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References
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Part II
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Extraocular Signs
Pupillary Signs
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16
16.1 Anatomical Considerations
The pupil is an aperture in the iris diaphragm that
regulates light entry into the eye to optimize
image formation on the retina. It constricts in
bright light and dilates in dim light. The pupil
size is controlled by two autonomic muscles, the
sphincter pupillae and the dilator pupillae, under
parasympathetic and sympathetic control,
respectively.
16.1.1 The Sphincter Pupillae
The sphincter pupillae is a 1-mm wide circumferentially oriented smooth muscle located in the
iris stroma at the pupillary border just in front of
the anterior pigmented iris epithelium and is covered with melanocytes and broblasts. It is innervated by the postganglionic bres of the short
ciliary nerves arising from the ciliary ganglion.
16.1.2 The Dilator Pupillae
The dilator muscle bres are radially oriented
myoepithelial cells embedded in the pigmented
iris epithelium and run from the sphincter pupil-
lae to the peripheral iris, where these end up as a
circumferentially oriented sphincter bundle. It is
connected to the elastic bromuscular ciliary
mesh with tent-like iridial strands anterior to the
ciliary muscle [1].
16.1.3 The Ciliary Ganglion
The ciliary ganglion is a 1–2 mm parasympathetic ganglion lying medial to the lateral rectus
in the posterior orbit. It contains, on average,
2500 neurons, fewer in women [2]. The ciliary
ganglia receive three types of neural bres: (1)
somatic motor bres from the inferior division of
the oculomotor cranial nerve (CN III), (2) postganglionic sympathetic bres, and (3) parasympathetic bres projecting from the
Edinger-Westphal nucleus. Only the parasympathetic bres synapse in the ciliary ganglion. The
postganglionic parasympathetic bres leave the
ganglion with short posterior ciliary nerves. Only
5% of the bres innervate the sphincter pupillae,
and the rest innervate the ciliary muscles located
in the ciliary body. The postganglionic sympathetic bres course along the long ciliary nerves
(branches of the nasociliary nerve, itself a branch
of CN V1) and innervate the dilator muscle.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. Gupta et al., Ophthalmic Signs in Practice of Medicine,
https://doi.org/10.1007/978-981-99-7923-3_16
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16 Pupillary Signs
16.1.4 Pupil Size
In mesopic light conditions, neither too bright
nor too dark, the size of the pupil varies from 2 to
4 mm. There is a progressive decrease in pupil
size with each decade. The pupils do not remain
constant in size, but show rhythmic oscillations
called Hippus (pupillary athetosis) at a rate of
~1Hz. The Hippus may get exaggerated in aconitine (a plant alkaloid) poisoning, trauma, renal
disease, and altered sensorium, generally indicating a frontal lobe dysfunction. The hippus originates from the parasympathetic system [3]. It
may also indicate non-convulsive status epilepticus [4] and early mortality in hospitalized patients
[5].
16.2 Pathway forthePupil Light
Reex
The afferent limb of the pupil light reex (PLR)
arc starts in the melanopsin-containing intrinsic
photosensitive retinal ganglion cells(ipRGC)
(Fig. 16.1). The ipRGC are few and constitute
less than 1.5% of all the RGC, distributed mainly
in the perifoveal retina. Nearly half of the ipRGC
are found in the ganglion cell layer, and the rest
in the inner or outer border of the inner plexiform
layer. The ipRGC show decline with ageing [6]
and, notably, in Alzheimer’s and Parkinson’s disease [7]. Although intrinsically photosensitive,
the ipRGC also receive inputs from the rod and
cone photoreceptors [8, 9].
The ipRGC are resistant to degeneration in
Leber’s hereditary optic neuropathy and dominant optic atrophy. [10]. PLR may be elicited in
these patients, even in total blindness.
The spectral sensitivity of the ipRGC peaks
in the blue region of the light spectrum, consistent with their role in the non-visual tasks, especially the circadian rhythm (day-night cycle by
suppression of melatonin), cognition, heart rate,
ght, or ight response [11]. On the other hand,
the spectral sensitivity of the rods and cones
mediated PLR peaks in the red light. PLR mediated by red light is short-duration and illsustained; the pupil dilates even while the light
is on. Pupil constriction in PLR mediated by
blue light sustains so long the light is on. The
ipRGC represent the retinohypothalamic tract.
Patients with multiple sclerosis (MS) who show
Fig. 16.1 Ultrastructure of the retina. Reproduced with
permission from the publishers from Gupta, A. (2022).
Bench-to-Bedside Research in Ophthalmology. In: Sobti,
R., Ganju, A.K. (eds) Biomedical Translational Research.
Springer, Singapore. https://doi.
org/10.1007/978- 981- 16- 8845- 4_5
16.2 Pathway forthePupil Light Reex
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thinning of the Ganglion cell-inner plexiform
layer show a signicant decline in pupillary
constriction response to blue light compared to
MS patients who do not have thinning of the
GCL-IPL layers [12]. Thus, in MS, the attenuation of the retinohypothalamic pathway, as
determined by blue light pupillometry, may be
responsible for disturbed circadian rhythm and
the perception of fatigue experienced by MS
patients [13].
Nasally arising axons from the RGCs and the
ipRGCs cross in the optic chiasm, while the temporal axons pass uncrossed through the chiasm
and proceed along the optic tracts (Fig. 16.2).
However, instead of ending up in the lateral
geniculate nucleus, these bres from the ipRGCs
project to the ipsilateral pretectal nucleus in the
oculomotor complex in the rostrodorsal midbrain
in front of the superior colliculus. The pretectal
nucleus sends projections to the ipsilateral and
contralateral Edinger-Westphal (EW) nuclei
which lie medial to the oculomotor nuclei in the
midbrain (Fig.16.3).
The efferent path of the PLR starts as preganglionic bres from the EW nuclei and course
477
Fig. 16.2 Inferior aspect of the human brain showing
some of the components of the visual pathway. Image
courtesy of Prof Daisy Sahni (Ex-Professor) and Prof
Anjali Aggarwal (Head), Department of Anatomy, Post
Graduate Institute of Medical Education and Research,
Chandigarh, India
Fig. 16.3 Highly schematic pupillary light reex (PLR)
pathway, midbrain, optic tracts, chiasma, and optic nerves.
The afferent pupillomotor bres from the nasal retina (blue
from the right eye and red from the left eye) cross in the
optic chiasma, travel in the optic tracts, but instead of ending up in the lateral geniculate nucleus like the visual bres,
proceed to the ipsilateral and the contralateral pretectal
nucleus and end up in the Edinger-Westphal (E-W) nucleus.
The efferent PLR bres (shown in green) start from the
E-W nucleus and reach the ciliary ganglion along the inferior division of the 3rd cranial nerve, from where the postganglionic bres accompany the short posterior ciliary
nerves to the iris and the ciliary body. Abbreviations; LGN,
lateral geniculate nucleus. Graphics by Kritka Thakur
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16 Pupillary Signs
along the oculomotor nerve and synapse in the
ciliary ganglion. The postganglionic bres innervate the iris and ciliary muscles.
16.2.1 Sympathetic Pathway
The rst neuron of the sympathetic pathway is
located in the hypothalamus, where the bres
descend in the brain stem, run in the periphery of
the anterolateral funiculus of the spinal cord, and
cross to the intermediolateral grey matter (ciliospinal centre of Budge) synapse here. They also
cross over the contralateral ciliospinal centre at
the level of C8 to T2 [14]. The second neuron,
preganglionic bres, emerges along the ventral
roots of the spinal cord and ascends in the thorax
to end in the superior cervical ganglion, which
lies in the adventitial wall of the carotid artery at
its bifurcation. The postganglionic pupillomotor
sympathetic bres travel along the periarterial
plexus along the internal carotid artery, while the
vasomotor sympathetic bres pass along the
external carotid artery. The oculomotorsympathetic bres pass through the superior
orbital ssure and the ciliary ganglion to travel
with the long posterior ciliary nerves and innervate the dilator pupillae [15] (Fig. 16.4). The
sympathetic bres also innervate the thin Muller
muscle bres that lie under the levator palpebrae
superiors in the upper lid and the retractor bres
of the lower lid.
16.2 Pathway forthePupil Light Reex
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479
Fig. 16.4 A highly schematic diagram of the sympathetic
pathway. The rst neuron of the sympathetic pathway is in
the hypothalamus, from where the bres descend along
the brain stem, medulla oblongata, and reach the ciliospinal centre of Budge, where the 2nd neuron is located.
Here the interneurons are located in the grey matter at the
level of T2 to C8. The preganglionic bres emerge along
the ventral roots of the spinal cord. These bres ascend in
the thorax to reach the superior cervical ganglion located
in the adventitia of the carotid artery at the level of its
bifurcation. The bres synapse in the superior cervical
ganglion, where the 3rd neuron is located. The postganglionic bres travel along the internal carotid artery,
enter the orbit along the branches of the ophthalmic
branch, and travel with the long ciliary nerves to reach the
dilator pupillae muscle. Graphics by Kritika Thakur
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16 Pupillary Signs
16.3 Testing forPupillary Reexes
Before eliciting PLR, pupil size should be
checked in dim and bright light. Normally, the
pupils are isocoric and are slightly bigger in blue
vs the dark irides. Nearly, 20% of the people may
show a difference in the size of the pupils of
<0.3mm. In encountering patients with signicant anisocoria, the larger pupil is the abnormal
pupil if it remains dilated in light, and the smaller
pupil is the abnormal pupil if it remains small in
the dark. The colour of the iris has no bearing on
the pupil light reex (PLR) when tested by automated pupillometry [16]. If the PLR is normal,
the near reex is always normal, so it need not be
tested. However, if the PLR is absent, the near
reex must be tested.
Pupil constriction in the ipsilateral eye when
the light is shown into the eye is called the direct
reex, and constriction of the contralateral eye is
called the consensual reex. Each eye should be
tested individually. Lack of direct reex indicates
either an afferent or an efferent defect in the ipsilateral eye. For instance, if shining light into the
right eye does not elicit constriction of the right
pupil, it could either be an afferent or an efferent
defect. However, if shining the light through the
left eye still does not elicit constriction of the
right pupil, it indicates an efferent defect in the
right eye. If, however, shining the light into the
left eye elicits a pupillary constriction of the right
pupil, it indicates an afferent defect in the right
eye (Fig.16.5).
Bilateral absent pupillary responses generally
indicate unfavourable outcomes in patients with
severe brain injury and coma. Occasionally, false
positive absent pupillary responses may be seen
up to 3 days in traumatic or infective brain injury,
but not in ischaemic encephalopathy beyond
which no false positive tests are seen [17].
Notably, pupillary reexes are absent in preterm babies with less than 30weeks of gestation;
they develop gradually beyond this age, and by
35weeks, the reex is present in all babies [18].
a
b
c
d
Fig. 16.5 Relative afferent pupil defect in the right eye.
In ambient light, pupil size is equal in both eyes (a). When
the light is shone in the right eye, the pupil constricts in
both the right and left eyes (b). When the light is shone
into the left eye, the pupil constricts in both eyes (c).
When light is swung back into the RE, the pupils in the
right and left eyes start dilating (d). Graphics by Kritika
Thakur
16.4 Pupillary Changes inLesions ofParasympathetic Pathways
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481
16.3.1 Swinging Flashlight Test
The swinging ashlight test is the most critical
subjective clinical test to detect conduction
defects in the optic nerve in unilateral or bilateral
asymmetric cases and is termed the relative afferent pupil defect (RAPD). Although rst described
by Marcus Gunn as a response to darkness,
Levatin [19] described the RAPD test as a pupillary escape phenomenon due to unequal light
sense in the two eyes due to gross retinal or optic
nerve disorders.
In a semi-dark room, bright pen torch light
(Halogen 3.5v) is shone from 45° below the optic
axis for 2s or a count of two, swinging (not more
than four times with a pause time of 3s) alternately between the eyes. If both eyes are normal,
when light is shone on one eye, the pupil constricts in both eyes. However, if there is a conduction defect in one eye, on swinging the light from
the normal eye (the pupils in both eyes get constricted) to the abnormal eye, the pupil of the
abnormal and the normal eye starts dilating
(Fig.16.5). The RAPD can be measured by putting a series of neutral density lters (0.3–1.6 log
units) in front of the good eye till the pupil constriction becomes equal in both eyes [20].
However, the major disadvantage of using neutral
density lters is the poor visibility of the pupil by
the examiner. Clinical grading of RAPD has also
been done in the past [21].
16.3.2 Phases ofPupil Light Reex
Once stimulated with light, there is a latent period
before the pupil starts constricting, attains maximum constriction velocity, and achieves max
constriction, followed by pupillary escape in
which the pupil dilates to some extent and on
switching off the stimulus, it gets back to the prestimulus size [22]. These phases of pupil reaction
can be reproducibly captured on an automated
pupillometer.
16.3.3 Causes ofRAPD
The RAPD is not seen in refractive errors, media
opacities, or feigned blindness. In patients with
amblyopia, the diagnosis of RPAD should be
made with caution as it rarely exceeds 0.3 log
units [23]. However, RAPD can be elicited if
there is an asymmetric conduction defect in the
optic nerve or the optic chiasm [23]. Lesions in
the optic tracts and superior colliculus show a
contralateral RAPD.However, the latter is without concurrent homonymous hemianopia [24,
25].
The most common cause of RAPD is conduction defect, as seen in optic neuritis, ischaemic
optic neuropathy, asymmetric glaucoma, traumatic optic atrophy, optic nerve gliomas, and
optic nerve sheath meningiomas. RAPD is also
present in diffuse and extensive retinal disorders
like retinal ischaemia, central retinal artery occlusion, ischaemic central retinal vein occlusion,
rhegmatogenous retinal detachment, and destruction and scarring of the retina in extensive
chorioretinitis.
16.4 Pupillary Changes inLesions
ofParasympathetic
Pathways
The efferent bres of the parasympathetic pathways travel from the Edinger -Westphal nucleus
and course along the oculomotor nerve (Cranial
nerve III), lying supercially on the dorsal aspect
of the nerve. The CN III emerges from the ventral
aspect of the midbrain into the interpeduncular
fossa and lies below the posterior cerebral artery
and above the superior cerebellar artery. At this
location, it is vulnerable to compression by a posterior communicating artery (PCA) aneurysm. As
it proceeds to enter the cavernous sinus, it lies on
the edge of the tentorium cerebelli. It becomes
vulnerable to brain herniation in an acute rise in
ICP due to subarachnoid haemorrhage. It pierces
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