in 90% of
patients, which was improvement in at least one of 9 symptoms and at least one of 11
signs. It is not clear how many symptoms or signs each patient had, or which improved.

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Vision therapy in mTBI

iii. The Ciuffreda group’s studies of 2013/2014

The main support for vision therapy is a study published as a series 2, 80, 81 . Because

these articles are the main support for vision therapy in mTBI, we discuss them in detail.
The trial involved 12 young adults (ages 23 to 33 years) with mTBI by undefined criteria,
occurring 1-10 years prior. A crossover design was used. Subjects trained in 12 sessions
over 6 weeks, with each session having three 15-minute segments, one each for vergence,
accommodation, and versions. The latter included fixation for 60 seconds, making
predictable horizontal or vertical saccades, and a simulated reading task in which they
made saccades to targets arranged in horizontal rows. For the placebo control of version
training, subjects fixated the middle of an empty screen, completed visual puzzles, and
scanned pictures for a memory test. They found that horizontal but not vertical stability
of fixation improved with training, and subjects made fewer saccades during simulated
reading with multiple lines but not with a single line 80 . Saccadic gain increased for 3 of 4
conditions but latencies did not.
Reading effects were described separately 81 . Reading speed improved from 142 to
177 words per minute and subjects made fewer saccades during reading. Comprehension
did not change. Improved reading speed correlated with improvements in
accommodation, vergence and attention, but not with saccadic changes. Statistical
methods were not described beyond giving p values, which were not provided for placebo
effects. Later they reported on the durability of effects 6 months later, now with 15
subjects trained, but follow- up in only eight and no details about the other seven.
ANOVA details were not given, but they reported that reading rate remained good and
comprehension improved in a delayed fashion 68 .

This same group reported on effects of training on VEPs in a separate set of 7


subjects 82 . This paper listed criteria for mTBI, but had no control group or placebo
intervention. Training had a number of VEP effects and improved scores on the Visual

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Vision therapy in mTBI

Search and Attention Test. They attributed VEP changes to more stable vergence and
accommodation, but did not provide data on the latter.
These studies are important to the field but have several weaknesses, which led a
recent Cochrane review to classify their evidence as ‘very low certainty’ 83 . First is the
lack of diagnostic criteria for mTBI. Second is the small cohort size, made smaller
because three subjects who did training first dropped out before doing the placebo arm.
Third, it is not stated if assignment was randomized. Fourth, the narrow age range (24-33
years) limits generalization to older adults, who form a significant proportion of patients
with head injury from falls or traffic accidents 84 . Fifth, medication use is not detailed,
apart from a statement that exclusion criteria included “Medications that alter ocular
motor function and/or attentional state” (p. 132) 81 . Sixth, the dropout rate of 25% in the
initial studies and 45% in the follow-up report 68 may cause over-estimation of benefit.
Seventh, the crossover design is problematic 83 . While this has the advantage of each
subject acting as their own control, it is more appropriate for interventions whose effects
decay after cessation, with washout periods that can reset the baseline between the first
and second interventions and allow assessment for carry-over effects (see 85 ). If the
durability of training effects is unknown, then it is difficult to designate an appropriate
baseline for the placebo arm in those who train first. In this scenario it is better to
randomly assign separate groups for training and placebo, as done by some studies of
vestibular therapy in mTBI 86, 87 .

Eighth, the statistical analyses relied on multiple t-tests comparing initial and post-
training assessments, without correction for multiple comparisons. For example, there
were eight lab-based measures of vergence, and Bonferroni adjustment would set
significance at p < .006. They did not provide specific p values once they exceeded 0.01,
but their t-values suggest that changes in the near point of convergence as well as the
velocity and time constant of vergence may have been significant. With 14 parameters in

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Vision therapy in mTBI

the versions study, the threshold for significance would be p < .0036. One result met this
bar, the number of saccades when scanning multiple lines.
A better analysis would be an ANOVA of the 9 subjects who completed both placebo
and treatment. They reported separate ANOVAs on the four who did training first (group
A), and the five who did placebo first (group B). For versions, the horizontal stability of
fixation improved in group A but not group B, while saccadic gain and velocity increased
in group B but not group A 80 . These inconsistencies could reflect their small sample, but
still raise concern about the conclusions based on t-tests.
The training of vergence, accommodation and versions in all patients regardless of
individual findings raises some issues. First, mTBI is heterogeneous: subjects vary in
which and how many of these functions are impaired 21, 25 , and not all patients will need
training of all three. Second, this approach makes it difficult to determine which aspects
of training were effective. Given the efficacy of training for primary convergence
insufficiency 5-7, 10 , and the fact that their strongest results related to vergence 2 , their
vergence training may have had some effect. However, it is difficult to infer any
symptomatic utility of training saccades or fixation. Indeed, gains in reading rate
correlated with improvements in vergence rather than saccades 81 .
One interesting final point is their use of rapid serial visual presentation in training
versions. This technique has subjects report how many times a certain target appears in a
rapid series of images. To do this requires sustained attention, concentration and working
memory. Given that attentional dysfunction is common after head injury 88 , a valid
question is whether any benefits derived inadvertently from the training of attention
rather than eye movements. A propos, their improved reading rates correlated with
improvement on a test of attention 81 . The arguments made against this attribution 82 are
not convincing, being based on inferences from studies of pediatric reading disabilities
that may not be accurate 89, 90 .

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Vision therapy in mTBI

5. Conclusions and future directions

Visual complaints occur after mTBI. Some can be linked convincingly to problems
such as convergence or accommodative insufficiency, and the best candidate for
treatment efficacy may be therapy for post-traumatic vergence dysfunction, and possibly
for accommodative insufficiency, but randomized trials are needed to establish that there
is benefit beyond natural recovery. On the other hand, one can question the utility of
training fixation, pursuit and saccades. First, there is little evidence that abnormalities of
these eye movements cause post-traumatic symptoms. Second, it is not clear whether
these abnormalities reflect ocular motor or cognitive dysfunction. Third, current studies
do not show convincing evidence of efficacy: some were retrospective, others had too
few subjects, lacked appropriate controls, or performed inadequate statistical analyses.
How can we advance from the current state of affairs? Future trials should have
design virtues such as adequate sample size, random assignment, blinding of subjects if
possible, and blinded evaluators. Specific diagnostic criteria should be used and clinical
details given, since it is unclear whether all types of mTBI (e.g. military blast injury
versus traffic accident) create equivalent effects 15 . While we await clarification regarding
whether the mechanism of injury is an important source of heterogeneity, one might
consider analyses of sub-groups with different etiologies. The natural improvement of
mTBI should be reflected in study design, with an untrained cohort matched for duration
and severity, and reassessment after several months, not only to ensure that treatment
effects persist, but also to show that the control group does not improve eventually to the
same level 75 . Effects of cognitive dysfunction, medications and co-morbid conditions
need to be considered. Studies should evaluate outcome measures relevant to function,
with a statistical analysis comparing trained and untrained groups. While the value of
binocular VEPs as currently used is limited, newer methods of studying perfusion,
connectivity, or task-related activation, may provide secondary outcome measures that

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Vision therapy in mTBI

could also advance our knowledge of the underlying neurophysiology of mTBI and its
treatment 91, 92 .

One should also consider the possibility that treatment effects actually derive from
improved cognition and attention. If so, there are two implications. First, the inclusion of
measures of attention among outcome variables would be important. While the use of a
visual search test in prior studies was commendable 2, 82 , it may be important to assess
multiple types of attention 93, 94 to determine which respond to treatment and/or correlate
best with ocular motor dysfunction. New tests of attention such as multiple object
tracking that appear to be particularly sensitive to mTBI 95 may prove to be good indices
of treatment effects. Second, an important control or comparison group would be one
undergoing cognitive rehabilitation. This could include not only standard but also novel
approaches. For example, recent reviews detail the mounting evidence that video games
can improve attention and spatial cognition 96-98 , and these have been applied recently to
the study of TBI patients 99 . It would be of interest to see how the efficacy and
compliance rates of these various approaches compare in the clinical setting.
Treatment of the many facets of persistent symptoms after mTBI remains a challenge.
Fifteen years ago others identified conceptual difficulties, lack of clarity about natural
history, and a paucity of good prospective trials as limiting factors in the field 100, 101.

There are similar issues regarding the treatment of ocular motor aspects of mTBI, not
only for vision therapy but also for pharmacologic interventions 83 . Further work
incorporating the features discussed above is required to determine the role of vision
therapy in mTBI management.

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Vision therapy in mTBI

Acknowledgements: JB is supported by Canada Research Chair (950-228984) and the


Marianne Koerner Chair in Brain Diseases. We thank Craig Smith for helpful comments
and review.
Author contributions: JJSB and PJR participated jointly in the conception of the review,
literature review, writing of the first draft and revisions.
Potential conflicts of interest: none.

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Vision therapy in mTBI

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Vision therapy in mTBI

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Table. post-trauma vision syndrome

Symptoms Signs
diplopia exotropia or exophoria
blurred vision convergence insufficiency
avoidance of near tasks accommodative insufficiency
reading difficulties pseudo-myopia
illusory motion of stationary objects ocular motor dysfunction
sensitivity to visual motion
intolerance of complex environments
Accepted Article

asthenopia
headaches
photophobia
short-term visual memory
concentration/attention
balance/posture/coordination
vertigo/dizziness

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