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Eye Diseases > Eyelids

Ptosis

Evidence-based assessment and management of drooping upper eyelid. Comprehensive guide covering etiology, pathogenesis, classification, diagnosis, and treatment protocols for optometry practice.

NormalPtosisMRD 4mmMRD 1mmStrong ContractionReduced ContractionMRD-1: Margin Reflex Distance (corneal light reflex to upper lid margin)

Left: Normal upper lid with MRD-1 of 4 mm reflecting full levator function. Right: Ptotic upper lid with MRD-1 of 1 mm due to reduced levator contraction. The levator palpebrae superioris (CN III) is the primary elevator; compensatory frontalis overaction is common.

Ptosis (blepharoptosis) is the abnormal drooping of the upper eyelid below its normal position. It may be unilateral or bilateral, congenital or acquired, and can range from cosmetically minor to visually significant. When the upper lid covers the pupil, ptosis threatens vision — in children it can cause permanent amblyopia.

ParameterNormalPtosis
MRD-14–5 mm<4 mm
Asymmetry<2 mm>2 mm difference
Palpebral fissure8–11 mmReduced
Levator function≥15 mmVariable (<15 mm)
~1/1000
Prevalence
congenital
Aponeurotic
Most Common
acquired type
Age 0–7
Amblyopia Risk
deprivation
Urgent
Urgency
if acute onset

Congenital Ptosis

  • •Isolated myogenic: Levator muscle dystrophy/maldevelopment — most common cause; typically unilateral
  • •Birth trauma: Forceps delivery causing levator damage
  • •Neurogenic: CN III palsy (rare), Horner syndrome (also rare)
  • •Syndromic: Blepharophimosis syndrome, Marcus Gunn jaw-winking, CFEOM

Acquired Ptosis

  • •Aponeurotic/involutional: Dehiscence or disinsertion of levator aponeurosis; most common acquired type; associated with aging and CL wear
  • •Neurogenic: CN III palsy (aneurysm, DM), Horner syndrome (carotid dissection, Pancoast), myasthenia gravis
  • •Myogenic: CPEO, oculopharyngeal muscular dystrophy, myotonic dystrophy
  • •Mechanical: Lid tumours, dermatochalasis, chalazion, orbital mass
  • •Traumatic: Lid laceration, orbital fracture, haematoma

Singapore Context

  • •Myasthenia gravis: relatively higher prevalence among Chinese population with ocular MG subtype common
  • •Aponeurotic ptosis from blepharoplasty complications increasingly seen with popular double-eyelid surgery
  • •Diabetic third nerve palsy: pupil-sparing, painful ptosis in context of DM — blood glucose control critical

Normal Lid Elevation Mechanism

  • •Levator palpebrae superioris (LPS): primary elevator, innervated by CN III (superior division); provides 12–15 mm excursion
  • •Müller's muscle: smooth muscle innervated by sympathetic chain; contributes ~2 mm of lid elevation
  • •Aponeurosis: thin fibrous extension of levator that inserts into anterior surface of tarsus
  • •Normal MRD-1: 4–5 mm; palpebral fissure 8–11 mm

Congenital Ptosis

  • •Levator muscle maldevelopment or dysgenesis — fibrous/fatty tissue replaces normal muscle fibres
  • •Poor levator function: typically <5 mm — lid may elevate less than 5 mm on upgaze
  • •Characteristic finding: lid lag in downgaze (fibrous restriction prevents full lowering)
  • •Often presents as asymmetric eyelid crease height or complete absence of crease

Aponeurotic (Involutional) Ptosis

  • •Age-related stretching, dehiscence, or disinsertion of levator aponeurosis from tarsus
  • •Levator muscle itself remains normal — function preserved (≥12 mm)
  • •Results in high lid crease (>10 mm) and deep superior sulcus from aponeurosis displacement
  • •Accelerated by: chronic contact lens wear, eye rubbing, ocular surgery, prolonged eyelid oedema

Neurogenic Ptosis

  • •CN III palsy: complete ptosis (levator denervated); associated with EOM restriction and pupil involvement if compressive
  • •Horner syndrome: disrupted sympathetic supply to Müller's muscle; mild ptosis 1–2 mm + miosis + anhidrosis
  • •Myasthenia gravis: autoantibodies against acetylcholine receptors at NMJ; fatigable weakness; variable, worse with sustained upgaze

Myogenic Ptosis

  • •CPEO (chronic progressive external ophthalmoplegia): mitochondrial DNA mutation causing bilateral symmetric EOM and levator involvement
  • •Levator muscle itself is directly affected; poor to fair LF; progressive course
  • •Kearns-Sayre syndrome: CPEO + cardiac block + pigmentary retinopathy
  • •Oculopharyngeal muscular dystrophy (OPMD): PABPN1 gene mutation; onset 40–60 years; ptosis + dysphagia
By Severity (MRD-1)
GradeMRD-1Notes
Normal4–5 mmNo ptosis
Mild3 mm1–2 mm below normal; cosmetic concern
Moderate2 mmSuperior VF partially obscured
Severe≤1 mmVisual axis nearly covered; amblyopia risk in children
By Levator Function
GradeLF RangeImplication
Normal/Excellent≥15 mmNormal levator; aponeurotic cause likely
Good12–14 mmAponeurotic; levator advancement/resection
Fair5–11 mmLevator resection; moderate disease
Poor<5 mmCongenital/myogenic; frontalis sling required
EtiologyMechanismKey Feature
MyogenicMuscle dystrophy / CPEOPoor LF; bilateral; progressive
AponeuroticDehiscence/disinsertionGood LF; high crease; deep sulcus
NeurogenicCN III / Horner / MGVariable; systemic associations critical
MechanicalMass effect on lidTumour / chalazion / dermatochalasis
PseudoptosisApparent, not trueGlobe retraction, contralateral retraction, brow ptosis

Demographic

  • •Advanced age (involutional)
  • •Family history (blepharophimosis, OPMD)
  • •Asian ethnicity (ocular MG subtype more common in Singapore)

Medical Conditions

  • •Diabetes mellitus (CN III palsy)
  • •Hypertension / vascular disease (CN III)
  • •Autoimmune disease (MG, thyroid)
  • •Mitochondrial disorders (CPEO, Kearns-Sayre)

Lifestyle / Environmental

  • •Chronic eye rubbing (aponeurotic dehiscence)
  • •Long-term contact lens wear (hard/rigid lens esp.)
  • •Eyelid trauma or surgery (blepharoplasty)
  • •Prolonged topical steroid use (Horner, myopathy)

Ocular Factors

  • •High myopia (superior sulcus deformity)
  • •Blepharitis / chronic eyelid inflammation
  • •Eyelid or orbital tumours (mechanical ptosis)
  • •Prior intraocular surgery (post-surgical ptosis)

Primary Signs

  • •Reduced MRD-1 (<4 mm) — hallmark finding
  • •Narrowed palpebral fissure height
  • •Asymmetry >2 mm between eyes
  • •Superior visual field obstruction on confrontation / FDT

Signs by Ptosis Type

Aponeurotic: elevated lid crease >10 mm, deep superior sulcus, good levator function ≥12 mm, thin lid on eversion
Congenital: poor LF <5 mm, absent or low lid crease, lid lag in downgaze, chin-up head posture, strabismus / amblyopia in children
Neurogenic (CN III): complete ptosis, EOM restriction, pupil dilation if compressive aneurysm — requires urgent imaging
Neurogenic (Horner): mild ptosis 1–2 mm + miosis + anhidrosis; lower lid inverse ptosis; anisocoria worse in dim light
Neurogenic (MG): fatigable ptosis — worsening with sustained upgaze; Cogan lid twitch sign; variable throughout the day; orbicularis weakness
Myogenic (CPEO): bilateral symmetric ptosis, progressive EOM restriction, reduced Bell's phenomenon, frontalis overaction

Compensatory Mechanisms

  • •Frontalis overaction: brow elevation to raise ptotic lid; causes brow asymmetry and horizontal forehead wrinkles
  • •Chin-up posture: backward head tilt to bring visual axis below lid margin
  • •Hering's law effect: bilateral levator co-innervation means treating one eye may unmask ptosis in the other

Visual

  • •Superior visual field obstruction
  • •Difficulty reading (need to tilt head)
  • •Blurred vision if astigmatism induced
  • •Diplopia (if EOM involved, e.g. CN III)

Functional

  • •Heaviness / fatigue of eyelid
  • •Manual lid elevation with finger
  • •Difficulty looking upward
  • •Eye fatigue / asthenopia

Secondary Musculoskeletal

  • •Brow and forehead ache (frontalis overaction)
  • •Neck pain (chin-up posture)
  • •Headaches from sustained effort
  • •Difficulty showing facial expressions

Cosmetic / Psychosocial

  • •Visible asymmetry and "tired" appearance
  • •Social withdrawal / reduced confidence
  • •Parental concern in children
  • •Occupational impact (appearance-sensitive roles)

Clinical Note: Sudden-onset ptosis — particularly with associated orbital pain, diplopia, or systemic weakness — warrants urgent investigation to exclude life-threatening causes such as posterior communicating artery aneurysm or myasthenic crisis.

Ocular Complications

  • •Amblyopia (deprivation type): most serious in children under 8 years — urgent surgical correction required
  • •Astigmatism: mechanical pressure of ptotic lid on cornea induces with-the-rule astigmatism
  • •Exposure keratopathy: incomplete lid closure (lagophthalmos in downgaze — congenital); post-surgical risk
  • •Strabismus: coexisting EOM weakness (CN III, CPEO) or amblyopia causing suppression

Functional Complications

  • •Superior visual field defect: documented on Humphrey VF or Esterman binocular VF; relevant for driving
  • •Reduced quality of life: difficulty with sustained tasks, reading, screen use
  • •Increased fall risk: reduced superior VF in elderly patients with ptosis

Musculoskeletal Complications

  • •Cervical strain: chronic chin-up head posture; may cause neck and upper back pain
  • •Frontalis hypertrophy: chronic overuse of frontalis muscle causes brow elevation and forehead asymmetry
  • •Tension headaches: from sustained frontalis contraction

Psychological / Psychosocial

  • •Reduced self-esteem and body image
  • •Social anxiety and withdrawal
  • •Depression if longstanding cosmetic concern without treatment

Neurological

  • •Myasthenia gravis: autoimmune NMJ disorder; AChR antibodies; ocular MG may be first presentation; thymoma association
  • •CN III palsy: posterior communicating artery aneurysm (pupil-involving, painful) vs. microvascular DM/HTN (pupil-sparing)
  • •Horner syndrome: sympathetic chain lesion — hypothalamus to eye; carotid dissection, Pancoast, brainstem stroke
  • •Multiple sclerosis: demyelination affecting CN III nucleus; associated with internuclear ophthalmoplegia

Mitochondrial / Metabolic

  • •CPEO: bilateral symmetric ptosis + progressive EOM restriction; mitochondrial DNA deletion
  • •Kearns-Sayre syndrome: CPEO + cardiac conduction defect + pigmentary retinopathy — cardiac monitoring essential
  • •MELAS: mitochondrial encephalopathy, lactic acidosis, stroke-like episodes
  • •Diabetes mellitus: CN III palsy (pupil-sparing), facial nerve palsy

Muscular Dystrophies

  • •Oculopharyngeal MD (OPMD): PABPN1 GCG expansion; onset 40–60 years; ptosis + dysphagia + proximal limb weakness
  • •Myotonic dystrophy: CTG repeat; ptosis + facial weakness + cataracts + cardiac conduction; autosomal dominant
  • •Facioscapulohumeral MD: facial weakness including orbicularis; bilateral symmetric ptosis less common

Congenital Syndromes

  • •Blepharophimosis syndrome (BPES): autosomal dominant FOXL2 mutation; blepharophimosis + ptosis + epicanthus inversus + telecanthus
  • •Marcus Gunn jaw-winking: aberrant CN V / CN III synkinesis; lid elevates with jaw opening
  • •CFEOM (congenital fibrosis of EOMs): KIF21A mutation; ptosis + EOM restriction from birth

Singapore Referral Pathways

  • •Myasthenia gravis: Refer to neurology (NNI) for AChR antibody measurement, CT chest (thymoma), EMG, tensilon test
  • •Acute CN III palsy: Refer to ED for urgent MRI / CT angiography to exclude posterior communicating artery aneurysm
  • •Pediatric amblyopia: Urgent referral to pediatric ophthalmology (SNEC / KKH); do not delay for cosmetic scheduling
  • •Mitochondrial disease: Refer to genetics / neurology; cardiac referral for Kearns-Sayre (conduction block risk)

Clinical History

  • •Onset and duration (congenital vs. acquired; acute vs. chronic)
  • •Variability: worse morning vs. evening (MG worse evening); worse with fatigue
  • •Laterality (unilateral vs. bilateral) and symmetry
  • •Associated symptoms: diplopia, pain, dysphagia, limb weakness, sweating changes
  • •Medical history: DM, HTN, autoimmune, cancer, prior surgery
  • •Medications: topical/systemic steroids, alpha-blockers (floppy iris syndrome)
  • •Family history: blepharophimosis, OPMD, congenital ptosis

Clinical Examination — Measurements

  • •MRD-1: corneal light reflex to upper lid margin; normal 4–5 mm; <4 mm = ptosis
  • •MRD-2: corneal light reflex to lower lid margin; normal 5 mm; check for inverse ptosis
  • •Palpebral fissure height: normal 8–11 mm; measure both eyes and compare
  • •Levator function (LF): eyelid excursion from maximum downgaze to upgaze with frontalis blocked; <5 mm = poor; ≥12 mm = good
  • •Lid crease height: normal 6–8 mm women, 5–7 mm men; elevated >10 mm = aponeurotic

Special Tests

  • •Phenylephrine 2.5% test: instil 1 drop; recheck MRD-1 at 5 min; >1.5 mm lift predicts Müller's muscle resection candidate — performed by oculoplastic surgeons; not within Singapore optometric scope (no prescribing rights)
  • •Ice pack test: apply ice pack over closed lids for 2 minutes; improvement in MRD-1 ≥2 mm suggests MG (sensitivity ~80%)
  • •60-second upgaze fatigue test: maintain sustained upgaze; progressive ptosis = positive fatigability sign for MG
  • •Cogan lid twitch sign: after returning from sustained downgaze to primary position, observe transient upward overshoot of upper lid — classic MG sign
  • •Hering's test: manually elevate more ptotic lid — if fellow lid drops, bilateral ptosis is present (caution pre-surgically)

Associated Examination Findings

  • •Extraocular motility (CN III, CPEO, MG — EOM restriction)
  • •Pupil examination: dilation (CN III compressive), miosis (Horner), normal (MG, aponeurotic)
  • •Bell's phenomenon: reflex upgaze on attempts to close eye; assesses risk of exposure keratopathy post-surgery
  • •Orbicularis strength: ask patient to squeeze eyes shut firmly; weakness suggests MG or CPEO
  • •Corneal sensation (reduced in herpes) and corneal integrity (exposure changes)

Ancillary Testing

  • •Visual field testing (Humphrey / Esterman) to document superior VF defect and functional impact
  • •Clinical photography (standardised): document baseline MRD-1, crease height, head posture
  • •Refraction and corrected VA: ptosis-induced astigmatism; amblyopia detection in children
  • •Amblyopia screening: crowded optotype VA in children; cycloplegic refraction if amblyopia suspected

Laboratory & Imaging (Specialist Level)

  • •AChR antibodies, anti-MuSK antibodies: MG confirmation
  • •MRI brain/orbits: CN III pathway, orbital mass, brainstem lesion
  • •CT angiography / MR angiography: posterior communicating artery aneurysm (acute CN III with dilated pupil)
  • •Thyroid function (TFT, TSH, Free T4): thyroid eye disease if lid retraction suspected
  • •Mitochondrial DNA testing, muscle biopsy: CPEO, Kearns-Sayre

Red Flags — Urgent Referral Required

  • •Acute ptosis + EOM restriction + dilated pupil = posterior communicating artery aneurysm until proven otherwise → ED immediately
  • •Progressive ptosis + generalised weakness + dysphagia = MG crisis → neurology urgent
  • •Pediatric ptosis covering visual axis or causing abnormal head posture = amblyopia risk → pediatric ophthalmology urgent
  • •Horner syndrome in child = neuroblastoma / NF1 until excluded → pediatric oncology / radiology
  • •Severe headache / neck pain + acute ptosis = carotid dissection / subarachnoid haemorrhage → ED
SeverityMRD-1LFPreferred Surgical Approach
Mild>2 mmGood–excellent ≥8 mmLevator advancement or Müller's resection (if phenylephr. positive)
Moderate1–2 mmFair 4–7 mmLevator resection (larger amount)
Severe≤1 mmPoor <4 mmFrontalis sling (autogenous fascia lata or synthetic)

Singapore Scope Note

Singapore-registered optometrists can identify, classify, and document ptosis, but do not have prescribing rights and cannot administer the phenylephrine 2.5% test. Surgical correction is oculoplastic surgery scope — refer to SNEC or restructured hospital oculoplastics. Children with ptosis threatening the visual axis should be referred urgently. Acute neurological ptosis (CN III, Horner's, MG crisis) requires immediate medical referral.

Management Principles

  • •Prevent amblyopia in children — primary priority; reduce anisometropia with glasses; patch if indicated
  • •Restore functional lid position — eliminate superior VF defect, allow normal visual axis
  • •Cosmetic symmetry — achieve bilateral eyelid symmetry within 0.5–1 mm
  • •Treat underlying systemic condition (MG, CN III, Horner's) — ptosis often improves with systemic treatment

Non-Surgical Management

  • •Observation: mild ptosis without functional impact; monitor 3–6 monthly for progression
  • •Medical — MG: pyridostigmine (AChE inhibitor); immunosuppressants (prednisolone, azathioprine); thymectomy if thymoma
  • •Medical — CN III (microvascular): optimise DM and HTN; 50–70% spontaneous recovery in 3–6 months; defer surgery until stable
  • •Medical — Horner's syndrome: phenylephrine 2.5% drops (temporary sympathomimetic lid elevation); treat underlying cause
  • •Ptosis crutch spectacles: wire frame attachment to spectacle lens physically supports lid; useful in poor surgical candidates or temporary ptosis
  • •Amblyopia management: refractive correction (glasses/CLs); occlusion therapy (patching) if VA difference; cyclopentolate or atropine penalisation

Surgical Management

Performed by oculoplastic surgeons. Optometrists refer and co-manage pre/post-operatively.

Indications

  • •Visual axis obstruction (any age, especially children <8 years)
  • •Documented superior visual field defect affecting function
  • •Functional impairment (driving, work, reading)
  • •Chin-up head posture causing cervical spine strain
  • •Cosmetic concern with significant psychosocial impact

Surgical Techniques

  • •Levator advancement/resection: for aponeurotic or moderate myogenic ptosis with good LF ≥8 mm; most common technique
  • •Müller's muscle-conjunctival resection (MMCR): for mild ptosis + positive phenylephrine test; predictable 2–3 mm elevation; posterior approach
  • •Frontalis sling: for severe ptosis with poor LF <4 mm; uses autogenous fascia lata or synthetic material (silicone, Mersilene); suspends tarsal plate from frontalis
  • •Whitnall's sling / levator lengthening: for Marcus Gunn jaw-winking after levator extirpation; or myogenic ptosis with moderate LF

Surgical Timing Considerations

  • •Children: urgent if visual axis covered; otherwise defer elective surgery to 3–5 years (enflurane tolerance, fascia lata harvest)
  • •Bilateral ptosis: stage surgically or operate both sides simultaneously; beware Hering's law effect
  • •Dry eye: assess pre-operatively; relative contraindication if severe; lubricants mandatory post-op
  • •Goal: MRD-1 of 3.5–4 mm; symmetry within 1 mm; no lagophthalmos

Post-Operative Care

  • •Lubricating ointment 2–4 weeks (Lacrilube / Genteal Gel); antibiotic drops for 1 week
  • •Cold compresses for first 48 hours to reduce oedema
  • •Activity restriction: avoid strenuous exercise, bending, heavy lifting for 2 weeks
  • •Monitor for: overcorrection (lagophthalmos, exposure keratopathy), undercorrection, infection, haematoma
  • •Follow-up: 1 week, 1 month, 3 months — longer if revision anticipated

Optometrist's Role

  • •Identify, measure (MRD-1, LF, crease height) and document ptosis with standardised photography
  • •Visual field testing to document functional superior VF defect (Humphrey / Esterman)
  • •Amblyopia screening: VA, refraction, ocular alignment — especially in children
  • •Refer to oculoplastics for surgical evaluation; provide complete referral letter with all measurements
  • •Refer urgently to neurology (NNI) if MG suspected; to ED if acute neurological ptosis
  • •Co-manage post-operative care: dry eye management, refraction updates, monitor for complications
Ptosis TypeFirst-Line ManagementReferral
Aponeurotic (mild)Observe; refer if functional or cosmetic concernOculoplastics (elective)
Aponeurotic (mod-severe)Levator advancement; Müller's resection if phenylephr posOculoplastics (semi-urgent)
Congenital (visual axis)Frontalis sling or levator resection; amblyopia RxPediatric ophthalmology (urgent)
MGPyridostigmine; immunosuppression; thymectomy if thymomaNeurology NNI (urgent)
CN III palsyUrgent imaging; treat underlying cause; defer surgery 6+ monthsED / neurosurgery (emergency)
Horner's syndromeNeuroimaging (carotid, chest); phenylephrine symptomaticNeurology / vascular (urgent)
CPEO / MyogenicFrontalis sling; lubricants; cardiology if Kearns-SayreOculoplastics + genetics

Urgent Referral Criteria

  • •Acute ptosis + pupil dilation + EOM palsy → ED immediately (aneurysm excluded first)
  • •Pediatric ptosis obstructing visual axis → pediatric ophthalmology within days
  • •Suspected MG with systemic features → neurology within 1–2 weeks
  • •Horner's in child → rule out neuroblastoma — pediatric radiology urgently

Prognosis for ptosis is generally good with appropriate management. Surgical correction achieves high success rates for functional and cosmetic improvement. Long-term visual outcomes depend on timely intervention to prevent amblyopia in children and adequate treatment of underlying conditions.

Congenital Ptosis

  • •Surgical success: 80–90% achieve good symmetry with appropriate technique
  • •Visual prognosis: excellent if treated before amblyopia develops (age <7 years)
  • •Recurrence: 10–20% may require revision surgery as child grows

Aponeurotic Ptosis

  • •>90% surgical success with levator advancement/resection
  • •Recurrence: 5–10% due to continued aponeurotic dehiscence with aging
  • •Cosmetic outcome: generally excellent with high patient satisfaction

Neurogenic — CN III (Microvascular)

  • •50–70% spontaneous recovery within 3–6 months
  • •Defer definitive surgery until ptosis stable for ≥6 months
  • •Compressive CN III (aneurysm): depends on neurosurgical management

Neurogenic — MG

  • •Variable; depends on medical control; may not require surgery if well-controlled
  • •Ocular MG: ~50% progress to generalised MG within 2 years without treatment
  • •Early immunosuppression reduces generalisation risk

Neurogenic — Horner’s Syndrome

  • •Mild ptosis 1–2 mm; often does not require surgical intervention
  • •Prognosis depends on underlying cause (carotid dissection, Pancoast, central)

Myogenic (CPEO / Muscular Dystrophy)

  • •Progressive condition: ptosis worsens over time despite surgery
  • •Frontalis sling provides temporary improvement; higher exposure keratopathy risk
  • •Long-term prognosis depends on systemic disease progression

Surgical Outcome Rates

  • •Undercorrection: 10–15%; may require revision
  • •Overcorrection: 5–10%; risk of exposure keratopathy; may improve with time
  • •Asymmetry: 10–20%; often improves in first 6 months as oedema resolves
  • •Dry eye post-op: common early; chronic in 5–10%
  • •Infection: rare (<1%) with proper post-operative care

Several conditions may mimic ptosis or present with a narrowed palpebral fissure. Careful examination distinguishes true ptosis from pseudoptosis:

1. Dermatochalasis

  • •Excess upper eyelid skin overhanging the lid margin
  • •Normal MRD-1 and eyelid margin position; skin redundancy only
  • •Manually lifting redundant skin reveals normal lid position

2. Brow Ptosis

  • •Descended eyebrow position appears to lower upper eyelid
  • •Normal MRD-1 when brow is manually elevated
  • •Management: brow lift, not ptosis surgery

3. Contralateral Eyelid Retraction

  • •Elevated eyelid on one side makes normal contralateral lid appear ptotic
  • •"Ptotic" eye has normal MRD-1 (4–5 mm); contralateral eye has elevated MRD-1 (>6 mm)
  • •Common causes: thyroid eye disease, prior surgery, trauma

4. Enophthalmos

  • •Posterior displacement of globe within orbit
  • •Narrowed palpebral fissure due to globe retraction; both upper and lower lids affected
  • •Causes: orbital fracture, orbital fat atrophy, silent sinus syndrome

5. Hypotropia

  • •Vertical strabismus with downward eye deviation
  • •Normal eyelid position relative to eye; corneal light reflex displaced inferiorly
  • •Assess with cover test, Hirschberg test, extraocular motility

6. Hemifacial Spasm

  • •Involuntary tonic contraction of orbicularis oculi causing apparent narrowed fissure
  • •Intermittent; eyelid position normal between spasms
  • •Unilateral; may involve lower face; no true ptosis
ConditionMRD-1Eyelid MarginKey Differentiator
True Ptosis<4 mmLow positionReduced LF or aponeurotic issue
DermatochalasisNormal 4–5 mmNormal positionExcess skin; improves with manual lift
Brow PtosisNormal (brow lifted)Normal / pseudo-lowLow brow; improves with brow elevation
Lid Retraction (fellow)Normal 4–5 mmNormal positionContralateral MRD-1 >6 mm
EnophthalmosVariableBoth lids affectedGlobe sunken; narrow fissure
HypotropiaNormalNormal to lidEye deviated down; cover test positive

Always measure BOTH MRD-1 AND levator function. MRD-1 quantifies ptosis severity; levator function determines the surgical approach. A patient with MRD-1 of 1 mm but levator function of 12 mm gets levator resection — very different from the same MRD-1 with only 3 mm levator function, which requires a frontalis sling.

Horner's syndrome triad: ptosis + miosis + anhidrosis. This combination warrants urgent MRI of the entire sympathetic chain from hypothalamus to apex — carotid dissection and apical lung lesion (Pancoast tumour) must be excluded.

Phenylephrine 2.5% test predicts Müller's muscle resection response — >1.5 mm MRD-1 improvement indicates a good surgical candidate. This test is performed by oculoplastic surgeons. Singapore optometrists do not have prescribing rights and should not administer phenylephrine — include accurate pre-referral MRD-1 measurements to assist surgical planning.

Sustained upgaze fatigue test for myasthenia: ask the patient to maintain upgaze for 60 seconds — progressive ptosis during this period is a positive fatigability sign. Follow immediately with the ice pack test for confirmation (sensitivity ~80%).

Amblyopia risk in children under 8 — ptosis covering the visual axis must be repaired without delay. Do not postpone surgery for cosmetic scheduling reasons if the visual axis is obstructed; each week of deprivation risks irreversible amblyopia.

Singapore Optometry Scope Note: Singapore optometrists do not have prescribing rights and cannot perform the phenylephrine 2.5% test. Optometric scope covers identification, measurement (MRD-1, levator function, crease height), documentation, visual field testing, and referral. Urgent referral criteria: Horner's syndrome, suspected 3rd nerve palsy, acute onset ptosis, myasthenia features. All referral letters should include: MRD-1, levator function, and pupil status.

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