Investigative Ophthalmology & Visual Science, Vol. 31, No.

1, January 1990
Copyright Association for Research in Vision and Ophthalmology

Autonomic Components of the Human

Pupillary Light Reflex
Philip H. Heller,* Franklin Perry,f Don L. Jewerr.f and Jon D. Levinef
To investigate the autonomic components of the pupillary light reflex in humans, we used infrared
pupillometry combined with a partial local cholinergic (tropicamide) or alpha-adrenergic (thymoxamine) blockade. The pupillary response curve was analyzed using parameters identical or similar to
those employed previously to study the autonomic components of the pupillary light reflex. Tropicamide increased baseline pupil area and affected five of the eight measured parameters. Thymoxamine
lowered baseline pupil area but did not affect any of the parameters. We found the expected cholinergic contribution to the constrictive phase of the pupillary light reflex but no evidence for peripheral
alpha-adrenergic activity during redilation. We propose that redilation primarily involves parasympathetic relaxation, modulated by cholinergic inhibition of the dilator muscle and central sympathetic
inhibition of the Edinger-Westphal nucleus. Invest Ophthalmol Vis Sci 31:156-162, 1990

While it has been long known that constriction of

the pupil to a light flash depends on parasympathetic
outflow from the Edinger-Westphal (E-W) nucleus,1'2 the autonomic control of the individual
phases of the human pupillary light reflex is not well
established. Lowenstein and Loewenfeld employed
pharmacological agents and surgical ablation to study
the pupillary light reflex in cats and monkeys and
described two phases of constriction and primary and
secondary redilatory phases.3 They hypothesized that
the constrictive phases were due to a parasympathetic
activation modified at its conclusion by a superimposed central sympathetic inhibition of the E-W nucleus. The primary redilation was thought to be due
to parasympathetic relaxation, while the secondary
redilation was thought to be due to an increase in
peripheral sympathetic activity. Observations in a
small number of patients with neurological lesions4"7
suggest that this model also may apply in humans.
Information relevant to possible mechanisms underlying the pupillary light reflex in humans also is
available from pharmacological analysis of human
intraocular muscle. Several studies have demonstrated a cholinergic stimulation of the constrictor
From the *Kaiscr-Permanente Medical Center, Hayward, California, and the tSchools of Medicine and Dentistry, University of
California, San Francisco, California.
Supported in part by grants AM32634, DE05369 and NS21647
from the National Institutes of Health and from the Community
Service Program of Kaiser Foundation Hospitals.
Submitted for publication: November 13, 1987; accepted June 7,
1989.
Reprint requests: Jon D. Lcvine, MD, PhD, Division of Rheumatology, U-426 (Box 0724), UCSF, San Francisco, CA 94143.

muscle and an alpha-adrenergic stimulation of the

dilator muscle, as required by the Lowenstein and
Loewenfeld model.l>8f9 In vitro study has also demonstrated beta-adrenergic inhibition of both muscles,
alpha-adrenergic inhibition of the sphincter and cholinergic inhibition of the dilator.10"12 The physiological contribution to the light reflex of these latter effects, observed in vitro, is unknown. Other workers
have found that the beta-adrenergic blocker timolol
does not affect either baseline pupil area or the pupillary light reflex.1314
In the present study we measured the pupillary
light reflex by infrared pupillometry after applying
agents to produce a parasympathetic or sympathetic
blockade. Our data confirm the expected cholinergic
contribution to constriction but fail to confirm the
expected alpha-adrenergic contribution to the redilatory phase. Instead wefindthat the recently described
cholinergic inhibition of the dilator muscle may contribute to the rate of redilation. We present a hypothesis to explain redilation in the human pupillary light
reflex that includes this cholinergic inhibition.
Materials and Methods
The pupillary light reflex was studied in 27 normal
subjects (16 males and 11 females) between the ages
of 20 and 40 years. The experimental protocol for this
study was approved by the UCSF Committee on
Human Research and informed consent was obtained in writing.
Pupil area was measured every 50 msec by infrared
video pupillometry (Micromeasurements, Inc.,
Berkeley, CA). The light stimulus was a square-wave
pulse of collimated white light, generated by a glow-

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AUTONOMIC COMPONENTS OF THE PUPILLARY LIGHT REFLEX /.Heller er ol

No. 1

Table 1. Pupillary light reflex parameters in normals, drug and comparative normal subgroups"
Group (n)
mean
SE
mean
SE
mean
SE
mean
SE
mean
SE

NLS (27)
Tropic (4)
lgNLs(5)
Thymox (5)
smNLs(ll)

C(%)\

mrci

mrdrf

d2(%)

43.9
1.2
9-7*
2.3
38.5
2.7
50.9
1.5
46.3
1.7

43.4
2.4
19.8+
3.7
52.4
5.1
34.7
5.7
32.7
2.3

13.2
0.7
8.1
2.2
15.7
1.5
11.2
0.8
10.2
0.8

7.9
0.6
7.2
1.0
6.1
0.7
6.3
1.3
8.8
1.2

0.296
0.007
0.339*
0.010
0.255
0.016
0.298
0.009
0.306
0.010

imrc

tmrd,

rec (%)

0.515
0.007
0.543
0.017
0.511
0.007
0.493
0.014
0.500
0.010

1.29
0.02
1.195
0.075
1.283
0.054
1.228
0.036
1.269
0.035

83.4
1.5
95.0
2.8
81.8
3.7
86.7
2.9
82.8
3.0

* Tropicamide compared to large normals (IgNLs), thymoxaminc compared to small normals (smNLs). For parameters independent of pupil area,
comparison with the entire control group did not alter findings of statistical
significance.

t These parameters arc significantly correlated with baseline pupil area.

X P < 0.01.
P < 0.05.

modulator tube (Sylvania R-l 131C; Mountainview,

CA), focused in the plane of the pupil and contained
within the pupil (ie, a Maxwellian-view stimulus).1516
The duration of the stimulus (200 msec) was chosen
to be shorter than the latency to the light reflex4
(Table 1) to further ensure elimination of variation in
stimulus intensity. Microcomputer-controlled tracking was used to compensate for minor head and eye
movements. Pupil area data were stored in a PDP-8
computer.
Pupil area was found to be stable after 5 min of
adaptation to a constant dim level of illumination
(0.34 ft-candles, measured by a Tektronix J-16 photometer probe located on the wall one meter in front
of the subject). Starting shortly before a trial, the subject fixated on a red light-emitting diode, coaxial with
the stimulus and placed at optical infinity to elimi-

nate accommodation effects. The subject pressed a

button to begin each recording period, which continued until 5 sec after the stimulus was delivered.
Length of the prestimulus interval was randomly set

50

<3
-60
0

1 2

TIME (SEC)
- 1 0

TIME (SEC)
Fig. 1. A series of pupillary light reflex responses from a typical
subject. Responses to six 200 msec 1200 cd/m2 stimuli (S) presented at 1 min intervals at time t = 0. Pupil area (PA) measured at
20 Hz.

Fig. 2. A single response to light (top) and its time differential

(below): BPA, mean baseline pupil area over 1 sec prior to flash; tc,
time to constriction (latency); C (%), size of constriction (as % of
BPA); d2 (%), % secondary redilation (% redilation occurring between 2.2-2.6 sec after the stimulus (S); rcc (%), % redilation at 5
sec after the stimulus; mrc, tmrc, maximum rate of constriction
and its time after S and; mrdi, tmrdi, maximum rate of primary
redilation and its time after S.

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INVESTIGATIVE OPHTHALMOLOGY b VISUAL SCIENCE / Jonuory 1990

Vol. 31

100
90
9 . 7 + / - 2 . 3 **

80

Xlg

38.5 + / - 2.7

70
^

60

^J 50
40

""

V v

)O

XX
x

X
X
jX

30
20

50.9 +/- 1.5

Xsin

46.3 +/- 1.7

X X
X

X
X

10
0

a
-

10

20

30

1
40

50

60

70

BPA
100
90
A

80

Xsm

34.7 +/- 5.7

Xlg

32.7 +/- 2.3

19.8 +/- 3.7 **.

52.4 +/- 5.1

70

H 60
50

Fig. 3. (A, B) Five analysis parameters as a function

of baseline pupil area (BPA)
in normal (X) and after partial parasympathetic (tropicamidc, D) or sympathetic (thymoxaminc, A)
block. Dotted lines indicate
classification of normals
into small, medium and
large BPA groups. Small
BPA normals (Xsm) were
compared to subjects
treated with thymoxaminc
Large BPA normals (Xlg)
were compared to subjects
treated with tropicamidc
(see Table 1).

Al

X
X

40
Xy

30

*
IX

X*

a
a

20
10
0
10

20

30

40

50

60

70

BPA

at either 3 or 4 sec in order to reduce effects of flash

anticipation on the pupillary response. Up to 12 responses were obtained at 1 min intervals. Baseline
pupil area was determined from the prestimulus recording.
Nine subjects also were tested after conjunctival
administration, in the consensual eye, of one to two
drops of either 0.5% tropicamide (Alcon Laboratories, Forth Worth, TX) or 0.5% thymoxamine
(Warner-Lambert, Morris Plains, NJ). These agents
produce a parasympathetic or sympathetic (alphaadrenergic) block, respectively.1718 All subjects were

examined by tangential light beam to detect the presence of a narrow anterior chamber, before administration of tropicamide. The only adverse reaction
noted following either drug was the routinely observed transient burning sensation with thymoxamine.1819 The pupillary light reflex was studied during a partial blockade (ie, 10 to 15 min after drug
administration) rather than at the time of maximal
effect, after 30 min. This allowed us to obtain responses during a blockade but at levels of baseline
pupil area comparable to some normal subjects. This
simplified the data analysis since several parameters

No. 1

159

AUTONOMIC COMPONENTS OF THE PUPILLARY LIGHT REFLEX / Heller er ol

40

30

11.2 +/- 0.8

Xsm

10.2 +/- 0.8

Xlg

x
A

^ X

*A*

xX X

1.5

20

10

8.1 + / - 2.2 *
15.7 + / -

*x

x
x

yx

x
X

10

x*

I
20

.1

1, .

30

40

50

1 .
60

70

BPA

Fig. 3 (continued) (C, D).

See legend under Figure 3
(A, B).

30
A

6.3 +/-

1.3

Xsm

8.8 + / -

1.2

Xlg

7.2 + / -

1.0

6.1 + / - 0.7

20
CM
X |

10

X|

X
AX
X

a
X

a
a

xj x,

1
10

D
used in the analysis are dependent on pupil area in a
nonlinear fashion,20 confounding an interpretation of
control and drug data from the same individual. In
addition, since at the limits of pupil size mechanical
factors can influence pupillary response,21 it was important to compare groups with comparable baseline
pupil area.
For each pupillary response a smoothed curve22 of
pupil area versus time and its time differential curve
were plotted. These curves were analyzed using parameters either identical to or similar to those found
by Lowenstein and Loewenfeld to reflect the autonomic components of the pupillary light reflex: base-

20

30

40

50

60

70

BPA
line pupil area (BPA), latency to constriction (tc), size
of constriction [C(%)]} maximum rate of constriction
and its latency (mrc, tmrc), maximum rate of primary redilation and its latency (mrdi, tmrd^, and
percentage recovery [rec(%)].3 Under our experimental conditions, employing a short, Maxwellian-view
stimulus, unlike the stimulus used in the study of
Lowenstein and Loewenfeld,3 the secondary redilation was often partially overlapped by the primary
redilation. This has been observed by others employing a short stimulus.23 Therefore, we used the percent
redilation occurring during the time interval 2.2-2.6
sec after the stimulus (ie, 2.0 to 2.4 sec after the end of

160

100

90

XX

80

Vol. 01

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / Jonuory 1990

X
X

ixx

x x
X

xi

70

S 60
o
Q>
k_

Fig. 3 (continued) (E). See

legend under Figure 3 (A,
B).

50
86.7 + / - 2.9

40

Xsm

82.8 + / - 3.0

95.0 + / - 2.8

Xlg

81.8 + / - 3.7

30
20
10
0

10

20

30

40

50

60

70

BPA

the stimulus) to measure secondary redilation

[d2(%)]. This time interval was selected because: (1)
in some curves there was a distinct secondary redilation noted at this time interval; (2) evidence for a
secondary redilation at this time interval was consistently seen in the derivative curve; and (3) this time
interval corresponds to the time during redilation of
the distinct secondary phase observed by Lowenstein
and Loewenfeld.3
Statistical analysis was done using the student ttest.
Results
Mean baseline pupil area for the normal subjects
was 31.9 2.0 mm2 (mean SE). For tropicamidetreated subjects the mean baseline area was 53.9 2.6
mm2, and for thymoxamine-treated subjects the
mean was 19.2 2.6 mm2. Thus, both drugs produced the expected autonomic block (P < 0.05).
Several sequential measurements of the pupillary
light reflex in a single subject are shown in Figure 1.
The latency, maximum rates of change, time to peak,
and times of maximum rate of change showed little
variation from trial to trial. There was minor nonsystematic fluctuation in baseline pupil area. Figure 2
demonstrates a single response with its time differential and illustrates the parameters used to analyze the
response.
The values for the parameters for normal and
drug-treated subjects are listed in Table 1 and plotted
as a function of baseline pupil area in Figure 3 (A-E).
For statistical analyses drug-treated groups of subjects
were compared only to the subset of normal subjects
who had a baseline area comparable to that of the

drug-treated subjects, that is, tropicamide-treated

subjects were compared with controls with large baseline area and thymoxamine-treated subjects were
compared with controls with small baseline area (Fig.
3). Using this comparison, tropicamide significantly
affected five of the eight parameters, decreasing the
size of constriction [C(%)]; the maximum rate of
constriction (mrc) and the maximum rate of primary
redilation (mrd^, and increasing the latency to constriction (tc) and the percentage recovery [rec(%)].
The measure of secondary redilation [d2(%)]5 the
time to maximum rate of constriction (tmrc), and the
time to maximum rate of primary redilation (tmrdi)
were unaffected by tropicamide.
Thymoxamine treatment, despite significantly
lowering baseline pupil area, failed to produce significant differences in any of the parameters.
Discussion
In this study we used a partial, local cholinergic or
alpha-adrenergic blockade to investigate the autonomic components of the pupillary light reflex in
humans. Baseline pupil area, measured under mesopic light conditions, was similar to that observed by
others.24 The cholinergic antagonist tropicamide significantly increased baseline pupil area. This effect
was probably due to antagonism of the known cholinergic stimulation of the sphincter muscle, but an
effect on the recently described cholinergic inhibition
of the dilator muscle may have contributed. The
alpha-adrenergic antagonist thymoxamine significantly decreased baseline pupil area. This effect was
probably due to antagonism of the known alphaadrenergic stimulation of the dilator, but antagonism

No. 1

AUTONOMIC COMPONENTS OF THE PUPILLARY LIGHT REFLEX / Heller er ol

of alpha-adrenergic inhibition of the sphincter, which

has been reported,10"12 may have contributed.
Since the size of the pupillary constriction to light
is known to be a function of pupil area,21 we analyzed, as well, the dependence on pupil area, of all the
individual parameters in our analysis. Absolute magnitude of constriction, as mentioned above, is highly
dependent on pupil area (r = -0.8), while the percentage constriction [C(%)] was only moderately correlated with area (r = -0.4). The maximum rate of
constriction, mrc, and the maximum rate of primary
redilation, mrdi, both absolute measures, were
greater at larger pupil area (r = 0.8 and 0.7, respectively), presumably secondary to the increased constriction which occurred in a reflex of essentially the
same duration. The two percentage measures, secondary redilation [d2(%)] and percentage recovery
[rec(%)], were independent of pupil area. Of the temporal parameters, only latency (tc) was a function of
pupil area, inversely so, as has been previously observed.2325 The values we observed for the parameters
[except d2(%), a parameter we devised] were similar
to those previously observed.32627
Because of the dependence of some of the parameters on pupil area, we compared the data from drugtreated subjects with that from control subjects who
had a baseline pupil area comparable to that of the
drug-treated subjects.
Tropicamide affected five of the eight parameters:
C (%), mrc, mrdi, tc and rec (%). The decreases in C
(%) and mrc and the increase in tc are readily explained by the well established antagonism by tropicamide of the cholinergic parasympathetic activation
of the sphincter pupillae muscle. The maximum rate
of primary redilation, mrdi, which is thought to represent parasympathetic relaxation, was also decreased. This decrease in mrdi probably was due to
the significantly attenuated constriction after tropicamide in two of the four subjects. Unexpectedly, the
percentage recovery, rec (%), was increased in the
presence of tropicamide. This observation would not
be expected if redilation was due primarily to parasympathetic relaxation and peripheral sympathetic
activity. This finding can be explained, however, by
assuming that cholinergic inhibition of the dilator
pupillae10"12 plays a role in the light reflex. If phasic
cholinergic inhibition of the dilator normally is present during redilation then a cholinergic blocker such
as tropicamide would be expected to decrease this
inhibition, thereby enhancing redilation. Since rec(%)
was measured at 5 sec after the stimulus, we conclude,
that this cholinergic inhibition of the dilator still
would be present or have its effect still present at 5 sec
post-stimulus.
Thymoxamine did not significantly affect any of
the parameters, although it did decrease baseline

161

pupil area. If secondary redilation were due to peripheral sympathetic activity, we would predict a decrease
in the secondary redilation measure, d2(%), in the
presence of thymoxamine. Since we did not see any
change in d2(%), we also looked at redilation in thymoxamine-treated subjects during the time period of
2.6-5.0 sec post-stimulus to see if there was a later
effect of thymoxamine, but none was seen. The percentage recovery, rec(%), was also unaffected in thymoxamine-treated subjects, further suggesting a minimal or absent contribution by peripheral alphaadrenergic activity (either dilator stimulation or
sphincter inhibition) to the redilatory phase. The
thymoxamine-treated pupils were compared to normal pupils of similar size since this was the only appropriate control available. It is possible that normal
small pupils, which have increased central parasympathetic tone, have a generally inhibited sympathetic
system and thereby an inhibited dilator activity. A
small pupil also might have diminished dilator activity because of the length-tension curve properties for
the stretched dilator muscle. While it is not possible
to rule out these effects, if they were operative in the
normal small pupil controls, we should have observed an increased value for d2(%) (our measure to
detect secondary active sympathetic redilation) in
normal pupils with a larger BPA, but this was not
seen (ie, 62% was independent of BPA).
While it is true that adrenergic antagonists such as
thymoxamine are not pure in terms of receptor action (alpha vs. beta or between alpha subclasses) or
might have other actions, the biochemical evidence
suggests strongly that thymoxamine as employed by
us would have been expected to affect sympathetic
activity of the dilator. It is possible that the difference
between our finding and that of Lowenstein and
Loewenfeld is due to the different stimulus used. In
their study3 they employed a prolonged (1 sec) nonMaxwellian-view stimulus. Another possibility is that
in the ablation techniques they employed, on which
their interpretation was based, other components besides alpha-adrenergic efferents were affected (eg,
cholinergic inhibitory outflows28). Our data do bring
into question the role of peripheral sympathetic activity in the mechanism for the finding of a secondary
redilation of the pupil following a light stimulus. It
should be emphasized that there is ample evidence
that active central and peripheral sympathetic activity is necessary for the phenomenon of reflex pupillary dilatation in response to sensory or psychosensory stimuli.29
It is possible that redilation represents predominantly a continual return to baseline tone (ie, parasympathetic relaxation) modulated by changes in
cholinergic inhibition of the dilator as described
above. This model, however, does not easily explain

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INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / January 1990

the often observed abrupt attenuation in the rate of

redilation observed in mid-redilation (Fig. 1). This
attenuation, however, could be the result of a sudden
decrease in the level of the increased central sympathetic inhibition of the E-W nucleus, which is
thought to commence with and be responsible for the
secondary phase of constriction.3 A decrease in this
ongoing central sympathetic inhibition during the period of increased parasympathetic tone compared to
baseline would result in a decreased rate of redilation.
Indeed, Lowenstein and Loewenfeld proposed the
mechanism of rapidly alternating levels of central
sympathetic inhibition to explain the cyclical changes
in pupil area that they observed during pupillary light
reflexes in excited monkeys.
In summary, we have demonstrated the feasibility
of employing pupillometry combined with pupillary
pharmacological blockade to dissect the individual
parasympathetic and sympathetic contributions to
the pupillary light reflex in humans. We found the
expected cholinergic contribution to the constrictive
phase but no evidence for peripheral sympathetic activity during secondary redilation. We propose that
redilation may be a complex event involving parasympathetic relaxation, cholinergic inhibition of the
dilator muscle and central sympathetic inhibition of
the Edinger-Westphal nucleus.

9.

10.

11.
12.

13.

14.

15.
16.
17.
18.
19.

20.

Key words: pupil, human, autonomic, light reflex, cholinergic, adrenergic

21.

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