PTOSIS

By Dr Sukanya M K
JR dept of general medicine
 EYELIDS

The upper lid just covers the upper cornea, and the lower lid lies slightly
below the inferior corneal margin.

Eyelid opens
 levator palpebrae superioris muscle (oculomotor nerve)
 Accessory muscles include :

Muller’s muscle (sympathetic) -embedded in the levator and inserts

mainly on the tarsal plate

Frontalis muscle (temporal branch -facial nerve) retract the lid in

extreme upgaze.
 Eyelid closure
 levator motor neuronal activity ceases
 Rapid and firm eye closure is a function of the orbicularis
oculi (facial nerve)

VII palsy-blinking and firm eye closure are impaired

3 nerve-lid position, gentle eye closure, and lid-eye

coordination
 Supra nuclear control
 The cerebral cortex particularly the right
hemisphere, is associated with the voluntary control of
tonic levator activity

 Central caudate nucleus (midbrain) -unpaired

Contibute fibers to both occulomotor nerves and innervate

both LPS

It maintain a tonic contraction during eye opening, increased

with upward movement and decreases in downward
movement.
Vertical saccade
 In upgaze ,Rostral interstitial nucleus of the median
longitudinal fasciculus (riMLF) when activated, provides
excitatory input >SR & IO (subnuclei 3CN).
 riMLF activates the nearby M-group which excitation SR and
IO subnuclei, but its primary excitatory output is to the CCN,
resulting in an increase in firing rate which produces eyelid
elevation.
 The M-group also synapses on the facial nucleus, -assistance
from the frontalis in eyelid elevation when needed.
The opposite occurs during downgaze.
Eyelid retraction in midbrain dysfunction occurs due to M-
group overstimulation (in an attempt to overcome an upgaze
palsy) or underinhibition (from injury to the nearby
interstitial nucleus of Cajal and nucleus of the posterior
commissure).
During a blink

 LPS abruptly ceases firing and the orbicularis oculi(5)

contracts which coordinated by the superior colliculus
(SC).
 The SC projects to the supraoculomotor area (CCN )and
facial nuclei

SC is inhibited by the pars reticulata of the substantia nigra

(SNr).
In parkinsonism, there is increased activity in the
SNr ,reduced spontaneous blinking.

Afferents from the trigeminal nucleus and pretectum to the

SC, which mediate reflexive blinking to corneal stimulation
and bright light.
 Afferents from the limbic system and reticular formation
to SOA, both regions are functionally involved in level of
arousal.
 supraoculomotor area (ventral periaqueductal
graymatter ) destruction of the periaqueductal graymatter
may cause ptosis
 The region of the nuclear complex of the posterior
commissure is involved in lid-eye movement
coordination ;lesion results in lid retraction
 The rostral interstitial nucleus of the MLF (riMLF) is the
principal premotor structure concerned with the generation
of voluntary vertical saccades. Because of the close lid-
eye coordination in all types of vertical gaze changes, it is
likely that the premotor control of saccadic signals to
the levators also comes from the riMLF.
PCom project to the
 C/l interstitial nucleus of Cajal (InC),
 magnocellular part of the PCom,
 mlf (RI)
 supraoculomotor area
 descending fibers terminate in (PPRF),
 sparsely in the spinal cord at cervical levels
 superior colliculus
strong input
 frontal eye fields
 dentate nu.
PCom lead to an upward gaze paralysis often combined with
lid retraction
 PTOSIS

 Drooping of the eyelid (ptosis or blepharoptosis) can be

measured with the limbus or central light reflex used as
reference points.
 The usual position of the adult upper eyelid margin is 1.5
mm below the upper limbus or 3 to 4 mm above the light
reflex.
 The palpebral fissure and upper eyelid fold ( 5 to 7)are
measured in the primary position of gaze.
 Levator function :the amount of excursion of the upper eyelid
from maximal straight downgaze to maximal upgaze.(frontalis
muscle, overcomes the by pressing the thumb over the center
of the patient’s eyebrow while measuring).

 < 2 mm – no levator function

 < 4mm –poor

 5 to 7mm-fair

 >8mm-good

 10-12mm or more -normal

Etiologies

 Congenital
 supranuclear lesions
 lesions of the oculomotor complex
 oculosympathetic lesions
 NMJ
 diseases of the muscle
 local mechanical lid abnormalities
 Pseudoptosis
A unilateral ptosis may be associated with eye- lid retraction
on the opposite side due to Hering’s law of equal
innervation
 CONGENITAL PTOSIS

 Congenital ptosis usually is the result of abnormal

development of the levator ,coexist with superior rectus
muscle paresis (common embryologic tissue mass).
 With congenital ptosis the levator is fibrotic and
dystrophic, so that lid elevation in upgaze is poor (lack of
levator contraction), and the lid fails to follow the globe
in downgaze (inability of the muscle to relax).
 Levator function is thus poor (5 mm or less).
 NEUROGENIC CAUSES

Supranuclear ptosis may be unilateral or bilateral.

 Unilateral - usually due to a lesion of the opposite
cerebral hemisphere, especially ischemic lesions (e.g.,
middle cerebral artery infarction) ,tumor and
arteriovenous malformations .
Bilateral -unilateral or bilateral hemispheric disease

 The preponderance of right-sided lesions in cases of cerebral

ptosis suggests a dominance of the right hemisphere in lid

control.

 Large hemispheric infarcts may cause complete bilateral

ptosis that may be a premonitory sign of an impending

herniation
 acute right fronto-temporo-parietal lobe lesions all
associated with conjugate gaze deviation to the right .
(transient ptosis, implying intact hemisphere assumed motor
control)
Apraxia of eyelid (inability to open
voluntarily)

 Not have true ptosis but have difficulty in overcoming levator

inhibition.

 They must thrust their heads backward to attempt eyelid

opening or must open their lids manually.

 lesions of the right hemisphere or bilateral cerebral

hemispheric lesions ,also seen with diseases of the

extrapyramidal system.
 Bilateral ptosis associated with supranuclear downward
gaze paralysis, but with other ocular motor functions
relatively intact, has been described with midbrain
glioma.

Dorsal midbrain syndrome/perinauds

•Bilateral disturbance in vertical gaze
•Light -near dissociation
•Defective accommodation
•Lid retraction- colliers sign
The downward gaze paralysis was likely due to bilateral
riMLF involvement)

 The bilateral ptosis was due to the tumor destroying the

periaqueductal gray (i.e., the “supraoculomotor area”),
which is concerned with premotor control of the levator
motor neurons.
 Lesions of central caudate nucleus –B/L ptosis

 Ptosis may also occur with lesions of the oculomotor

nucleus, fascicle, or nerve and is often associated with

other signs of oculomotor dysfunction (e.g., mydriasis).

 oculosympathetic lesions (Horner syndrome)- associated

miosis.
Horner’s syndrome, sympathetic dysfunction produces ptosis,

miosis, and anhidrosis (1 to 3 mm)

The lower lid is frequently elevated 1 to 2 mm because of loss of

the action of the lower lid accessory retractor that holds the lid

down (inverse ptosis).

The resulting narrowing of the palpebral fissure causes apparent

enophthalmos.
 Cause of horner’s

brainstem lesions (especially of the lateral medulla), cluster

headache, internal carotid artery thrombosis or dissection,

cavernous sinus disease, apical lung tumors , neck trauma ,

an isolated manifestation of syringomyelia

Interruption of the sympathetic pathways between the

hypothalamus and the spinal cord (e.g., Wallenberg

syndrome) causes a first-order Horner’s syndrome.

• The second-order neuron lies in the ciliospinal center at

C8-T2 (e.g., syringomyelia, C8 root lesion) causes a second-

order Horner’s syndrome.

 Isolated, intermittent ptosis - the first sign of a posterior
carotid artery aneurysm
 In the Miller Fisher variant of Guillain–Barré syndrome,
unilateral or bilateral ptosis may occur.
 Intermittent ptosis with diplopia seen in Charcot– Marie–
Tooth disease
Mouth opening may be associated with ptosis (inverse
Marcus Gunn phenomenon) due to synkinesis between the
oculomotor and trigeminal nerves.

Ptosis may occur on the side of eye adduction (likely due to

paradoxical supranuclear levator inhibition) with Duane
syndrome .

Ptosis may also be psychogenic or functional in nature

 Diseases of NMJ

myasthenia gravis, Lambert–Eaton syndrome and

botulism.
 MG -Cogan “eyelid twitch sign” -asked to look up after
having kept the eyes directed downward for 20 to 30
seconds, the affected upper eyelid may twitch before
setting in a ptotic position.
 Ptosis, which may be temporarily abolished by sustained
upgaze, LEMS.
 Myopathies

 myotonic muscular dystrophy

 chronic progressive external ophthalmoplegia

 dermatomyositis

 diabetics Slowly progressive ptosis due to local

myopathy of the levator palpebrae or tarsalis muscles (or

both) by chronic local ischemia or hypoxia .

 APONEUROTIC PTOSIS

 Disinsertion of the levator tendon may occur with age, resulting in

unilateral or bilateral involutional ptosis in the elderly.

 The lid continues to move normally in upgaze and downgaze in

aponeurotic disinsertion (excursion of the eyelid from downgaze to

upgaze is usually 9 mm or more).
 Ptosis must be differentiated from dermatochalasis, which refers to

the stretched, redundant, baggy eyelid skin that occurs with age.
 MECHANICAL CAUSES
 levator tendon damage due to ocular surgery or thyroid eye disease.
 tumors or cysts of the conjunctiva
 infection (e.g., preseptal or orbital cellulitis)
 cicatricial scarring (e.g., posttraumatic, postsurgical, or postinflammatory),
 inflammation and edema (e.g., Graves’ disease),
 infiltration (e.g., amyloid, sarcoid, neoplastic, Waldenström macroglobulinemia),
 primary or metastatic tumors or orbital pseudotumor,
 contact lenses wear, contact lens migration,
 foreign body reaction, giant papillary conjunctivitis,
 disinsertion of the levator from excessive eyelid manipulation .
 PSEUDOPTOSIS

False ptosis (pseudoptosis) may occur due to

 mechanical impairment of upward eyelid movement (e.g., with orbital

tumor),
 orbital inflammation and eyelid swelling,

 an anophthalmic socket

 microphthalmia or phthisis bulbi,

 lid retraction in the opposite eye,

 on the side opposite a hypertropic eye (when the hypertropic eye fixes, the
opposite eye becomes hypotropic and demonstrates an apparent ptosis)
 Blows to the forehead, resulting in orbital roof fracture and

subfrontal epidural hemorrhage, may cause ptosis and

ipsilateral paralysis of globe elevation; in the context of an

ecchymotic lid, these findings indicate local damage to orbital

muscles rather than injury to the superior division of the third

nerve
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