1. PUPIL
DR. PIYUSHI SAO
DR. PIYUSHI SAO

2. PUPIL
• The pupil is an aperture located in the iris diaphragm of the eye that
allows light to enter the retina
• It appears black in contrast to the surrounding iris because most of
the light entering the pupil is absorbed by the tissues inside the eye.
• The size of the pupil determines the amount of light that enters the
eye.
• The pupil size is controlled by the dilator and sphincter muscles of the
iris.
DR. PIYUSHI SAO

3. PUPIL
• These muscles are derived from the neuroectoderm.
• The sphincter pupillae forms at about the 4th month of gestation,
when the optic cup differentiates into a circular band of muscle called
the sphincter irides.
• The dilator pupillae forms in the 7th month of gestation from the
outer layer of the primitive optic cup
DR. PIYUSHI SAO

4. PUPIL
• Based on its embryological
origins, the normal pupil is
not placed quite at the
center of the iris diaphragm
but slightly nasally and
inferiorly.
• The size in the normal adult
is between 3.0 to 3.5 mm
DR. PIYUSHI SAO

5. Normal Variations Seen In The Pupil Size
• 1. Age: -innervation of the pupil does not commence before the -----
31st week of gestation
• pupillary response does not occur prior to that.
• mydriasis in an infant less than 31 weeks along with unresponsive
pupillary reflexes-NORMAL
• while performing ROP evaluation in pre-term
DR. PIYUSHI SAO

6. • Gender: women -- larger pupillary size.
• Refractive error: Myopes --larger average pupillary size than hyperopes.
• Iris color: lighter colored iris larger pupils
than the ones with the dark colored iris (more melanin content)
• Emotions: pupillary size --autonomic innervation--emotional and
psychological state pupillary size
• Background illumination: Pupils constrict -bright light
dilate - dim light
light entering the visual system constant
DR. PIYUSHI SAO

7. Evaluation of the pupil
• great localizing value in neuro-ophthalmology
• macular function test
• permits clinical estimation of functional vision in a patient with media
opacity where the retina and the optic nerve cannot be evaluated.
DR. PIYUSHI SAO

8. Parameters recorded in pupil evaluation:
1. Size with respect to the level of illumination.
2. Reaction to light-direct and consensual.
3. Sustenance of reaction.
4. Relative afferent pupillary defect (RAPD) by swinging flash light/edge
pupil cycle time
5. Light near dissociation.
DR. PIYUSHI SAO

9. Direct Pupillary Response
• The best way to do this
• have the patient fixate on an object at least 3 m away
• in a dim lit room
• shine a light at one eye
• approaching it from slightly below
• This prevents the patient looking at the light source which could generate
accommodation and thus unwanted pupillary constriction.
• Note the briskness of the pupil response.
• If the pupils do not react briskly, vermiform constriction, iris notches, and
the response to near stimulus should be recorded.
DR. PIYUSHI SAO

10. Near Reaction
• The near reaction is best tested with an accommodative target, such
as a reading card.
• an illuminated light source as the accommodative target should not
be used
• the pupillary light response will be added to the near response.
DR. PIYUSHI SAO

11. light-near dissociation
• If the pupil reacts better to near than to light, the patient has light-
near dissociation.
• most common cause - optic neuropathy.
• Adie tonic pupil,
• Parinaud syndrome (i.e. dorsal midbrain syndrome),
• Argyll Robertson pupil (i.e. tertiary syphilis).
DR. PIYUSHI SAO

12. paradoxical pupillary constriction
• In children, paradoxical pupillary constriction in darkness has been
reported in patients with
• congenital stationary night blindness
• congenital achromatopsia,
• cone disorders and
• Lebers congenital amaurosis
• dominant optic atrophy, and
• amblyopia.
• In young children with nystagmus and paradoxical pupils,
electroretinogram testing should be considered
DR. PIYUSHI SAO

13. Relative Afferent Pupillary Defect (RAPD) (Or
Marcus Gunn Pupil)
• RAPD is detected by observing a change in the size of the pupils as
the light source is moved back and forth between the two eyes
• The designation of a “relative” afferent pupillary defect is important.
• Bilateral afferent pupillary defects are common (e.g. patients with
optic neuritis), but a bilateral RAPD cannot exist.
DR. PIYUSHI SAO

14. swinging torch (flashlight) test
• dimly illuminated room
• the patient fixates in the distance
• bright light is flashed for two to three seconds in one eye
• then quickly “flicked” across to the other eye
• place it there for a couple of seconds and then "flick" it back and so
on.
• Normally, each illuminated pupil constricts with associated
constriction of the opposite eye due to the consensual reflex.
• In ocular media disease like cataract, the pupils respond normally.
DR. PIYUSHI SAO

15. swinging torch (flashlight) test
• If the light is directed toward one eye and if the ipsilateral pupil
appears to dilate “paradoxically”, an RAPD is present.
• If the light is flashed on one eye and the pupil does not appear to
constrict
• or increased pupillary escape from constriction occurs
• RAPD present.
DR. PIYUSHI SAO

16. RAPD
• When the optic nerve is damaged
• the sensory afferent sent to the midbrain is reduced
• resulting in less vigorous constriction
• relative dilation from its previously constricted state
DR. PIYUSHI SAO

17. DR. PIYUSHI SAO

18. IF ONE EYE IS DILATED?
• The RAPD can also be tested in patients in whom one pupil is dilated
or unreactive due to a possible efferent defect that could be neural,
mechanical, traumatic or pharmacological.
• The physician examines the pupillary reaction of the undilated pupil
• light is flashed back and forth between the two eyes.
• In case the normal pupil dilates,
• it indicates an afferent pupillary defect (consensual reflex) in the eye
where the pupil is non-reactive.
DR. PIYUSHI SAO

19. One-eyed Patient Or Bilateral Pupillary
Involvement?
• an Edge Pupil Cycle Time is observed
• for detecting afferent pupillary defect (APD)
• This involves observation of the number of pupillary constriction and
dilatation in one minute after a thin optical section of light is placed
on the pupillary edge.
• Upon the placement of this optical section in this location, the pupil
would ideally constrict (light reflex) and move out of the zone of the
optical section.
• as the illuminance decreases, the pupil would dilate again and the
edge would again reach where the optical section is placed
DR. PIYUSHI SAO

20. Pupil cycle time
• Twenty-five such oscillations are timed in two
separate runs and the average time for each cycle calculated.
• Pupil cycle time can thus be used as a fast, simple and reliable clinical
test of optic nerve functions.
• not as reliable as the VER and the pupillary afferent defect
estimations
• advantage of being extremely easy to carry out
• especially of use in bilateral optic nerve disease.
DR. PIYUSHI SAO

21. RAPD
• RAPD may correspond with ipsilateral poor vision, this is not always
the case.
• a macular hole will result in poor acuity but not in an RAPD.
• marked unilateral field loss or unilateral dyschromatopsiaipsilateral
RAPD present.
• lesion confined to the optic tract an incongruous homonymous
field defect RAPD contralateral to the optic tract lesion.
• In patients with lesions of the brachium of the superior colliculus, a
contralateral RAPD without field loss (i.e. midbrain RAPD) may be
noted.
DR. PIYUSHI SAO

22. lesion confined to the
optic tract an
incongruous
homonymous field defect
RAPD contralateral to
the optic tract lesion.
RAPD +
DR. PIYUSHI SAO

23. RAPD
• Neutral density filters (NDF) can be used
to measure the relative afferent defect.
• Graded denomination of the filter (NDF)
is inserted in front of the better eye and
the RAPD is assessed.
• measurement of the NDF in log units
which results in equalization of the
pupillary reflexes gives the numerical
magnitude of the RAPD.
DR. PIYUSHI SAO

24. • It implies the amount of afferent input that has to be decreased in
the normal, unaffected eye so that it equals the input in the
diseased eye.
• numerically indicates the extent of pupillomotor deficit
in the diseased eye with afferent defect
DR. PIYUSHI SAO

25. DR. PIYUSHI SAO

26. ANISOCORIA
• When pupil size is recorded, a pupil gauge or millimeter rule is used
with the patient fixating in the distance,
• both dark and illuminated environments.
• If a difference in the size of the pupils (anisocoria) is present,
• it is noted if the anisocoria is greater in the dark or in the presence of
light.
• If the anisocoria is less than 1 mm and remains the same in both the
light and the dark, and if the pupils are round and reactive, the
patient may have physiologic anisocoria
DR. PIYUSHI SAO

27. ANISOCORIA
• Anisocoria greater in the dark
• suggests sympathetic disease
• Horner syndrome.
• Anisocoria greater in the light
• suggests parasympathetic disease
• Adie tonic pupil
• Note that even if one eye is completely blind, the pupil sizes should
be equal, in the absence of iris trauma or synechiae, i.e. afferent
disorders should not cause anisocoria.
DR. PIYUSHI SAO

28. Heterochromia Iridium
• congenital Horner syndrome
• SturgeWeber syndrome
• unilateral glaucoma treated with an antiprostaglandin, such as
latanoprost.
DR. PIYUSHI SAO

29. abnormal pupil
• Slit-lamp examination
• Irregularities in pupil shape
• congenital- iris coloboma
• acquired- synechiae (iritis),
• iris notches (trauma), and
• iridocorneal endothelial syndrome (glaucoma)
• In patients with type one neurofibromatosis, Lisch nodules closely
resembling iris nevi may be seen by using the slit lamp.
• Purse stringing of the pupil may be seen with Adie tonic pupil; it is
best elicited by quickly turning the slit-lamp beam on and off while
the pupil is examined.
DR. PIYUSHI SAO

30. Pupil gaze synkinesis
• is a sign of aberrant regeneration of cranial nerve (CN) III.
• Most commonly, the pupil constricts on adduction.
• While the patient is fixating in the distance
• the size of the pupils in primary gaze is compared with the pupil size
in adduction.
DR. PIYUSHI SAO

31. • The pupil size can be measured by different methods, especially prior to
refractive surgery.
• The Colvard pupillometer (Oasis Medical, Glendora, California, USA),
• the Zywave wavefront analyzer (Bausch and Lomb, Munich, Germany)
• a new technique used for measuring the dark adapted scotopic pupil size
with infrared digital photography.
• Pupil perimetry
• measuring involuntary pupil diameter changes in response to retinal visual
stimulation in the central 30 degrees of the visual field through an automated static
perimetry system.
• The pupil size is measured by video pupillography.
• By recording the pupil responses to light stimuli presented at different visual field
loci, it offers an objective method of visual field assessment.
DR. PIYUSHI SAO

32. The Pupillary Light Reflex Pathways
• The pupillary light reflex is a reflex that controls the diameter of the
pupil, in response to the intensity (luminance) of light that falls on the
retina of the eye.
• normal conditions :- the pupils of both eyes respond identically to a
light stimulus
• Light entering one eye  constriction of the pupil of that eye (the
direct response)
• + constriction of the pupil of the unstimulated eye (the
consensual response).
DR. PIYUSHI SAO

33. • Thus, this pathway has two limbs, the afferent pathway and the
efferent pathway.
• The efferent pathway is essentially parasympathetic in nature
Optic nerve Afferent
limb
It senses the
incoming light.
Oculomotor
nerve
Efferent limb It drives the muscles
that constrict the
pupil.
DR. PIYUSHI SAO

34. Afferent Pupillary Light Reflex Pathway
• The pupillary reflex pathway begins
with
• retinal ganglion cells convey
information from photoreceptors to
the optic nerve (via the optic disc).
• important measure :-of the
integrity of the anterior visual
pathways as it follows the visual
pathways till the posterior part of
the optic tract, with the nasal fibers
crossing at the chiasma.
DR. PIYUSHI SAO

35. Afferent Pupillary Light Reflex Pathway
• Thus, any lesion at this site, which
includes the retina, the optic nerve,
the optic chiasma and the optic tract
is likely to affect both, the visual and
the pupillary pathways.
• The pupillary fibers transmitting
through the optic tract subsequently
deviates from the visual pathways,
DR. PIYUSHI SAO

36. Afferent Pupillary Light Reflex Pathway
• just anterior to the lateral
geniculate body (LGB) and enter
the midbrain,
• connecting to the pretectal
nucleus of the upper midbrain,
• thus bypassing both, the lateral
geniculate nucleus (LGN) and the
primary visual cortex.
DR. PIYUSHI SAO

37. Afferent Pupillary Light Reflex Pathway
• This again has localizing
implications because lesions of
the LGB and the visual cortex
do not cause pupillary
abnormalities.
DR. PIYUSHI SAO

38. Afferent Pupillary Light Reflex Pathway
• From the pretectal nucleus,
these fibers traverse to the
Edinger-Westphal nucleus of
the oculomotor nerve
through the tectotegmental
tract and distributes equally
on both sides.
DR. PIYUSHI SAO

39. Afferent Pupillary Light Reflex Pathway
• This is the basis of the
consensual light reflex
as the optic tract carries
pupillary fibers from
both eyes and the
tectotegmental tract
distributes these fibers
equally to both the
Edinger-Westphal
nuclei.
DR. PIYUSHI SAO

40. Efferent Pupillary Light Pathway
(Parasympathetic)
• oculomotor cranial nerve
nucleus at the dorsal
mesencephalon at the level of
the superior colliculus.
DR. PIYUSHI SAO

41. Efferent Pupillary Light Pathway
• Efferent pupillary fibers
from the EWN are carried
in the superficial layer of
the oculomotor nerve on
both sides,
• through the cavernous
sinus,
• into the orbit
• through the inferior
division of the oculomotor
nerve
• till they synapse on the
ciliary ganglion.
DR. PIYUSHI SAO

42. Efferent Pupillary Light Pathway
• The
postganglionic
parasympathetic
fibers then
traverse through
the short ciliary
nerves to the iris
sphincter and the
ciliary muscles.
DR. PIYUSHI SAO

43. DR. PIYUSHI SAO

44. DR. PIYUSHI SAO

45. Efferent Pupillary Light Pathway
DR. PIYUSHI SAO

46. life saving importance
• The superficial location of the
pupillary fibres within the
oculomotor sheath in between the
brainstem and the cavernous sinus
• makes it more vulnerable to
compressive intracranial insults in
the form of aneurysms, and tumors,
DR. PIYUSHI SAO

47. Third cranial nerve palsy
• Pupillary involvement in CN III palsy  ptosis and limited ocular
motility
• the pupil is involved- MYDRIASIS
• an aneurysm must be excluded
• If the pupil is spared and all other functions of CN III are completely
paretic, an aneurysm is unlikely, and microvascular ischemic disease
is more probable.
DR. PIYUSHI SAO

48. DR. PIYUSHI SAO

49. DR. PIYUSHI SAO

50. DR. PIYUSHI SAO

51. DR. PIYUSHI SAO

52. DR. PIYUSHI SAO

53. Czarnecki's sign
• Aberrant regeneration of the right pupil in a man with
a large intracavernous sinus meningioma causing a
pupil-involving, incomplete third cranial nerve palsy.
• His pupil is round when he gazes straight ahead
(top).
• When he tries to rotate the eye medially, the pupil
constricts, but a segment of the iris from around 3-
to 6-o' clock (black arrow) constricts much better
than other segments of the iris (bottom).
• This phenomenon of segmental constriction of the
pupil in response to gaze, one of the signs of
aberrant regeneration, is referred to as
Czarnecki's sign
DR. PIYUSHI SAO

54. THE OCULOSYMPATHETIC PATHWAY
• sympathetic fibers supplying
the dilator pupillae muscles of
the iris
• originate in the posterolateral
hypothalamus,
• which descend through the
lateral part of the brainstem.
DR. PIYUSHI SAO

55. • After traversing the
mesencephalon and the pons,
these uncrossed fibers project
and synapse in the sympathetic
cell column from C8 to T2
vertebrae in the spinal cord,
called the ciliospinal center of
Budge.
DR. PIYUSHI SAO

56. • Upon exiting the spinal cord,
these then travel through the
stellate ganglion,
• the inferior cervical ganglion
and the middle cervical ganglion
to synapse in the superior
cervical ganglion at the carotid
artery bifurcation.
DR. PIYUSHI SAO

57. • From here, these fibers travel
along with the internal carotid
artery via the carotid plexus,
and enter the cavernous sinus
from where they travel
alongside the abducens nerve.
DR. PIYUSHI SAO

58. • They enter the orbit through
the superior orbital fissure
along with the nasociliary
branch of the trigeminal
nerve, and pass through the
ciliary ganglion without
synapsing, and finally enter
the eye through the long
ciliary nerves and terminate
on the dilator pupillae
muscle.
DR. PIYUSHI SAO

59. DR. PIYUSHI SAO

60. sympathetic pathways can be divided into:
• 1. A first order neuron (central):
This is from the hypothalamus to
the first synapse at first
ciliospinal center of Budge
• (uncrossed fibers)
• mainly located in the brainstem
and the cervical spinal cord.
DR. PIYUSHI SAO

61. • 2. second order neuron (pre-
ganglionic):
• This is from the brainstem to the
synapse of these fibers at the
superior cervical ganglion.
• These convolute and travel
upwards in the sympathetic chain.
• Here, they come in contact with
the apex of the lungs and the
subclavian artery in the thorax.
• Thus, here the location of the
sympathetic chain is essentially in
the neck area and the thorax.
DR. PIYUSHI SAO

62. • 3. A third order neuron (post-
ganglionic):
• This comprises the pupillary
pathway subsequent to the
superior cervical ganglion.
• The location of the post-ganglionic
sympathetic chain is thus from the
base of the skull, the cavernous
sinus and the orbit.
• These postganglionic fibers also
provide sympathetic innervation to
the lacrimal gland, the smooth
muscles of the upper and the lower
eyelids and blood vessels.
DR. PIYUSHI SAO

63. Horner Syndrome
• 1. Mild ptosis - of decreased
sympathetic innervation to the
Muller's muscle in the upper eyelid.
• 2. Relative enophthalmos because of
narrowing of the palpebral aperture
as a result of the sympathetically
innervated lower eyelid retractors not
acting (causing upside down ptosis).
• 3. Miosis because of decreased
sympathetic innervation to the dilator
pupillae muscle and relative
overaction of the sphincter pupillae
DR. PIYUSHI SAO

64. Horner Syndrome
• 4. Dilatation lag of the pupil because
the pupil with Horner's syndrome
does not have an effectively working
dilator pupillae because of
sympathetic paralysis
DR. PIYUSHI SAO

65. Horner Syndrome
• 5. Loss of the ciliospinal reflex, which
is a superficial reflex whereby upon
pressing the area of the ciliospinal
center of Budge, there is an increased
sympathetic stimulation, resulting in
pupillary dilatation, which is absent in
patients with Horner's syndrome.
DR. PIYUSHI SAO

66. ciliospinal reflex
• The ciliospinal reflex (pupillary-skin reflex) consists of dilation
of the ipsilateral pupil in response to pain applied to the neck,
face, and upper trunk.
• If the right side of the neck is subjected to a painful stimulus,
the right pupil dilates (increases in size 1-2mm from baseline).
DR. PIYUSHI SAO

67. Horner Syndrome
• 6. Ipsilateral facial anhidrosis
(head and neck) is specific
for the preganglionic variety
of Horner's syndrome
DR. PIYUSHI SAO

68. Horner Syndrome
• Congenital Horner's syndrome presents with iris heterochromia
hypothesized to occur because a lack of sympathetic stimulation in
childhood interferes with melanin pigmentation of the melanocytes in
the superficial stroma of the iris.
DR. PIYUSHI SAO

69. • Horner's syndrome- show relative non-dilatation of the pupil in the
affected eye when cocaine 5% is instilled into that eye causing an
increase in the anisocoria as the normal pupil will dilate well.
• This is because cocaine can only act upon the pupil when epinephrine
is released from the nerve endings and supplies the dilator pupillae
muscle.
• This drug test thus confirms the presence of Horner's syndrome.
DR. PIYUSHI SAO

70. DR. PIYUSHI SAO

71. DR. PIYUSHI SAO

72. • Apraclonidine test for Horner syndrome.
• A, suspected oculosympathetic defect (ptosis and miosis) on the right side.
• B, Following instillation of topical apraclonidine in both eyes, the right
pupil has dilated and the anisocoria is now reversed, confirming Horner
syndrome on the right side.
• Note also the resolution of eyelid ptosis, even to the point of retraction on
the right side.
DR. PIYUSHI SAO

73. Horner syndrome involving
the second-order neuron
• right-sided ptosis and miosis in bright
light.
• B, The anisocoria increases in the dark.
• C, Following instillation of
hydroxyamphetamine eyedrops (1%),
both pupils dilate, indicating that the
third-order neuron is intact
DR. PIYUSHI SAO

74. • CT scan demonstrates a right apical lung mass (Pancoast tumor)
DR. PIYUSHI SAO

75. NEAR SYNKINESIS
• Near synkinesis triad consists of
• convergence of eyes,
• accommodation of lenses and
• miosis of pupils.
• The pupillary constriction in such cases is however not dependent on
the associated convergence, accommodation or the amount of
ambient light present in the environment.
DR. PIYUSHI SAO

76. NEAR SYNKINESIS
• Near synkinesis pathway is more ventrally located than the pretectal
afferent limb of the light reflex
• comprises a supranuclear connection between the neurons
subserving
• the ciliary body muscles (accommodation),
• the pupillary sphincters (miosis)
• and the medial rectus muscle (convergence).
DR. PIYUSHI SAO

77. NEAR SYNKINESIS
• This forms the anatomical basis of some instances of
light near dissociation (dorsal midbrain syndrome where the pupillary
light reflexes are affected but the near reflex is not because of lesions
at the level of the dorsal midbrain).
• Though the pathways are not as well defined as the pathways for the
light reflex, the fibers subserving the near reflex, reach the striate
cortex and further relay of information is provided to the frontal eye
fields (FEF) and the EWN, bypassing the pretectal olivary nucleus, in
the dorsal midbrain.
DR. PIYUSHI SAO

78. • Though the pathways are not as well defined as the pathways for the
light reflex, the fibers subserving the near reflex, reach the striate
cortex and further relay of information is provided to the frontal eye
fields (FEF) and the EWN, bypassing the pretectal olivary nucleus, in
the dorsal midbrain.
• From the EWN, these fibers follow the efferent course through the
different components of the oculomotor nerve, the motor part
serving the medial rectus muscle and the parasympathetic part
serving the sphincter pupillae through the ciliary ganglion and the
short posterior ciliary nerves
DR. PIYUSHI SAO

79. Congenital and Acquired Abnormalities of the
Pupillary Shape and Number:
• Ectopic pupil: This implies a pupil located at a location away from its
normal location.
• It associated with ectopic location of the lens, the condition, usually
autosomal dominant, is termed as ectopia lentis et pupillae.
DR. PIYUSHI SAO

80. • Dyscoria: This refers to any abnormality of the shape of the pupil,
congenital or acquired.
Baerveldt glaucoma implant
DR. PIYUSHI SAO

81. • Polycoria: This refers to more than one pupillary aperture as may be
seen in the anterior segment dysgenesis syndromes.
DR. PIYUSHI SAO

82. • Correctopia: This refers to the
displacement of the pupil from its
normal position.
• Though this sound similar to ectopic
pupil, corectopia actually implies the
pupil, previously located at a normal
position, has been displaced while
ectopia pupillae implies and describes
the actual displaced position.
DR. PIYUSHI SAO

83. DR. PIYUSHI SAO

84. • Keyhole pupil in iris coloboma
DR. PIYUSHI SAO

85. Congenital miosis and mydriasis: These may be seen in certain
conditions like
• congenital Horner's Syndrome and
• congenital third nerve palsy.
• Miosis associated with heterochromia iridium is classical of a
congenital Horner's syndrome
DR. PIYUSHI SAO

86. Abnormal Pupillary Reflexes through the
Aperture:
• Leukocoria: This condition where a white retrolental reflex can be
seen through the pupillary aperture
• Retinoblastoma ( children )
DR. PIYUSHI SAO

87. • Bruckner’s reflex: The appearance of a red glow through a pupil in
a highly ametropic or strabismic eye due to retro-reflective optics, is
classically called the Bruckner's reflex and is of great use in the
screening of patients with anisometropia, ametropia and strabismus
in children.
DR. PIYUSHI SAO

88. • Iris transillumination: The red fundal glow through the pupil may
be visible in albinotic patients because of retro-reflection of the light
entering into the eye through the pupillary aperture and the
hypoplastic iris and transmitting out through both, the pupil and the
iris by a process called transillumination
DR. PIYUSHI SAO

89. Anisocoria:
• unequal size of the pupils.
• In the absence of any deformities
• defects in the efferent nervous pathways controlling the pupil size
• in the oculomotor nerve (parasympathetic fibers)
• or the sympathetic pathways
DR. PIYUSHI SAO

90. Physiological anisocoria
• slightly unequal pupils.
• i. Difference of less than 1.0 mm
• pupillary reactions -same in both light adapted and dark adapted
• no light near dissociation.
• ii. Occasionally the anisocoria may switch sides (called “alternating” or
“seesaw” anisocoria).
• iii. No associated features (diplopia, visual loss) are present.
• iv. Old photographs -dating the onset of anisocoria.
• Once established, no further evaluation or therapy is required for the
condition
DR. PIYUSHI SAO

91. Pathological Anisocoria:
• 1. pupillary reactions to light - If equal
• rule out- sphincter denervation as in traumatic mydriasis
• angle closure glaucoma
• Look for more central cause
• 2. check for the consensual reflex- normal- integrity of the afferent
system
• small or the large pupil size is essentially due to efferent defect
• 3. whether the anisocoria increases in bright light or dim light :
DR. PIYUSHI SAO

92. Pathological Anisocoria:
• whether the anisocoria increases in bright light or dim light :
• a. increases in darkness- smaller pupil is not able to react to the
physiological dilatation that occurs in darkness in an attempt to keep
the amount of light entering the eye constant and hence, it is the
pathological eye.
• b. increases in light- larger pupil is not able to react to the
physiological constriction that occurs in a bright background in an
attempt to keep the amount of light entering the eye constant and
hence, it is the pathological eye.
DR. PIYUSHI SAO

93. Pathological pupil is dilated
• 1. Early stage of coma (brainstem herniation)
• 2. Traumatic mydriasis (non-reacting pupil; does not constrict with
pilocarpine)
• 3. Mydriasis due to acute glaucoma (non-reacting pupil; constricts with
pilocarpine)
• 4. Drug induced like with atropine (non-reacting pupil; the mydriasis may
go away with time after the anticholinergic effect has been washed away
but no constriction occurs with pilocarpine due to receptor blockade)
• 5. Oculomotor nerve palsy (non-reacting pupil; constricts with pilocarpine
as the lesion is more central and hence, the receptivity to local pilocarpine
exists)
• 6. Tonic pupil (non-reacting to light, reacts to near stimulus, shows
supersensitivity to pilocarpine 0.125%)
DR. PIYUSHI SAO

94. Pathological pupil is constricted
• 1. Horner's syndrome (smaller pupil dilates less as compared to the normal
pupil with 10% cocaine, thus increasing the anisocoria)
• 2. Unilateral pilocarpine use (history of glaucoma to be elicited)
• 3. Localizing for ipsilateral pontine bleed/lesion in early stage
(recalcitrant to dilatation by topical mydriatrics as the cause is central)
• 4. Early stage of opiate overdose where unilateral constriction may be
there (recalcitrant to dilatation by topical mydriatrics as the cause is
central; may respond to naloxone)
• 5. Argyll Robertson pupil (usually bilateral; near reflex very markedly
present; response to light reflex is very poor; recalcitrant to dilatation by
mydriatrics)
• 6. End stage tonic pupil
DR. PIYUSHI SAO

95. Conditions leading to a relative afferent
pupillary defect include:
• 1. Optic nerve disorders:
• Unilateral optic neuropathies are common causes of RAPD.
• optic neuritis,
• Glaucoma
• optic neuropathy due to any cause that is unilateral,
• iatrogenic damage to the optic nerve which may occur following
orbital hemorrhage,
• orbital, sinus or plastic surgery, neuro-surgical procedures
• retrobulbar anesthesia.
DR. PIYUSHI SAO

96. • 2. Retinal disorders:
• Usually retinal disease has to be quite severe for an RAPD to be
clinically evident.
• ischemic retinal disease like CRVO, CRAO, BRVO, BRAO, diabetic
retinopathy, and sickle cell retinopathy.
• Severe retinal infections, retinal detachment, intraocular tumors and
macular degenerations
• Ocular ischemic syndrome
DR. PIYUSHI SAO

97. • 3. Amblyopia: Unilateral amblyopia is known to cause a mild RAPD
in the affected eye.
• 4. Light near dissociation and the Argyll Robertson pupil:
The neuroanatomical basis of light near dissociation has been
explained in the earlier part of this chapter.
DR. PIYUSHI SAO

98. Light near dissociation and the Argyll
Robertson pupil:
• light near dissociation  Argyll Robertson's pupil (ARP)
• Neurosyphilis--lesions in the intercalated neuron
• bilaterally miotic, and irregular pupils reacted poorly to light with a
normal near response
• recalcitrant to pharmacological dilatation.
• Generalized iris atrophy
• with loss of the normal pattern of the iris
DR. PIYUSHI SAO

99. Light near dissociation
• A true ‘light near dissociation’ is present only if
• the near response, tested in mesopic background illumination
exceeds the best constriction that bright light can produce.
• There is no clinical condition in which the light reflex is present but
the near response is absent
• Vision is not a prerequisite for near reflex.
DR. PIYUSHI SAO

100. Light near dissociation
• advanced diabetes mellitus,
• tumors of the pituitary gland,
• midbrain lesions (Parinaud's dorsal midbrain syndrome),
• myotonic dystrophy,
• Adie's tonic pupil,
• familial amyloidosis,
• peripheral neuropathies associated with alcoholism,
• Charcot-Marie-Tooth disease,
• Dejerine-Sottas disease and
• aberrant regeneration of cranial nerve III (pseudo-Argyll Robertson pupil).
DR. PIYUSHI SAO

101. True And Pseudo Argyll Robertson pupil
• true ARP  lesions in the pupillary pathway.
• pseudo-ARP third nerve palsy
• is due to aberrant regeneration of the nerve
• pupillary fibers find their way into the nerve sheath
• innervating the medial rectus muscle.
• Due to this, any action of the medial rectus muscle, including
convergence, results in miosis, thus simulating a strong near reflex
in the absence of normal constriction to light.
DR. PIYUSHI SAO

102. Holmes Adie’s tonic pupil:
• internal ophthalmoplegia
• denervation of the post-ganglionic supply to the sphincter pupillae
and the ciliary muscle
• The pupil is mid-dilated and tonic
• non-responsive to light
• though the response to accommodation slow
• simulating light near dissociation
• Redilatation after accommodation is slow.
DR. PIYUSHI SAO

103. Holmes Adie’s tonic pupil:
• The denervation hypersensitivity and up-regulation results in a
constriction response to 0.125 percent pilocarpine.
• overall sluggish response to light with vermiform-like movement of
the pupillary border iris sector paralysis, iris stromal streaming and
iris stromal spread.
• Deep tendon reflexes may also be decreased
DR. PIYUSHI SAO

104. • The pupil is not round.
The sphincter
contraction is strongest
along its superior
sector, seen as a
puckering or “bunching
up” of the iris stroma.
• The sphincter is
paralyzed between the
7-o’clock and 9-o’clock
sectors
• the adjacent area of
iris stroma appears
thinned out and
flattened.
DR. PIYUSHI SAO

105. Left Adie tonic pupil.
• The left pupil reacts poorly to
direct light stimulus, whereas the
right pupil demonstrates a strong
consensual response.
Both pupils constrict as the patient
fixates on a near target.
• The response of the left pupil to
near response is better than its
response to light (light–near
dissociation).
• After the patient refixates on a
distant target, the right pupil
quickly redilates.
• The left pupil is slow to redilate (it
is smaller than the right pupil), a
sign of tonicity
DR. PIYUSHI SAO

106. Right Adie tonic pupil
• Right Adie tonic pupil at
baseline in ambient room
lighting.
• After instillation of
pilocarpine (0.1%), the right
pupil becomes miotic,
supersensitivity.
DR. PIYUSHI SAO

107. Hutchinson’s pupil:
• ominous sign
• unilateral, fixed, dilated pupil is
• pathognomic of ipsilateral uncal herniation and cerebral edema
• precedes brainstem death.
• kinking of the oculomotor nerve across a displaced posterior cerebral
artery due to
• presence of the abnormal lesion and
• subsequent compression against the hiatus of the tentorium and the dural
roof of the cavernous sinus.
DR. PIYUSHI SAO

108. Hippus
• This comprises spasmodic and rhythmic pupillary movement between
the sphincter and the dilator muscles.
• It is prominent while testing the pupillary light reflex but may be
independent of changes in background illumination.
• When pathologicalaconite poisoning
• neurosyphilis, seizure disorders, multiple sclerosis, meningitis,
posterior fossa lesions, congenital chorea and barbiturate poisoning.
DR. PIYUSHI SAO

109. Tournay's Phenomenon
• Dilation of the pupil in the abducting eye on extreme lateral gaze is
known as Tournay's phenomenon.
• small percentage of the normal population
• mechanical traction caused by movement of the globe
• stimulates the long ciliary nerves in abduction
• short ciliary nerves in adduction or alternatively,
• co-innervation of the iris sphincter and the medial rectus muscle
• with both being inhibited in abduction, resulting in the dilatation in
abduction.
DR. PIYUSHI SAO

110. sphincter pupillae parasympathetic
innervation
dilator pupillae sympathetic innervation
DR. PIYUSHI SAO

111. Effect of Drugs
• 1. Substance P, which acts directly on the sphincter pupillae and
cause constriction of an atropinized eye.
• 2. Morphinepupillary miosis
• by cutting off the central inhibition of the Edinger-Westphal
nucleus.
• systemic ingestion of morphine causes pupillary miosis
• while topical instillation, even in very strong solutions (5%) does
not.
• Drugs like nalorphine, which are used as anti-narcotics, reverse the
miotic action of morphine by central mechanisms.
• This can be used to assess the effectivity of morphine detoxification.
DR. PIYUSHI SAO

112. Effect of Drugs
• 3. Stages of anesthesia.
• During the stage of induction
• anxiety and excitement dilated pupils,
• constricts  anesthesia deepens,
• supranuclear inhibition of the sphincter nuclei is cut off.
• However, if the anesthesia becomes dangerously deep and
encroaches on the midbrain, the pupils become dilated and fail to
react to light.
DR. PIYUSHI SAO

113. Effect of Drugs
• 4. Appropriate blood calcium levels facilitate acetylcholine release
and synaptic transmission.
• low calcium levels  miosis.
• high concentrations of magnesium may block transmission causing
dilatation of pupils.
• 5. Topical dexamethasone causes mild dilatation of the pupil, but
does not do away with the pupillary reactions.
DR. PIYUSHI SAO

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118. DR. PIYUSHI SAO

119. REFERENCES
• ZIA CHOUDHARY : THE PUPIL; PG-439 PDF –1558
• Neuro-Ophthalmology Illustrated 2nd Ed
• Aao neuroophathalmology ..pg 356
• Alberts Principles-occuloplastics and neuro - Volume III
• Khurana Comprehensive Ophthalmology 6th edition
DR. PIYUSHI SAO

120. THANKYOU
DR. PIYUSHI SAO