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Short-Wavelength Sensitivity Deficits in Patients With Migraine
Allison M. McKendrick, PhD;
George A. Cioffi, MD;
Chris A. Johnson, PhD
Arch Ophthalmol. 2002;120:154-161.
ABSTRACT
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Objective To examine short-wavelength sensitivity in patients with migraine using
short-wavelength automated perimetry (SWAP) and Stiles 2-color increment threshold
procedures.
Methods Twenty-five subjects with migraine with (n = 11) and without (n = 14)
aura and 20 age-matched headache-free subjects underwent testing. All subjects
underwent standard automated perimetry (SAP) and SWAP (using a Humphrey field
analyzer; 24-2 presentation pattern). In 2 migraine patients (one with and
another without aura), the 2-color increment threshold procedure was used
to determine whether sensitivity losses were specific to short-wavelength
sensitivity pathways or a generalized loss to multiple pathways.
Results No statistically significant differences between migraine patients and
controls were found for mean deviation (MD) or pattern-standard deviation
(PSD) for SAP. However, for SWAP, MD and PSD were worse for the migraine group
(P = .04). Twelve migraine patients had more than
4 locations with sensitivity worse than the 5% probability level (reference
value). Increment threshold determinations in the 2 selected migraine patients
indicated a selectively greater loss for short-wavelength sensitivity mechanisms.
Conclusions Approximately 50% of subjects with migraine (with or without aura) demonstrate
SWAP sensitivity losses, at times between migraine events. These findings,
in conjunction with previous results for SAP and flicker perimetry, suggest
that migraine patients should be excluded from normative databases of visual
function, and warrant further investigations of the relationship between migraine
and glaucoma.
INTRODUCTION
BETWEEN MIGRAINE events, the visual fields of many individuals with
migraine (hereafter described as migraine patients) are abnormal, with deficits
being demonstrated for achromatic perimetry1-2
and temporal modulation (flicker) perimetry.3
Because the symptoms of migrainous visual aura are consistent with a cortical
origin4 and are accompanied by changes in blood
flow within cortical areas responsible for vision,5-7
other visual field deficits associated with migraine would be expected to
be cortical. Although reports of homonymous deficits exist,8-10
these are the exception. Most deficits are reported to be unilateral and nonhomonymous,1, 3, 11 which implies involvement
of the prestriate visual pathways. Functional deficits have also been identified
in migraine patients using psychophysical methods that measure prestriate
function.12-13
The potential significance of visual field loss in migraine patients
should be considered in light of evidence of an increased prevalence of migraine
in patients with glaucoma.14-17
However, this finding has not been universal.18-19
Vasospastic disorders, including migraine, have been suggested to be more
common in individuals with glaucoma, and these conditions may share etiologic
factors such as abnormalities in vascular regulation.20-24
Although a relationship between migraine and glaucoma may exist, prestriate
visual field deficits have been demonstrated between migraine attacks in young
migraine patients with normal intraocular pressures and optic disc appearance.3
Although visual field deficits have been demonstrated in migraine patients
using standard achromatic perimetry (SAP),1, 11
more substantial visual field loss has been identified using flicker perimetry,3 a technique that has also been shown to be effective
in detecting glaucomatous visual field loss.25-28
These tests are designed to assess the magnocellular pathways, which are likely
to be sensitive for early loss because these cells are sparse (approximately
10%-20% of ganglion cells29-30).
Therefore, if even a small proportion of neurons are affected by disease,
a deficit may be manifest owing to reduced redundancy.31
Other visual mechanisms that are sparsely represented may also manifest
deficits in migraine patients, particularly the short-wavelength sensitivity
(SWS) pathways. The SWS deficits have been demonstrated in glaucoma,32-33 diabetes,34-38
and retinitis pigmentosa.34, 39
The SWS pathways may be sensitive to damage, as SWS photoreceptors are particularly
susceptible to vascular insult and light damage.38, 40
However, the presence of SWS pathway deficits in a wide variety of diseases
implies receptoral and postreceptoral (involving the SWS neural pathways)
sites of damage. Psychophysical evidence of damage at postreceptoral sites
has been measured in diabetic patients.41 Alternatively,
a non–SWS-specific loss may be manifest earlier in the sparsely represented
SWS system owing to reduced redundancy.31 The
sensitivity of the SWS pathway is commonly assessed in glaucoma using short-wavelength
automated perimetry (SWAP).32-33
This method has been shown to be superior to SAP for detection of early functional
glaucomatous damage.32, 42-44
In this study, SWAP was used to measure the sensitivity of the SWS pathway
across the central visual field. In 2 migraine patients who demonstrated SWAP
deficits, the sensitivities of SWS (blue/pi-1) and middle-wavelength sensitivity
(MWS) (green/pi-4) pathways were compared using the Stiles 2-color increment
threshold technique45 to determine whether
a selective loss of SWS pathway sensitivity or losses in MWS pathway sensitivity
were present. Two-color increment thresholds have been used previously to
demonstrate selective losses of SWS pathway sensitivity in early diabetic
retinopathy34, 36 and deficits
in MWS and SWS pathway sensitivity in glaucoma and retinitis pigmentosa.34, 36
PATIENTS AND METHODS
Twenty-five individuals with a history of migraine participated in the
study. Migraines were classifed as with (n = 11) and without (n = 14) aura
to meet the classification criteria of the International Headache Society.46 All subjects in the aura group had visual symptoms.
The test protocol was approved by the Institutional Review Board of Legacy
Health Systems, Portland, Ore, and all subjects gave written informed consent
before commencement of the test procedures, in accordance with the tenets
of the Declaration of Helsinki.
The control group consisted of 20 subjects free of headache as established
by means of a questionnaire and a clinical interview. Subjects were aged 18
to 40 years. No statistically significant difference was found among the mean
(± SD) ages of the 3 groups (migraine patients with aura, 32.4 ±
5.9 years; migraine patients without aura, 27.7 ± 6.5 years; and controls,
29.9 ± 5.6 years; analysis of variance, P
= .16). Migraine patients and controls were recruited from within Legacy Health
Systems or by means of advertisement in local newspapers. Three migraine patients
(2 patients with aura and 1 without), and 4 controls were recruited from within
our laboratory. Only these subjects had previous SAP experience. Only 1 subject
had previous SWAP experience.
A routine eye examination was performed to ensure that all subjects
had normal optic disc appearance, intraocular pressure of less than 21 mm
Hg, results of slitlamp examination within the reference range, visual acuity
of 20/20 or better, and refractive errors of less than 6.00 diopters (D) sphere
and 2.00 D cylinder. Subjects were required to be free of systemic disease
and systemic medications known to affect visual function. None of the migraine
patients was receiving preventive drug therapy.
Migraine patients underwent testing at least 4 days after a migraine
to minimize possible transient effects on performance due to medications,
nausea, or postmigraine fatigue.
We performed SAP and SWAP using a Humphrey field analyzer II (Model
750; Humphrey Systems, Dublin, Calif). For SAP, we used a Goldmann size III
white target projected on a 31.5-apostilb (asb) (10 candelas per square meter
[cd/m2]) white background. For SWAP, we used a Goldmann size V
blue target (Omega 440-nm interference filter) projected on a 315-asb (100
cd/m2) yellow background (Schott OG530 filter; Coherent, Inc, Auburn,
Calif). These SWAP test conditions provide approximately 17 dB of isolation
of the SWS mechanisms throughout the central visual field.47
We used the 24-2 test pattern for SAP and SWAP. We used the Swedish Interactive
Threshold Algorithm standard strategy for SAP and the full threshold strategy
for SWAP.
Subjects underwent SAP first on each eye, followed by a brief rest,
and then SWAP.
The Humphrey field analyzer II statistical analyses use an internal
normative database. Current migraine prevalence estimates suggest approximately
12% to 15% of the "normal" subjects included in the database may have migraine,48-51 thereby
confounding comparisons of visual field performance in migraine patients with
those of migraine-free subjects. To avoid this problem, we included test results
of age-matched controls who were known to be migraine free, and visual field
indices and individual sensitivity values were compared between groups. Right-
and left-eye data were analyzed separately to determine whether unilateral
or bilateral involvement was present.
Group comparisons were performed using the mean deviation (MD) and the
pattern-standard deviation (PSD) visual field indices. Groups were compared
using a t test. Because of multiple comparisons and
the likelihood of correlation between the measures, we used the Hochberg step-up
multiplicity adjustment procedure52-53
to determine statistical significance while maintaining an overall type I
error rate of P = .05. Performance on SAP and SWAP
were considered separately; hence the Hochberg procedure was applied twice,
each time with 4 measures (MD and PSD for right and left eyes).
Individual migraine subject performance was also analyzed on a pointwise
basis, using the control group to determine a 95% confidence interval for
each point in the visual field. If the thresholds at individual points are
independent (which they may not be), the probability that n points (from of a total of N) fall below
the lower confidence limit (CL) is determined using the following equation54:
where  is the probability an individual
point will fall outside the control CL ( = .025), and NCn is the binomial coefficient
that determines the number of uniquely different ways in which a subset of n points may be chosen from a larger set of N points and is equivalent to N!/[n!(N - n)!].
The factorial expansion is signified by !, which determines the number of
ways that a set of numbers can be ordered and is equal to N! = N x (N -
1) x (N - 2) x (N - 3) x ... x 3 x 2 x 1, where N is a positive integer.
For the 24-2 test pattern, the number of test points is 54. The points
above and below the blind spot were excluded from analysis, resulting in 52
points. From equation 1, visual fields were judged to be abnormal (P<.05) if they had 4 or more points below our lower CL (P = .025 for a single point) determined from the control data.
We used a modified Humphrey field analyzer I to perform a Stiles 2-color
increment threshold procedure to assess SWS (blue) and MWS (green) pathway
sensitivity. We measured thresholds using a Goldmann size V blue target superimposed
on a yellow background (Schott OG530 filter).55
Conditions were selected to measure Stiles pi-4 (MWS) and pi-1 (SWS) mechanisms.45 This concept has been described in detail by Demirel
and Johnson.55 For low-luminance yellow backgrounds,
detection of a large blue target is mediated by MWS pathways (or rods if very
low luminances). For the SWS mechanism to become responsible for detection
of the blue target, sensitivity of the MWS mechanism must be reduced. This
reduction is achieved by displaying a bright yellow background. Adaptation
to the bright yellow background reduces the sensitivity of the MWS pathway,
and the SWS mechanism becomes responsible for detection of the blue target.
If sensitivity to the blue target is measured at a range of yellow background
intensities (from dim to very bright), a characteristic 2-branch curve is
obtained as illustrated schematically in Figure 1. It is well documented that the lower branch represents
detection by MWS mechanisms, and the upper branch, detection by SWS mechanisms.45
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Figure 1. Schematic of a threshold-vs-intensity
curve for detection of a large blue target displayed on a yellow background.
At low background luminances, detection is mediated by middle-wavelength sensitivity
(MWS) mechanisms. At high background luminances, the short-wavelength sensitivity
(SWS) mechanisms become responsible for detection.
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Thresholds to the blue target were measured at 16 adapting field intensities,
beginning at 0.1 cd/m2. After 10 minutes of dark adaptation, thresholds
were measured at 2 locations (one of normal SWAP sensitivity, and the other
of reduced SWAP sensitivity at the same eccentricity) using the Humphrey full-threshold
algorithm. Thresholds were measured twice at each location for each background
intensity, and the mean of both measurements was taken as the final threshold.
After each increment in background intensity, 2 minutes of adaptation to the
new background was required before measuring thresholds.
The background intensity levels and the mean thresholds provided by
the Humphrey field analyzer at each background intensity were converted to
quantum units (quanta · sec-1· degree-2) as recommended by Wyszecki and Stiles,45
using the method detailed by Sample et al.47
The threshold-vs-intensity (TVI) curves were the best fit of the following
equation56-57:
where I is the increment threshold; A, the ordinate intercept; I, the background
intensity; Ie, the background intensity
where the TVI curve begins to adapt; and n, the exponent that describes the
slope of the function.
RESULTS
Figure 2 presents the MD and
PSD values for SAP and SWAP for the migraine (with and without aura) patient
and control groups. The significance level of the t
tests after adjustment by means of the Hochberg procedure are also given in Figure 2. No significant difference was found
between the group means for MD or PSD for SAP. However, for SWAP, significant
differences were present between the combined migraine and the control groups
for MD and PSD.
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Figure 2. Box plots of mean deviation (MD;
A and B) and pattern-standard deviation (PSD; C and D) for standard automated
perimetry (SAP; A and C) and short-wavelength automated perimetry (SWAP; B
and D). Data are presented for right and left eyes in migraine and control
groups. Probability levels for group mean comparisons are also presented.
Boxes represent the 25th, 50th (median), and 75th quantiles; whiskers, the
10th and 90th quantiles. Data falling outside the range of the 10th to 90th
quantiles are represented by solid symbols.
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For SAP, 5 (20%) of 25 migraine patients had 4 or more points outside
the lower bounds of the control group 95% CL. Within this group of 5 subjects,
3 had bilateral and 2 had unilateral involvement. The bilateral involvement
was not homonymous and not obviously consistent with a cortical origin. For
SWAP, 12 (48%) of 25 migraine patients had 4 or more points outside the lower
bounds of the control group 95% CL. Of this group of 12 patients, 6 had unilateral
and 6 had bilateral deficits. Six of the subjects had the depressed locations
clustered in the superior arcuate nerve-fiber bundle region, 3 had abnormal
locations clustered in the inferior arcuate nerve-fiber bundle region, and
3 had scattered locations of loss. None of the subjects had bilateral homonymous
deficits. None of the controls had 4 or more points outside the 95% CLs for
SAP or SWAP.
Table 1 shows the number
of subjects in each migraine group with abnormal performance measured on a
pointwise basis for SAP and SWAP. Inspection of Table 1 shows similar involvement in both migraine groups. No significant
difference was found between the migraine groups for MD or PSD on SAP or SWAP
(t test, P>.05). This result
should be viewed with caution, as our limited sample size (11 migraine patients
with and 14 without aura) results in a power of 0.70 to detect a difference
of 2 dB. Nevertheless, no trend for different performance was found between
the migraine groups.
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Subjects With Visual Field Deficits
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We measured TVI curves for 2 migraine patients, one with and one without
aura, who had abnormal performance on SWAP. Both subjects demonstrated normal
thresholds for SAP.
The migraine patient with aura was a 28-year-old woman with a typical
migraine frequency of 2 weeks. Her initial SWAP visual field assessment was
conducted 9 days after migraine (Figure 3A). She returned on 2 further occasions for measurement of TVI curves.
These visits were performed 24 hours and 14 days after the same migraine.
On both occasions, increment threshold data were collected for her left eye
at a relatively depressed visual field location (3° nasal and 9° superior)
and a location of normal sensitivity at the same eccentricity (3° nasal
and 9° inferior). The increment threshold data collected at 24 hours after
migraine is displayed in Figure 3B
and at 14 days after migraine in Figure 3C.
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Figure 3. Left eye short-wavelength automated
perimetry visual field performance measured 9 days after migraine in a patient
with migraine with aura (A). Increment threshold data were measured 24 hours
(B) and 9 days (C) after migraine in the left eye of the same subject. Solid
symbols represent thresholds measured at a location of normal sensitivity
(3° nasal and 9° inferior); open symbols, thresholds for a location
of depressed sensitivity (3° nasal and 9° superior). MD indicates
mean deviation; PSD, pattern-standard deviation.
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The migraine patient without aura was an 18-year-old woman with a typical
migraine frequency of 1 month. Her initial SWAP visual field was measured
2 weeks after migraine (Figure 4A).
She returned for 2 further examinations to measure increment threshold data,
at 6 days and 3 weeks after the same migraine. Increment thresholds were measured
at 3° nasal and 9° superior and at 3° temporal and 9° inferior
in her left eye. The increment threshold data collected at 6 days after migraine
is displayed in Figure 4B and at
3 weeks after migraine in Figure 4C.
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Figure 4. Left eye short-wavelength automated
perimetry visual field performance measured 2 weeks after migraine in a patient
with migraine without aura (A). Increment threshold data were measured 6 days
(B) and 3 weeks (C) after migraine in the left eye of the same subject. Solid
symbols represent thresholds measured at a location of normal sensitivity
(3° nasal and 9° superior); open symbols, thresholds for a location
of depressed sensitivity (3° temporal and 9° inferior). MD indicates
mean deviation; PSD, pattern-standard deviation.
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Both migraine patients show sensitivity losses for MWS and SWS pathways;
however, the relative loss of SWS pathway function was greater than that of
the MWS pathway. The logarithm decrease in sensitivity at background intensities
of 7 quanta · sec-1· degree-2
(a measure of MWS pathway function) and 9 quanta · sec-1· degree-2 (a measure of SWS pathway function)
for the affected location of visual field is plotted in Figure 5. For each subject, the data presented are the mean of the
2 visits. Figure 5 demonstrates
the relatively greater loss of SWS pathway function in these 2 individuals.
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Figure 5. Logarithm threshold difference
in sensitivity between the normal and depressed region of visual field for
the 2 patients with migraine described in Figure 3 and Figure 4. The measures
of short (SWS) and middle-wavelength sensitivity (MWS) pathway functions were
determined at 9 and 7 quanta · sec-1· degree-2, respectively. The data are the mean of 2 measures, as shown
in Figure 3B-C and Figure 4B-C.
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COMMENT
The SWS deficits were common in migraine patients (12/25 [48%]) when
compared with a group of headache-free subjects of similar age. The visual
field loss was suggestive of prestriate rather than cortical involvement,
as there was an absence of bilateral homonymous deficits. This does not necessarily
exclude cortical involvement; however, we found no direct evidence of such
involvement in our subject group. Migraine patients with and without visual
aura showed similar degrees of loss (Table
1, Figure 3 and Figure 4), suggesting that the visual field
deficits are independent of the cortical involvement present during the aura
phase of the attack.
Migraine patients are reported to demonstrate increased susceptibility
to glare and ocular discomfort between attacks, and these hypersensitivities
may arise owing to interruptions in cortical inhibition.58-60
No evidence of hypersensitivity was found in our migraine group, and subjects
did not report excessive discomfort during assessment. As our experiments
were not designed specifically to consider these issues, we cannot rule out
the possibility of heightened aversive responses in our migraine group resulting
in losses of concentration and elevated thresholds. Visual discomfort in migraine
patients has been demonstrated previously for foveal viewing using grating
stimuli of 3 to 4 cycles per degree.59-60
However, our measures were for spot targets in the periphery, and we think
cortical hypersensitivity to illusory stimuli was unlikely to be a significant
factor in the visual dysfunction measured in this study.
The mechanism and site of SWS loss in migraine remains to be elucidated.
Increment threshold data from 2 subjects (Figure 3 and Figure 4)
suggest that the SWS pathway is more affected than the MWS pathway, although
a larger cohort of subjects must undergo testing. The SWS pathways are particularly
vulnerable to retinal disease, with evidence of dysfunction of the photoreceptors
and postreceptoral sites. In diabetes, metabolic abnormalities and hypoxia
are thought to contribute to the selective SWS pathway deficits in early diabetic
retinopathy.34 Abnormalities in ocular vascular
regulation may be present in migraine, as abnormalities in cold-induced vascular
regulation in the finger have been reported in migraine patients.61-62 Although recent studies of cortical
function find no evidence of ischemia during migraine events,63-64
similar studies have not been performed to verify the presence or absence
of peripheral hypoxia during the course of a migraine or at other times.
What is the clinical significance of SWS loss in migraine? Although
visual dysfunction in migraine likely arises owing to attrition caused by
disease, at present no data support or reject this hypothesis. Longitudinal
data are required to determine whether such visual field deficits are transient
or permanent, or whether they are progressive. A relationship between time
after migraine and visual field deficit severity has been reported using kinetic
perimetry,2 and using flicker perimetry for
several individual patients.3, 65
Most estimates of migraine prevalence range from 12% to 15%, with the
prevalence for women being about twice that for men.48-51
Although visual field studies have only been conducted on small samples of
migraine patients, reports suggest that 20% to 40% demonstrate visual field
deficits for SAP,1, 3, 11
approximately 67% for flicker perimetry,3 and
about 48% (12/25) for SWAP (present study). If these estimates are representative
of migrain patients, we predict that 2.5% to 7% of the general population
may demonstrate some form of visual field abnormality in association with
migraine.
The possibility of large numbers of migraine patients demonstrating
abnormal visual fields raises several interesting issues. First, migraine
patients should be excluded from normative databases of visual performance.
The high prevalence of SWAP sensitivity loss in migraine patients may account
for part of the greater individual variability for SWAP compared with SAP.66-68 Second, a challenge
remains in determining the relationship, if any, between prestriate visual
dysfunction in migraine and glaucoma. Migraine has been suggested as a vascular
risk factor for glaucoma20-24;
however, the relationship between these conditions is not a simple one. Primary
open-angle glaucoma affects approximately 3% of the population older than
40 years.69-70 Within this glaucomatous
population, estimates of migraine prevalence vary, but most range from 17%
to 25%.14-15,19, 71
Hence, approximately 0.6% of the general population has glaucoma and migraine.
Within the general population, 2.5% to 7% may have visual field dysfunction
in association with migraine in the presence of normal optic nerve appearance
and normal intraocular pressure. Whether this group of patients has a higher
risk for glaucoma is currently unknown.
AUTHOR INFORMATION
Accepted for publication September 5, 2001.
Supported in part by research grant EY-03424 from the National Eye Institute,
Bethesda, Md (Dr Johnson).
Corresponding author and reprints: Chris A. Johnson, PhD, Discoveries
in Sight, Devers Eye Institute, Legacy Clinical Research and Technology Center,
1225 NE Second Ave, PO Box 3950, Portland, OR 97208-3950 (e-mail: cajohnso{at}discoveriesinsight.org).
From the Devers Eye Institute, Legacy Clinical Research and Technology
Center, Portland, Ore.
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