Plus–Minus Lid Syndrome

Plus–minus lid syndrome is a rare eye–lid problem where one upper eyelid droops (ptosis) while the other upper eyelid pulls up too far (retraction). Both changes happen at the same time. The droopy lid is the “minus,” and the pulled-up lid is the “plus.” This pattern usually points to a tiny injury in the upper midbrain (the area deep in the brain that helps control eyelid opening and some eye movements). Doctors first described this pattern in the early 1990s. In many patients, the cause is a small stroke in the midbrain. In a few others, the same look can be mimicked by diseases of the eyelid muscles or nerves (for example myasthenia gravis), and that is called a “pseudo” plus–minus lid picture. PubMedBioMed Central

Plus-minus lid syndrome means one upper eyelid droops (ptosis) while the other upper eyelid pulls up higher than normal (eyelid retraction). The “minus” is the droopy lid; the “plus” is the lifted lid. Most reported cases come from a small stroke or other lesion in the midbrain (the part of the brainstem behind the eyes) that involves the oculomotor (third cranial) nerve pathway. In many patients, PMLS accompanies other midbrain signs such as ataxia (clumsiness), upgaze problems, or pupil abnormalities. EyeWikiPMC+1

Anatomy

You have a single levator control center in the midbrain called the central caudal nucleus. This center lifts both upper lids through the levator palpebrae superioris muscle. Nearby, a small cluster of cells around the posterior commissure normally sends “brake” signals down to the levator center to prevent excessive lid elevation. If a lesion damages this brake area, the levator can be over-active, and the lid retracts (pulls up). If that same lesion also injures the oculomotor (third) nerve fascicle on one side, the levator on that side becomes weak, and the lid droops. The result is ptosis on the injured-nerve side and retraction on the opposite side—the classic plus–minus picture. BioMed CentralPMC

A closely related sign is Collier’s sign, which is bilateral lid retraction from injury around the posterior commissure (often seen with Parinaud/dorsal midbrain syndrome). Plus–minus lid syndrome is like Collier’s sign plus a same-side third-nerve problem that creates ptosis and masks retraction on that side. PMCNCBI

Types

1. True Plus–Minus Lid Syndrome (neurogenic/dorsal midbrain type).
   This is the classic brain-based form. It happens with unilateral midbrain lesions that both disinhibit the levator (causing contralateral lid retraction) and injure the nearby third-nerve fascicle (causing ipsilateral ptosis). Many patients also show other dorsal midbrain signs (for example, upgaze trouble, convergence-retraction nystagmus, pupillary light-near changes) or ataxia depending on which fibers are involved. BioMed CentralPubMedEyeWiki

2. Pseudo Plus–Minus Lid Syndrome (mimickers).
   Some disorders outside the brain can imitate the appearance. Ocular myasthenia gravis may cause a droopy lid on one side, while compensatory innervation and Hering’s law can make the other lid look retracted; in these cases, lifting the droopy lid often makes the “retracted” lid fall, which gives away the mimic. Thyroid eye disease or orbital inflammatory/myositis can also pull a lid up on one side while the other lid droops from a different cause. Doctors call this a pseudo form because the midbrain brake-and-levator pathway is intact. PubMedSpringerLinkNCBI

Grading

• Type 1: True neurogenic plus–minus lid syndrome.
  A unilateral midbrain lesion disinhibits the levator (retraction opposite side) and damages the third-nerve fascicle (ptosis same side). Often linked to midbrain infarction (small stroke). BioMed Central

• Type 2: True plus–minus lid with associated brainstem syndromes.
  The eyelid pattern can come with ataxia or features of Claude, Benedikt, Weber, Nothnagel, or Wernekink commissure syndromes, depending on which nearby tracts are hit. PMC

• Type 3: Pseudo plus–minus lid due to neuromuscular disease.
  Ocular myasthenia gravis produces fluctuating ptosis; the other lid may look retracted from compensatory drive. The key bedside clue: when you lift the droopy lid, the other lid relaxes. PubMed

• Type 4: Pseudo plus–minus lid due to orbital or thyroid disease.
  Thyroid eye disease is the most common cause of upper lid retraction in general; orbital myositis or other orbital problems can also pull the lid up. If the other eye has ptosis from a different reason, the face may mimic the plus–minus pattern. NCBIPMC

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Causes

Brain/brainstem (most common “true” cases):

1. Small midbrain ischemic stroke (paramedian mesencephalic infarct). This is the classic cause. BioMed Central

2. Thalamo-mesencephalic infarct (stroke at the junction of thalamus and midbrain). PubMed

3. Midbrain hemorrhage (bleed affecting posterior commissure and third-nerve fascicle). (Inference based on reports of nuclear III syndromes in midbrain hemorrhage.) PubMed

4. Midbrain tumors (e.g., glioma) compressing the posterior commissure and third-nerve fascicle. Taylor & Francis Online

5. Pineal region tumors (e.g., germinoma) causing dorsal midbrain/Parinaud features with lid retraction; if fascicle is involved, the opposite lid droops. PMC

6. Cavernous malformations of the midbrain (vascular malformation that can bleed or compress local tracts). (Mechanistic plausibility and brainstem case spectrum.) Mayo Clinic Proceedings

7. Demyelinating disease (e.g., multiple sclerosis) affecting the dorsal midbrain pathways. (Collier/Parinaud physiology supports this when lesions hit the posterior commissure area.) PubMed

8. Inflammatory or infectious midbrain lesions (e.g., neurocysticercosis), which can inflame or compress the oculomotor nucleus/fascicle region. PMC

9. Vascular narrowing or “top of the basilar” issues producing combined dorsal midbrain signs with eyelid asymmetry. ScienceDirect

10. Post-traumatic midbrain injury causing focal damage to posterior commissure or III fascicle (a recognized cause of dorsal midbrain signs). Wikipedia

Mimickers and mixed mechanisms (“pseudo” or dual-cause pictures):

1. Ocular myasthenia gravis with compensatory lid retraction on the fellow eye. PubMed
2. Thyroid eye disease (levator/Müller over-action, inferior rectus restriction, or fibrosis) leading to lid retraction, paired with unrelated ptosis in the other eye. NCBI
3. Orbital myositis / idiopathic orbital inflammation pulling one lid up, paired with ptosis from another cause. PMC
4. Aberrant oculomotor regeneration after third-nerve palsy, altering levator control and lid level asymmetrically. EyeWiki
5. Iatrogenic eyelid change (e.g., botulinum toxin, surgery, contact lens effect) on one side, with opposite-eye ptosis from another reason. EyeWiki
6. Facial nerve palsy with compensatory levator overaction affecting lid position balance (listed in clinical differentials). EyeWiki
7. Congenital ptosis with contralateral retraction from compensatory drive (Hering’s law) creating a look-alike pattern. Ento Key
8. Pineal/tectal inflammatory lesions or encephalitis involving posterior commissure, producing retraction that can pair with ptosis from another source. Wikipedia
9. Paraneoplastic brainstem involvement that disrupts midbrain lid pathways. (Paraneoplastic brainstem ophthalmoplegia is reported.) PubMed
10. Unknown/undetermined cases with normal imaging (rare). Some case reports document the sign clinically without a clear lesion on early scans. BioMed Central

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Symptoms and signs

1. Droopy upper eyelid (ptosis) on one side. The lid sits low and may cover part of the pupil. PubMed

2. Over-elevated upper lid (retraction) on the other side. You can see a rim of white above the iris. Wikipedia

3. Double vision (diplopia). Often from partial third-nerve palsy or other eye movement imbalance. BioMed Central

4. Vertical gaze problems. Trouble looking up or down, depending on which midbrain fibers are affected. NCBI

5. Convergence-retraction nystagmus. Eyes jerk backwards during attempted upgaze (a dorsal midbrain sign). NCBI

6. Pupil light–near changes. Pupils may react poorly to light but better to near (part of dorsal midbrain syndrome). NCBI

7. Eyelid fatigue or fluctuation (especially with myasthenia mimics). Symptoms can change during the day. AAO

8. Imbalance or clumsiness (ataxia) when nearby cerebellar pathways (e.g., superior cerebellar peduncle) are involved. BioMed Central

9. Apathy or slowed thinking in some midbrain stroke cases. (Reported rarely alongside plus–minus lid with ataxia.) PMC

10. Headache, nausea, or vomiting when there is pineal/tectal pressure or acute brainstem events. PMC

11. Eyelid twitching or abnormal movements if there is aberrant reinnervation or associated ocular motor instability. EyeWiki

12. Eye pain or tenderness if the problem is orbital myositis rather than brainstem. PMC

13. Vision blur during episodes of diplopia or when the droopy lid covers the pupil. (General neuro-ophthalmic effect.) BioMed Central

14. Photophobia or glare in the eye with lid retraction because the eye is more exposed. (Physiologic consequence of retraction.) PMC

15. Neck/eye strain from head postures used to compensate for double vision (common in ocular motility disorders). (General principle supported by motility literature.)

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Diagnostic tests

A) Physical examination (bedside viewing and measurements)

1. Direct eyelid observation (primary position). The doctor looks for one droopy lid and one retracted lid at rest—this is the core sign. PubMed

2. Margin–reflex distance (MRD1) and levator function measurement. Simple ruler/penlight checks quantify how high the lid sits and how strongly the levator moves. This helps track change over time. (Standard oculoplastic exam practice.)

3. Full eye-movement exam (ductions/versions). The goal is to find any third-nerve weakness (down-and-out position, limited adduction/elevation) and any vertical gaze changes suggesting dorsal midbrain involvement. BioMed CentralNCBI

4. Pupil and near responses. Poor light response with better near response supports dorsal midbrain involvement in true cases (part of the Parinaud spectrum). NCBI

5. Look for Collier’s sign and convergence-retraction nystagmus. These are sister signs of posterior commissure injury and help confirm a central cause. NCBI

B) Manual/bedside maneuvers (simple in-office tests)

6. Passive lift of the ptotic lid (“Hering’s law” check).
   In true plus–minus lid, lifting the droopy lid does not make the “retracted” opposite lid fall. In pseudo cases (like myasthenia), the opposite lid often drops when you lift the ptotic lid. This one-minute bedside maneuver helps separate true from mimic. EyeWiki

7. Fatigue/sustained upgaze test.
   Holding upgaze for 1–2 minutes can worsen ptosis in myasthenia but not in pure brainstem lesions; a quick clue toward a pseudo source. AAO

8. Ice-pack test (for myasthenia mimic).
   Cooling the droopy lid for 2–5 minutes can improve ptosis in myasthenia by boosting neuromuscular transmission; improvement supports the pseudo diagnosis. Lippincott Journals

9. Sleep/rest test (for myasthenia mimic).
   Short rest may improve myasthenic ptosis; helpful when equipment is limited. EyeWiki

C) Laboratory and pathological tests (tailored to likely cause)

10. Stroke risk labs (e.g., fasting lipids, HbA1c/fasting glucose, CBC, coagulation). These look for vascular risk in suspected midbrain infarct (the common “true” cause). (Routine stroke work-up supported by vascular neurology practice and case reports.) BioMed Central

11. Thyroid function tests (TSH, free T4/T3) and thyroid antibodies (TRAb/TSI, TPO) when thyroid eye disease is suspected in a pseudo pattern. NCBI

12. Autoantibodies for myasthenia gravis (AChR and MuSK). A positive result supports a pseudo mechanism. (Standard MG diagnostics.) AAO

13. Inflammatory markers (ESR/CRP) and autoimmune screens when an inflammatory orbital or brainstem process is considered. (General practice supported by orbital inflammation literature.) EyeWiki

14. Infectious testing (e.g., TB, cysticercosis serology as regionally appropriate) if imaging suggests infectious midbrain/orbital disease. Lippincott Journals

D) Electrodiagnostic tests (when myasthenia is on the table)

15. Single-fiber EMG (SFEMG) of orbicularis oculi or frontalis. This is the most sensitive test for ocular myasthenia (often 85–100% sensitivity in studies). A normal result does not prove it is not MG, but a positive test strongly supports a pseudo mechanism. PMC

16. Repetitive nerve stimulation (RNS). Helpful in generalized MG but less sensitive in purely ocular MG; still useful context if positive. AAO

17. Ocular VEMP-based fatigability paradigms (roVEMP) in specialty centers as a noninvasive way to detect decrement in extraocular pathways. Frontiers

18. Standard nerve conduction/EMG when broader neuromuscular disease is suspected; supports the overall differential but is usually adjunctive here. (General MG work-up principles.) AANEM

E) Imaging tests (core for the “true” brain form and for orbital mimics)

19. MRI brain with DWI/FLAIR focused on the midbrain (thin sections through the posterior commissure and oculomotor fascicles). This is the key study to confirm a true midbrain lesion (stroke, demyelination, tumor, cavernous malformation). Early scans can be negative after very small brainstem strokes, so clinical exam matters. BioMed Central

20. MRA/CTA of the posterior circulation to look for artery disease supplying the midbrain; add orbital MRI/CT if thyroid eye disease or orbital myositis is suspected in a pseudo pattern. EyeWikiPMC

Non-pharmacological treatments (therapies & practical measures)

These support comfort, safety, and vision while the underlying condition is treated or recovers.

1. Eye patching for double vision
   Purpose: immediate relief of diplopia.
   Mechanism: occludes one eye so the brain receives a single image. Often used short-term. nanosweb.org

2. Temporary Fresnel prisms on glasses
   Purpose: align double images during recovery.
   Mechanism: shifts light to reduce diplopia without surgery. Review of Optometry

3. Lubricating drops/ointment and preservative-free tears
   Purpose: protect the cornea if the retracted lid exposes the eye.
   Mechanism: adds a tear film layer; ointment protects overnight. vagelos.columbia.edu

4. Nighttime eyelid taping
   Purpose: keep the eye closed during sleep to prevent exposure keratopathy.
   Mechanism: gentle tape or shields maintain closure. EyeWikiAAO

5. Moisture-chamber goggles/sleep masks
   Purpose: trap humidity and reduce evaporation.
   Mechanism: creates a humid micro-environment around the eye. EyeRoundsAAO

6. Humidifier use indoors
   Purpose: lessen dryness from environmental factors.
   Mechanism: raises ambient humidity to slow tear evaporation. AAO

7. Blink training and screen-break habits
   Purpose: counter reduced blink when concentrating.
   Mechanism: the “20-20-20” habit and conscious complete blinks protect the surface. (Supportive best-practice.)

8. Warm compresses & lid hygiene (if meibomian gland dysfunction contributes to dryness)
   Purpose: improve oil layer of tears.
   Mechanism: heat softens oils; gentle cleaning reduces inflammation. (Supportive best-practice.)

9. Protective sunglasses outdoors
   Purpose: reduce wind/UV and reflex tearing.
   Mechanism: physical barrier to evaporation. (Supportive best-practice.)

10. Occupational therapy for reading and task adaptation
    Purpose: adjust lighting, font size, and work distance during recovery.
    Mechanism: practical compensations reduce eye strain. (Supportive best-practice.)

11. Physical therapy & balance training (if ataxia present)
    Purpose: reduce falls and improve gait after midbrain events.
    Mechanism: task-specific balance/strength exercises. (Stroke rehab standard of care.)

12. Driving pause and vision-safety counseling
    Purpose: legal and safety compliance until diplopia/lid issues stabilize.
    Mechanism: avoids high-risk activities temporarily. (Safety best-practice.)

13. Sleep posture: head-of-bed elevation
    Purpose: may reduce eyelid swelling and morning exposure symptoms.
    Mechanism: lowers venous congestion. (Supportive best-practice.)

14. Allergy control measures if surface irritation worsens exposure
    Purpose: reduce itch/rub cycle.
    Mechanism: avoidance and non-sedating strategies to minimize ocular rubbing. (Supportive best-practice.)

15. Punctal occlusion (office procedure; non-drug) when dryness persists
    Purpose: keep natural tears on the eye longer.
    Mechanism: tiny plugs block tear drainage. WebEyeWikipedia

16. Temporary botulinum-induced ptosis (selected cases)
    Purpose: deliberately lower a retracted lid short-term to protect cornea.
    Mechanism: weakens levator for ~3 months; used judiciously. EyeWiki

17. Tarsorrhaphy (temporary suturing the eyelids partly closed)
    Purpose: protect the cornea when exposure is severe or persistent.
    Mechanism: narrows the palpebral opening. EyeWiki

18. Careful follow-up with neuro-ophthalmology
    Purpose: track recovery and spot red flags.
    Mechanism: serial measurements guide prism or surgical timing. (Standard care.)

19. Stroke-rehab lifestyle bundle
    Purpose: accelerate neurologic recovery.
    Mechanism: graded aerobic activity + task-specific practice under therapy supervision. (Guideline-concordant.) AHA Journals

20. Education on “pseudo-plus-minus”
    Purpose: prevents misinterpretation when droop on one side causes apparent over-elevation on the other.
    Mechanism: explains Hering’s law; avoids unnecessary interventions. PMC

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Drug treatments

Important: The medicines below treat causes that commonly produce the plus–minus lid pattern. Doses are typical adult references—must be individualized and confirmed by the treating clinician.

1. Aspirin (81–325 mg daily) for secondary stroke prevention
   Purpose/Mechanism: antiplatelet to reduce recurrent ischemic events after non-cardioembolic stroke/TIA. AHA Journals

2. Clopidogrel (75 mg daily) as an alternative antiplatelet
   Purpose/Mechanism: P2Y12 blockade; option if aspirin-intolerant or per guideline scenarios. AHA Journals

3. Short-course dual antiplatelet therapy (DAPT) in specific high-risk minor stroke/TIA windows (e.g., aspirin + clopidogrel for 21–90 days per guideline contexts)
   Purpose/Mechanism: transiently lowers early recurrence risk; not for long-term use. AHA Journals

4. High-intensity statin (e.g., atorvastatin 40–80 mg nightly)**/**lipid therapy per guideline
   Purpose/Mechanism: plaque stabilization and LDL lowering; additional agents (e.g., icosapent ethyl in selected patients with elevated triglycerides) based on lipid profile. professional.heart.org

5. IV thrombolysis (alteplase/tenecteplase) in eligible acute ischemic stroke within time window
   Purpose/Mechanism: clot dissolution; emergency-department protocol only. www.heart.org

6. Blood pressure, diabetes, and AFib management (evidence-based antihypertensives, glucose-lowering therapies, and anticoagulation for AFib when indicated)
   Purpose/Mechanism: reduces recurrent stroke risk; exact regimen is individualized. AHA Journals

7. High-dose corticosteroids for inflammatory demyelinating relapses (e.g., IV methylprednisolone up to 1 g daily for 3–5 days)
   Purpose/Mechanism: speeds relapse recovery in MS/optic neuritis–spectrum presentations; taper per clinician. PMCPractical Neurology

8. Therapy for ocular myasthenia gravis, when PMLS-like signs come from MG
   Typical start: pyridostigmine (e.g., 30–60 mg 3–4×/day, titrated), with corticosteroids or other immunotherapy if needed; biologics for refractory disease.
   Purpose/Mechanism: improves neuromuscular transmission; immunotherapy suppresses autoimmunity. PMCClinical Care Journal of Medicine

9. Short-term topical agents to modulate eyelid position (adjuncts)

   • Oxymetazoline 0.1% eye drops (Upneeq®; 1 drop once daily) can temporarily raise a mild acquired ptosis by stimulating Müller’s muscle; use is off-label for neurogenic ptosis and should be clinician-directed.

   • Apraclonidine 0.5–1% can lift a Horner’s ptotic lid transiently (also used diagnostically). PMCWebEye

10. Short-term botulinum toxin for severe eyelid retraction (specialist use)
    Purpose/Mechanism: weakens the overactive levator to reduce exposure; typically lasts ~3 months. EyeWiki

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Dietary molecular supplements (supportive, not curative)

There is no supplement proven to cure PMLS. These options may support neuro-vascular health or ocular surface comfort, mainly when a deficiency is present. Always confirm need and dose with a clinician (interactions are common).

1. Vitamin B12 (cyanocobalamin) — 1,000 µg/day orally (or clinician-directed injections)
   Function/Mechanism: cofactor for myelin; corrects deficiency-related neuropathy risk. Evidence supports treatment when deficient; benefits in normal levels are uncertain. PMC+1

2. Vitamin D3 (cholecalciferol) — often 1,000–2,000 IU/day if low, dose guided by blood levels
   Function/Mechanism: pleiotropic neuro-immune and vascular effects; mixed data for stroke outcomes; treat documented deficiency. PMCFrontiers

3. Omega-3 (EPA/DHA) — food-first (fatty fish); supplement ~1 g/day EPA+DHA if diet is poor
   Function/Mechanism: cardiometabolic support; not a proven dry-eye cure in large RCTs. PubMedNew England Journal of Medicine

4. Alpha-lipoic acid — 600 mg/day (monitor for hypoglycemia in diabetics)
   Function/Mechanism: antioxidant studied in neuropathy; trial results are mixed but sometimes symptomatic benefit reported. Diabetes JournalsPubMed

5. Coenzyme Q10 — 100–200 mg/day
   Function/Mechanism: mitochondrial antioxidant; human neuroprotective evidence is limited/heterogeneous; do not replace guideline stroke care. PMCJAMA Network

6. Magnesium (e.g., glycinate) — 200–400 mg/day
   Function/Mechanism: nerve/muscle excitability; helpful if deficient; watch renal status. (General evidence base; supportive.)

7. B-complex (B1 50–100 mg, B6 25–50 mg with B12 as above)
   Function/Mechanism: supports peripheral nerve function; avoid chronic high-dose B6 neuropathy risk. actaneurologica.com

8. L-carnitine/Acetyl-L-carnitine — 1–2 g/day
   Function/Mechanism: mitochondrial fatty-acid transport; mixed neuropathy data. (Supportive evidence; use with clinician oversight.)

9. N-acetylcysteine (NAC) — 600–1,200 mg/day
   Function/Mechanism: glutathione precursor/antioxidant; evidence for neuro protection is emerging but not disease-specific. (Exploratory.)

10. Zinc (if deficient) — ~8–11 mg/day
    Function/Mechanism: immune and healing cofactor; correct deficiency only to avoid copper imbalance. (Standard nutrition guidance.)

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Regenerative & “stem-cell” therapies

There are no FDA- or EMA-approved regenerative or stem-cell drugs to treat midbrain lesions or PMLS. Multiple clinical trials have explored mesenchymal stem cells, neural stem cells, CD34+ cells, and allogeneic products for stroke, but results are mixed and not practice-changing; these remain experimental and, if offered, should only be within regulated clinical trials. Key points:

1. Mesenchymal stem cells (MSCs) — under study for ischemic/hemorrhagic stroke; not approved for restoring midbrain eyelid control. NaturePMC

2. Neural stem cell lines (e.g., CTX) — safety-focused pilot trials exist; no established efficacy. ClinicalTrials.gov

3. Allogeneic cell products (e.g., MultiStem) — RCT data are mixed; no standard-of-care role. JAMA Network

4. Meta-analyses vary, but several conclude no clinically important benefit to date; research continues. PMC

5. Press reports of new cell approvals (e.g., remestemcel for GVHD) do not apply to stroke or PMLS. Wikipedia

6. Bottom line: if a provider markets “stem-cell cures” for eyelid or brainstem problems outside a trial, be cautious and seek a second opinion. (Safety guidance.)

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Surgeries

Surgery is usually delayed until the condition is stable for months. The choice depends on whether the problem is ptosis, retraction, exposure, or persistent strabismus/diplopia.

1. Levator advancement/resection (ptosis repair)
   Procedure: shorten/advance the levator aponeurosis to raise the droopy lid.
   Why: corrects stable neurogenic ptosis when levator function is adequate. Lippincott Journals

2. Frontalis suspension (sling)
   Procedure: connect the lid to the forehead muscle with fascia/silicone so brow lift raises the lid.
   Why: used when levator function is poor; common for severe or recurrent ptosis. NCBIEyeWiki

3. Upper-lid retraction repair (e.g., Müllerotomy, levator recession, full-thickness anterior blepharotomy, sometimes spacer grafts)
   Procedure: weaken or recess the over-elevating structures to lower the lid and protect the cornea.
   Why: treats exposure and asymmetry from persistent retraction. EyeWikiJAMA NetworkNature

4. Temporary or permanent tarsorrhaphy
   Procedure: partially sew eyelids together to narrow the opening.
   Why: protects the cornea when exposure keratopathy is severe or refractory. EyeWiki

5. Strabismus surgery (after 6–12 months stability)
   Procedure: adjust extraocular muscles to correct persistent misalignment.
   Why: long-standing diplopia that prisms can’t solve. Review of Optometry

Note: If an aneurysm/tumor causes PMLS, neurosurgical/endovascular treatment addresses the source rather than the eyelids.

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Prevention tips (focused on the common vascular causes)

1. Control blood pressure to guideline targets. AHA Journals

2. Treat cholesterol aggressively (statins ± add-ons per profile). professional.heart.org

3. Don’t smoke or vape; enroll in a cessation program if needed. AHA Journals

4. Manage diabetes (A1c goals individualized). AHA Journals

5. Move your body (aim ≥150 minutes/week moderate activity unless told otherwise). AHA Journals

6. Heart-healthy eating pattern (Mediterranean/DASH-style). PubMedBMJ

7. Screen and treat sleep apnea if suspected (snoring, daytime sleepiness). (Guideline-consistent risk reduction.)

8. Limit alcohol; avoid recreational drug use (e.g., sympathomimetics) that raise stroke risk. (Guideline-consistent.)

9. Keep up with vaccinations (influenza/COVID) to reduce systemic illness that can destabilize vascular disease. (Public health guidance.)

10. Know FAST for stroke (Face droop, Arm weakness, Speech trouble, Time to call emergency)—early care saves brain. AHA Journals

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When to see a doctor—right away vs routine

• Go to emergency care now if eyelid changes are sudden and you have double vision, new weakness/numbness, slurred speech, severe headache, imbalance, or vision loss. These can signal stroke or aneurysm. www.heart.org

• Arrange urgent neuro-ophthalmology review if one lid is up and the other down, or if diplopia/pupil changes appear—even without other symptoms. EyeWiki

• Schedule follow-up if you already have a diagnosis and need prism updates, exposure-care tweaks, or to discuss surgery once things are stable. Review of Optometry

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What to eat and what to avoid

1. Base meals on vegetables, fruits, whole grains, legumes, nuts, and seeds. (Fiber + micronutrients) PubMed

2. Choose healthy fats: olive/canola/other unsaturated oils; fatty fish 1–2×/week. PubMed

3. Prioritize lean proteins: fish, skinless poultry, legumes, tofu. PubMed

4. Limit salt (especially with hypertension). Aim for low-sodium choices. PubMed

5. Limit added sugars: sweet drinks, pastries, candy. PubMed

6. Cut back on processed/charred red meats; enjoy legumes and fish more often. PubMed

7. Avoid trans fats; keep saturated fats low (swap butter for olive oil). PubMed

8. Watch portions & weight—calorie needs drop with age. American College of Cardiology

9. If you drink alcohol, keep it light or avoid (some should abstain entirely). PubMed

10. Food first for omega-3s (fish, walnuts); use supplements only when advised. PubMed

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Frequently Asked Questions

1) Is plus-minus lid syndrome a disease by itself?
No. It’s a pattern of eyelid positions that points doctors to a location in the midbrain or a mimic. The true “disease” is the underlying cause (often a small stroke, demyelination, or less commonly a tumor/aneurysm). EyeWiki

2) Can it permanently damage vision?
The lid changes themselves don’t damage the eye, but exposure from a retracted lid can injure the cornea. Protecting the surface with lubrication, moisture chambers, and (if needed) procedures is important. vagelos.columbia.edu

3) Will it go away on its own?
If caused by a small ischemic cranial-nerve or midbrain event, a lot of patients improve within 6–12 weeks. Your team monitors recovery and adjusts prisms or considers surgery if it stays stable but bothersome. PMC

4) How is it different from Collier’s sign?
Collier’s sign is bilateral lid retraction from disinhibition of the levator center. PMLS adds ptosis on one side because adjacent third-nerve fibers are also involved. EyeWiki

5) What is “pseudo plus-minus”?
A true droopy lid on one side can trick the brain into raising the other lid (Hering’s law), mimicking PMLS without a midbrain lesion. Careful testing separates the two. PMC

6) Which scans do I need?
MRI brain (with attention to midbrain) is typical; vascular imaging if aneurysm is possible; additional tests if MG or orbital disease is suspected. EyeWiki

7) Can eye drops fix it?
Drops like oxymetazoline 0.1% can temporarily lift some acquired ptosis; apraclonidine lifts a Horner’s ptosis. These are adjuncts—not cures—and should be clinician-directed. PMCWebEye

8) Do prisms help?
Yes, Fresnel prisms or patching often help diplopia while nerves recover; long-term prisms or surgery can be discussed if misalignment remains. Review of Optometry

9) Is surgery always needed?
No. Surgery is considered after stability if ptosis, retraction, or misalignment persist and bother function/appearance or threaten the cornea. Review of OptometryEyeWiki

10) Can stem cells or “regenerative” shots cure it?
No approved stem-cell therapy exists for PMLS/midbrain lesions; current stroke trials are experimental with mixed results. Avoid clinics offering cures outside trials. PMCJAMA Network

11) What lifestyle changes matter most?
Blood pressure, lipids, diabetes, physical activity, and smoke-free living are the big levers for stroke prevention and brain health. AHA Journals

12) Which doctor should I see?
A neuro-ophthalmologist coordinates eye and brain causes; a stroke neurologist or neurosurgeon may be involved if imaging finds a vascular or mass cause. EyeWiki

13) How do doctors decide between frontalis sling vs levator surgery?
It depends on levator strength: good function favors levator advancement; poor function favors a frontalis suspension. NCBI

14) What about botulinum toxin?
Select cases with disabling eyelid retraction may benefit from carefully placed botulinum to lower the lid temporarily—often as a bridge to surgery or recovery. EyeWiki

15) Can diet really help my eyelids?
Diet doesn’t change lid wiring, but heart-healthy patterns (Mediterranean/DASH) support the vascular system, lowering risks for the kinds of events that can cause PMLS. PubMedBMJ

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Last Updated: August 22, 2025.