pupil

Dr. Durga prasad

 Pupillary function depends on the integrity of the structures
along the course of the pupillomotor pathway
 include: (1) retinal receptors;
 (2) ganglion cell axons in the optic nerve, optic chiasm, and
optic tract (but not the lateral geniculate body);
 (3) brachium of the superior colliculus;
 (4) pretectal area of the mesencephalon and the interconnecting
neurons to pupilloconstrictor motor cells in the oculomotor
nuclear complex;
 (5) the efferent parasympathetic outflow to the pupillary
sphincter and ciliary muscle; and
 (6) the efferent sympathetic pathway from the hypothalamus
to the pupillary dilator muscle.
Light reflex
parasympathetic supply
Anisocoria
 Inequality of the pupils
 Retina, ON, optic chiasma, tracts—
afferent pathway
 Half of the fibers decussate in optic
chiasma
 So input to each p.s nuclei in the
brainstem remains equal
 So RAPD do not cause anisocoria
Sympathetic supply
Ciliospinal reflex
 Painful stimuli over the neck, face or
upper trunk
 Bilateral pupil dilatation 1-2 mm
 Reflex is prominent in coma ,sleep
EXAMINATION OF THE PUPIL
 LOW ROOM ILLUMINATION

 FIXATE AT A DISTANCE

 BRIGHT FLASH LIGHT

 NO EYEDROPS
 SIZE

 4.5-7 mm in dark
 2.5-6mm in light
 Larger in young, smaller in the old
 Miosis -3mm
 Mydriasis-6mm
 Anisocoria-1mm
shape
 Oval-severe brain disease
 Tadpole-horner’s

Position
 Eccentrically placed pupil-midbrain
corectopia
Abnormal pupils
Lesions of parasympathetic pathway
 Toxic
 Adie’s
 Paralytic
 Argyll –Robertson
 Deafferented pupil

Lesions of sympathetic pathway

 Horner’s
 HT
H
O
1st Order
R AR PUPIL
N
E PTN
SC
R’
S 2nd Order SENSORY EWN

SCG
Afferent pupillary MOTOR III N
3 Order
rd defect

PARALYTIC

CG
CILIARY ADIE’S
MUSCLE

TOXIC
Toxic pupil
 Sudden unilateral dilatation
 Inadvertent finger to eye transmission of
anticholinergic agents
 Perfumes, medicines
 plants contain scopolamine— (patches )self
limited (cruiseship anisocoria)
 Belladonna alkaloids
 Pupil is dilated & no response to light/near
 1% pilocarpine-parasympathetic agonist
 Also cannot constrict pupil
 Because of NM blockade

 In 3rd nerve palsy –constricts

 Because of NM junction is normal
 Exposure to jimson weed,
 ingestion of datura seeds –
 Acute botulism- bilateral fixed
pupil
ADIE’S PUPIL
 FEMALE 20-50 yrs
 C/O photophobia,
 Episodes of blurred near vision or
blurred vision when switching from near
to far viewing
 Or simply c/o unequal pupil
Paralytic pupil

 Pre ganglionic parasympathetic fibers

denervation –
 Compression, contusion, infiltration,
inflammation
 Aneurysm of the posterior
communicating artery
 Pupil sparing 3rd nerve palsy
Occulomotor nerve palsy
 Anisocoria –head injury--level of
consciousness—
 uncal herniation –expanding
supratentorial lesion forces the uncus
against the edge of the tentorium-
 Compressing the adjacent midbrain &
3rd nerve
 Contralateral cerebral peduncle is
compressed
ARGYLL ROBERTSON PUPILS
 In 1869, Douglas Argyll Robertson
 miosis,
 unresponsive to light stimulus,
 and contraction on near effort in eyes with
intact visual function.
 central nervous system syphilis.
 A-R pupils with impaired, rather than absent,
light reaction are by far more common.
RAPD classification
1+ ---- minimally detectable asymmetry

2+ ---- fail to constrict or dilate slightly

3+ ---- dilate readily

4+ ---- non reactive dilated pupil

Lesions of sympathetic pathway
 Horner’s pupil
 Miosis
 Partial ptosis
 Enophthalmos
 Anhidrosis-lesion proximal to carotid
bifurcation
 Loss of ciliospinal reflex -2nd ,3rd order
neurons
Horner’s syndrome
 Disruption of sympathetic innervations
to the eyes
 Dilatation lag is classical finding
 Delayed response to reduced
illumination
 Anisocoria is > 5 sec after entering a
dark environment than it is after 15-30
sec
 Cocain test-
 Cocain prevents reuptake of norepinephrine
 Normal pupil –dilates in 30-40 min after 10%
cocain
 Honer’s pupil- because of denervation-
norepinephrine is low-- no effect of 10%

 No localising value- so not using

 Paredrine test
 It stimulates nor epinephrine release at
NM junction—leads dilatation
 3 rd order neurons—not much of nor
epinephrine —dilatation is poor
 1st & 2nd order neurons much of nor
epinephrine -- dilatation
Approach to the pt. of anisocoria
 First to establish which muscle is not
working properly
 Anisocoria always ses in the direction
of paretic muscle
 If the iris sphincter is paretic ,--
---Bright light will accentuate
weakness & ses anisocoria
 Iris dilator - viceversa
Pupillary inequality that increases in
bright light
 Sphincter tears, traumatic mydriasis, iris sphincter
atrophy (HZV uveitis)
 medication-atropine
 3rd nerve palsy
 Post ganglionic lesion-tonic pupil
 ACG
 IOFB –iron mydriasis
 Adrenergic mydriasis
 segmental paralysis of sphincter-adie’s, partial 3rd N
palsy
 Fixed pupil after anterior segment Sx
Pupillary inequality that increases in
dark
 SIMPLE / PHYSIOLOGICAL

 HORNER’S

 LOCAL OPHTHALMIC CAUSES—

inflammatory response
Simple anisocoria
 20% of normal population
 In most pts. <1mm anisocoria, no
ptosis, dilatation lag or vasomotor
dysfunction
Pupillary signs in coma-
 Hypothalamic lesions-ipsilateral
horner’s syndrome ,anhidrosis half of
the body
 Transtentorial herniation- ipsilateral
H.S/anhidrosis
 Carotid artery disease- ipsi-H.S /
contra. anhidrosis