1) Drooping of the eyelid, known as ptosis or blepharoptosis, can have many causes including congenital issues, neurological problems, diseases of the neuromuscular junction, myopathies, mechanical issues, and pseudoptosis. 2) Measurement of levator function helps localize the cause of ptosis to either problems with the levator muscle itself or supranuclear issues. 3) Common etiologies include congenital ptosis affecting the levator muscle, Horner's syndrome causing sympathetic dysfunction, myasthenia gravis impairing the neuromuscular junction, and aponeurotic disinsertion seen with aging.

1. PTOSIS
By Dr Sukanya M K
JR dept of general medicine

2. 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.

3. 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

4. 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.

5. 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.

6. 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).

8. 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).

9. 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.

10. 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

12. 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.

13. 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

14. strong input
 frontal eye fields
 dentate nu.
PCom lead to an upward gaze paralysis often
combined with lid retraction

15. 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.

17.  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

18. Etiologies
 Congenital
 supranuclear lesions
 lesions of the oculomotor complex
 oculosympathetic lesions
 NMJ
 diseases of the muscle
 local mechanical lid abnormalities
 Pseudoptosis

19. A unilateral ptosis may be associated with eye- lid
retraction on the opposite side due to Hering’s law of
equal innervation

20. 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).

21. 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 .

22. 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

23.  acute right fronto-temporo-parietal lobe lesions all
associated with conjugate gaze deviation to the
right .
(transient ptosis, implying intact hemisphere assumed
motor control)

24. 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.

25.  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

26. 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.

27. 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.

28. 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.

29. 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

30. 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.

32. 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

33. 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

34. 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.

35. 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

36. 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.

37. 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 .

38. 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)

39. 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

40. THANK YOU