Ocular Motility
Clinic
Royal Victorian Eye
& Ear Hospital;
University of
Melbourne Dept of Ophthalmology;
The Private Eye
Clinic, Melbourne
The information in this talk is based on an examination of
several hundred patients with head injury over a fifteen year period. The core group is
290 consecutive patients who were first seen during the period 1984-1994. Nearly all of
these patients were referred from Neurology Rehabilitation Units.
Epidemiology of Head Injury
In the
state of Victoria, Australia (population greater than four million), there are
approximately 5,000 hospital admissions per year for head injury. Two thirds of these victims are male. Two thirds
of the total are under twenty-five.
Two
hundred and ninety patients were seen over the period 1984-1994 and all were referred
because symptoms or signs were detected by the non-ophthalmic medical staff in a
Rehabilitation Unit.
Eighty
percent of the patients were seen in the first year after head injury. Follow-up was
achieved in 43% of patients. The other 57% were not seen for follow-up. The reasons for
this were varied and included geography (having been discharged from the Neurology Rehab
Unit, they no longer found it convenient to attend a metropolitan ophthalmologist), being
cured or disinterested. There is some anecdotal evidence to suggest that most of the
patients who do not return for follow-up are in fact cured, as there is often significant
medicolegal and fiscal advantage to them returning for care if they have persisting
problems.
The
Neurology Rehabilitation source of these patients means there is under referral of
patients who would normally not be admitted to a Neurology Rehabilitation Unit and
therefore there is under referral of the mildest cases and under referral of the severest
cases of the head injury. Even though this is a different population to that in other
studies, the similarity of the findings when compared to other head injury studies is
striking.
Following
a closed head injury (CHI) there are problems that one can anticipate and can expect to
find, eg. cranial nerve palsy or marked optic atrophy. There are also findings that effect
many of these patients that are peculiar to the
head injury population and are somewhat unexpected. These findings are not well
acknowledged in the literature, are not well known by Ophthalmologists, are sometimes
vague, often ignored by Ophthalmologists and if not ignored are misunderstood or
undiagnosed.
The
groups of symptoms and signs peculiar to head
injury are:
1.
Problems with accommodation and
convergence (35%)
2.
Non paretic motility
disturbances (15%)
3.
Subtle optic atrophy (20%)
4.
Other non-specific visual
disturbances
The groups of symptoms and signs that are expected are:
1.
Cranial nerve palsies (50%)
2.
Marked OA (5%)
These are seen in 1/3 of patients. The three types of problems
that are seen singly or in combination are:
1.
Convergence
insufficiency (19%)
This
is defined as crossed diplopia for near in someone who is straight for distance.
2.
Accommodative
insufficiency (14%)
This
is defined as someone under the age of thirty-five who develops symptomatic
“presbyopia” whilst wearing the full manifest hyperopic correction for distance.
3.
Pseudomyopia (13%)
This
is someone who has never been myopic who suddenly becomes myopic, or someone who had a
lesser degree of myopia who suddenly needs a much stronger myopic correction. The acquired
or change in myopia is abolished with cyclopentolate.
The
treatment of convergence insufficiency can be:
1.
No treatment.
Monocular eye closure when required.
2.
Prisms for reading.
3.
Surgery. Bimedial
resection and slanted bimedial resection have been tried.
The
early results of surgery are variable and the medium-long term results are worse. Today I
would only offer this to a patient who was not coping with conservative techniques and
found a less that 50% expectation of improvement to be an attractive proposition.
The
treatment of accommodative insufficiency is to give the appropriate plus that allows the
patient to function for near. I tell the patient that they are likely to improve with
time.
The
treatment of pseudomyopia is to give the appropriate script as a crutch. The natural
history of pseudomyopia is somewhat variable. There is the odd patient who gets worse from
year to year. There is the odd patient who ends up needing different pairs of glasses at
different times of the day. Early on in my experience, I would give cyclopentolate and
bifocals as this seems to be a theoretically purer approach, but this was abandoned after
a small number of trials because of patient complaints.
If we
assume that all those patients who are lost to follow-up are OK, then convergence and
accommodative insufficiency persists in 1/3 of patients and pseudomyopia persists in a
little over half of the patients in whom it is first an issue.
The data on cranial nerve palsies is offered largely so you can
compare this series with your own experience to get a “feel” for the overall
severity of this patient population.
Fifty percent of the patients had a cranial nerve palsy.
Fourth Nerve Palsy
One in three patients had a fourth nerve palsy and of these one
in three were bilateral. Most get better. Forty percent end up requiring surgery. Of those
that require surgery most end up requiring a superior oblique tuck for a Knapp class 2
palsy.
Sixth Nerve Palsy
One in eight patients had a sixth nerve palsy and one in eight
of these were bilateral. Of the unilateral ones most get better and only one in four have
surgery. Of the bilaterals only one in four get better and most have surgery.
Third Nerve Palsy
One in eight patients had a third nerve palsy. Of these nearly
all were unilateral. It is probable that most patients with injury severe enough to cause
a bilateral third nerve palsy don’t survive. One in three have surgery to make their
appearance normal or to lessen diplopia.
How long does it take for cranial nerve palsies to recover?
The “old” rules were that it takes a year for cranial
nerve palsies to recover and that it is reasonable to offer surgery beyond twelve months.
We had a small number of patients with fourth and sixth nerve
palsies who continue to improve beyond twelve months and continue to improve through to
eighteen months. We had a small number of patients with third nerve palsies who continue
to improve beyond two years. Miller has reported a similar experience in a small number of
patients whose third nerve palsies had not improved at all by twelve months, but then did
improve in the second year.
We thus recommend careful longitudinal assessment of these
patients and intervention only when it is quite clear that they have stopped spontaneously
improving, or have begun to get worse on measurements.
OTHER (NON-PARETIC)
MOTILITY DISTURBANCES
These were seen in 15% of all the patients. None of these
findings were anticipated and they are all probably peculiar
to closed head injury population.
The commonest was exotropia (8%). This behaved just like a
comitant childhood exotropia, but childhood exotropia was ruled out by history and there
was no evidence of any third or partial third nerve palsy or INO. Some of these patients
had surgery and in general the result was not as good as the results in
“standard” childhood exotropia surgery.
Other motility disturbances that were seen and seem to be peculiar to the closed head injury population
include:
a.
Binocular diplopia without any
tropia. A small number of patients were seen who complained of binocular diplopia for whom
no cause was ever found.
b.
Esotropia. A small number of
patients have comitant esotropia and another similar small number of patients have
divergence insufficiency. These may be partly resolved sixth nerve palsies.
c.
Tropia, no diplopia. A small
number of patients quite clearly have an acquired tropia, but never experience diplopia.
This may be due to poor cognitive function. It may be due to acquired suppression.
Diplopia may become symptomatic as cognition improves in, say, the second year after head
injury.
d.
Skew deviation. Apparent IO
palsy.
e.
Supranuclear gaze palsy.
OPTIC ATROPHY
Severe optic atrophy is an expected situation, and is seen in approx 5% of
the total group of patients. It is easily diagnosed. The vision is 6/60 or worse and the
disc is pale. There may be a chiasmal injury underlying it.
Subtle optic atrophy
is a condition that is peculiar to head injury.
Many of the patients complain of very non-specific symptoms, eg. blur which the examiner
may not understand.
The
condition of subtle optic atrophy is typically a constellation of several of the
following:
1.
Snellen acuity of
6/12 or better
2.
Low contrast acuity
(especially 10% acuities) are particularly bad.
3.
Colour vision is
often non-specifically abnormal. Desaturated colour vision tests many be more abnormal.
4.
Non-specific field
constriction is seen.
5.
Unilateral mild
pallor is easier to detect than bilateral mild pallor. NFL drop out or thinning can be
appreciated especially with the direct ophthalmoscope.
Approximately 20% of
patients have this mild optic atrophy and their symptoms can be misinterpreted if elegant
psychophysical tests are not carried out. Standard Snellen acuity is quite inadequate in
understanding the symptoms that these patients have.
NON-SPECIFIC VISUAL
DISTURBANCES
There
are many other non-specific (sensory) visual disturbances that seem to be peculiar to head
injury patients.
Some
of these symptoms may be a manifestation of the excessive introspection that patients may
experience following a near death experience.
These
include:
a.
Optically insignificant
spectacle prescription is required for clear vision.
b.
Acquired reading
disorder
c.
Loss of stereo
d.
Typical
blepharospasm
e.
Acquired colour
vision defect
f.
Palinopsia
Are these “peculiar” symptoms functional or due to
malingering or are they “real”?
By the label
“functional” one means there is no organic basis to these symptoms. By the label
“malingering” one means the patient is trying to deceive the examiner in some
way. Ophthalmologists are very lucky in that we can examine “our organ” well and
can do lots of different tests. It is thus easier for us to recognise
“malingering” than, say, the neurologist who has to evaluate the patient who
comes in with a weak arm.
Too many patients
described the same symptoms for them to be imagined. The same symptom complexes are
described in different patient populations! This strongly suggests that these peculiar problems are indeed “real”.
Most commonly,
standard neuro-radiological investigations are either normal or non-specifically abnormal.
SPECT (a nuclear medicine investigation) demonstrates diffuse multi-focal areas of damage
following the acute head injury and these changes may persist. This test may be valuable
for some patients in order to convince sceptical observers that there is indeed an organic
problem.
Visual problems following head injury are common. The commonest
symptom seen in this patient group is diplopia which can be due to a variety of causes.
Many of the visual symptoms and signs that are found are peculiar to this group of
patients and if the clinical patterns are not appreciated they may be inappropriately
ignored or mislabelled.