Neuro-Ophthalmologic Manifestations of Amyotrophic Lateral Sclerosis

Neuro-ophthalmologic manifestations of ALS are the eye and vision problems that come from changes in the brain and nerves that control eye movement, eyelids, and visual processing. ALS mainly injures motor neurons. These are the nerve cells that make muscles move. The muscles that move the eyes are often spared early in ALS. But the brain circuits that command and coordinate eye movements can be affected. When that happens, a person can have slow eye jumps, shaky fixation, trouble tracking a moving object, or other issues that make reading, screen use, and daily communication harder. These eye and vision problems can appear at any time in the disease, but are usually milder early and more noticeable later, especially if the brainstem or frontal “eye control” areas are involved. Research shows that abnormalities in saccades (fast eye jumps), smooth pursuit (slow tracking), and fixation can occur in ALS and may be more common in people with bulbar onset (speech and swallowing symptoms first). EyeWiki

ALS is a disease that gradually damages motor neurons—the nerve cells that tell muscles to move. Most people think of weakness in the arms, legs, breathing muscles, or swallowing muscles. But the eyes can be involved too—not usually at the very beginning, but more often as ALS advances or when there is also frontotemporal brain involvement. The eye problems come mainly from brain and brainstem control systems that coordinate eye movements and eyelids, and from practical issues like reduced blink rate and difficulty closing the eyes completely. Put simply: the eyes themselves are usually healthy, but the “wiring and control” for moving and protecting them can be affected. Typical changes include trouble holding gaze steady, small unwanted eye jumps (“square-wave jerks”), slightly inaccurate saccades (quick eye jumps), slower smooth-pursuit tracking, eyelid-opening apraxia, and dry, irritated eyes from less frequent blinking. These findings vary by person and stage and can be subtle; careful neuro-ophthalmic examination or eye-tracking tests pick them up best. EyeWikiPMC+1

Some studies also explore changes in retinal structure (the light-sensing layer in the back of the eye) using OCT scans. Results are mixed. Some studies suggest small changes; others show no meaningful difference from healthy people. So retinal measurements are being studied, but they are not yet a reliable standalone marker. PMCthejcn.com

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Types

Below are 10 practical “types” of eye/vision involvement you might encounter in ALS. Each type is explained in simple terms.

1. Slow or small saccades (fast eye jumps).
   You look from one word or object to another using quick eye jumps called saccades. In ALS, these jumps can be slower or undershoot the target. This makes reading feel stop-and-go and tiring. These findings reflect problems in brain circuits that start and shape saccades. EyeWikiFrontiers

2. Trouble tracking a moving target (smooth pursuit).
   Following a slow moving object, a scrolling line, or a moving cursor can feel unsteady. You may need extra “catch-up” saccades. This is common when cerebellar or brainstem control is affected. PMCFrontiers

3. Fixation instability (little unwanted eye hops).
   While trying to hold gaze on a word or face, tiny unwanted eye movements (like square-wave jerks) can break fixation. Reading then feels jumpy. EyeWiki

4. Mild gaze limitation (late or rare).
   In early ALS, the nerves that directly drive the eye muscles are usually spared. Later, some people develop mild limitations, especially for fast horizontal movements, because the higher-level control system is affected. True nuclear cranial nerve palsy is uncommon. EyeWiki

5. Alignment symptoms (occasional diplopia).
   Most people with ALS do not have constant double vision. But fatigue, secondary conditions, or rare late involvement can produce intermittent misalignment and brief diplopia.

6. Blink and eyelid problems.
   Facial weakness or reduced blink can cause dry eye and irritation. Rarely, some patients can feel “stuck” with the eyelids closed (a phenomenon called apraxia of eyelid opening), but this is far more typical of Parkinsonian disorders than ALS. NCBI

7. Visual comfort problems (dryness, strain, light sensitivity).
   Less frequent blinking dries the cornea. Dry corneas feel gritty, sting in wind or air-conditioning, and make lights feel harsh.

8. Reading and screen-use difficulty.
   Slow saccades, poor fixation, and tracking trouble make reading slow and tiring. People may use larger fonts, more spacing, or text-to-speech.

9. Cognitive control of eye movements (ALS–FTD spectrum).
   Some ALS patients have executive function changes. These can show up as errors on “antisaccade” tasks (you should look away from a sudden target, but the brain fails to inhibit the automatic look-toward movement). This is a marker of frontal lobe control change. Frontiers

10. Retinal or visual pathway signals (research area).
    OCT and specialized tests sometimes suggest subtle retinal or pathway changes, but results are inconsistent, so they are not used for diagnosis on their own. PMC

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Causes

These “causes” explain why eye/vision problems can appear in someone with ALS. They include direct disease mechanisms, indirect contributors, and mimics that doctors must not miss. Each item is written in very simple terms.

1. Frontal eye field involvement.
   These brain areas start voluntary eye jumps. Injury here slows saccades and increases errors on tasks that need inhibition.

2. Brainstem saccade generator stress.
   The pons houses burst neurons and the omnipause system that gate saccades. Stress in this network can make eye jumps slow or small. EyeWiki

3. Cerebellar modulation problems.
   The cerebellum fine-tunes saccades and smooth pursuit. When its connections are affected, pursuit becomes jerky and fixation becomes unstable. PMC

4. Bulbar-onset disease spread.
   Bulbar involvement often means more brainstem involvement, which can increase smooth-pursuit and saccadic abnormalities. EyeWiki

5. Executive control changes (ALS–FTD spectrum).
   Frontal networks that control attention and inhibit reflexive saccades can be affected, raising antisaccade error rates. Frontiers

6. Reduced blink from facial weakness.
   Weakness in eyelid closing muscles lowers blink rate, dries the eye, and blurs vision.

7. Ocular surface exposure at night.
   Incomplete lid closure during sleep can dry and irritate the cornea, causing morning blur and burning.

8. Fatigue and general weakness.
   Total body fatigue can worsen eye control through reduced endurance and attention.

9. Respiratory CO₂ retention or low oxygen (late).
   Poor gas exchange can cause diffuse symptoms like headache, fogginess, or vague blur, which may be felt as “vision trouble.”

10. Medication side effects.
    Anticholinergics, baclofen, or sedatives can blur vision, slow focus, or cause drowsy tracking.

11. Dehydration and poor tear film.
    Less fluid intake and poor nutrition reduce tear quality and comfort.

12. Coexisting small-vessel ischemia (older adults).
    Microvascular palsies of cranial nerves III, IV, or VI can cause new double vision that is not from ALS itself.

13. Coexisting myasthenia gravis (rare but important).
    MG causes fatigable ptosis and diplopia. It can coexist and must be excluded when symptoms fluctuate.

14. Thyroid eye disease (separate disorder).
    TED causes eye muscle inflammation and diplopia; it is a key mimic to consider.

15. Diabetic retinopathy or neuropathy (comorbidity).
    Diabetes can blur vision and cause nerve palsies independent of ALS.

16. Cataract or macular disease (age-related).
    Common eye diseases can be the main reason for poor vision in an ALS patient.

17. Retinal pathway changes under study.
    Some research suggests subtle retinal changes; other studies do not. This inconsistency itself is important. PMC

18. Dry eye from CPAP/BiPAP airflow leaks.
    Air blowing across the eyes overnight dries the surface.

19. Blepharospasm or rare eyelid-opening apraxia.
    These are uncommon in ALS and are more typical of Parkinsonian disorders, but very rarely may be seen or misattributed. NCBI

20. Environmental strain (screen glare and small fonts).
    Small text, glare, and poor lighting magnify minor oculomotor problems and make symptoms feel worse.

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Symptoms

Each symptom is described in one or two short, clear sentences.

1. Slow reading.
   Words seem to “jump,” and you need extra time to move from word to word.

2. Trouble tracking moving things.
   Following a cursor, a ball game, or a scrolling feed feels jerky or tiring.

3. Eyes that undershoot targets.
   You look at a button or word and land a little short, needing a tiny extra jump.

4. Shaky fixation.
   When you try to hold steady on a point, the eyes make little unwanted hops.

5. Intermittent blur, worse with fatigue.
   Blur improves after blinking or resting the eyes.

6. Dry, gritty, burning eyes.
   Dryness is worse in wind, air-conditioning, or overnight.

7. Light sensitivity from dryness.
   Bright light or screens feel harsh until tears are restored.

8. Occasional double vision.
   This is not common in early ALS, but can happen with fatigue or separate eye problems.

9. Heavy lids or trouble opening the eyes.
   More often this is dryness or fatigue; true “eyelid opening apraxia” is rare and usually tied to other disorders.

10. Droopy eyelids (ptosis), usually mild.
    If it fluctuates a lot during the day, doctors check for myasthenia gravis.

11. Head turning to compensate.
    People move the head more to help the eyes lock onto targets.

12. Screen intolerance.
    Small fonts and dense pages become hard to sustain.

13. Difficulty maintaining eye contact.
    Holding gaze on a face can be tiring due to fixation issues.

14. More reading mistakes under time pressure.
    Timed tasks feel harder because saccades and attention are both taxed.

15. General eye fatigue by evening.
    Symptoms ramp up with long days or poor lubrication.

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Diagnostic tests

Below are 20 tests grouped into Physical Exam, Manual/Bedside Functional Tests, Lab & Pathological Tests, Electrodiagnostic Tests, and Imaging/Structural Tests. Each item explains what the test is and why it helps, using very simple words.

A) Physical Exam

1. Visual acuity (Snellen/ETDRS).
   Measures how clearly you see letters at a set distance. It tells us if basic clarity is normal or reduced from common causes like refractive error or cataract.

2. Contrast sensitivity (e.g., Pelli-Robson).
   Checks how well you see faint gray letters on white. ALS studies report reduced contrast in some patients, so this test can pick up subtle visual changes even when standard acuity seems fine. PMC

3. Color vision (Ishihara or D-15).
   Screens for color mistakes that may suggest retinal or optic pathway problems unrelated to ALS.

4. Pupil exam (light and near response).
   Looks for nerve pathway problems or medication effects. Pupils are usually normal in ALS; abnormal pupils point to other diagnoses.

5. Eyelid and blink exam.
   The clinician observes blink rate, eyelid closure strength, and corneal surface. This detects dry eye from reduced blinking and any droop or fatigue signs.

6. Alignment and motility (cover tests and “H” movements).
   Simple tests show whether the eyes stay aligned and how well they move in all directions. They help separate subtle control problems from true nerve palsies.

B) Manual / Bedside Functional Tests

7. Prosaccade testing (look quickly to a new target).
   The examiner asks you to jump your eyes between two targets. Delayed or small jumps suggest saccade system stress seen in ALS. EyeWiki

8. Antisaccade task (look away from a sudden dot).
   This checks frontal lobe control. Making many errors or being slow can signal executive control changes sometimes present in ALS. Frontiers

9. Smooth pursuit tracking (follow a slow target).
   The clinician moves a small object slowly and watches your tracking. Jerky pursuit and frequent catch-up saccades fit with ALS-related pursuit changes. PMC

10. Fixation stability (look at a tiny dot).
    The examiner looks for small “hops” (saccadic intrusions). Excess intrusions make reading hard and are reported in ALS. EyeWiki

11. Near point of convergence (NPC).
    A target is moved toward the nose to see where the eyes lose convergence. This helps explain eye strain at near and separates common convergence issues from ALS-related control changes.

C) Lab & Pathological Tests

12. Myasthenia tests (AChR, MuSK antibodies ± ice pack test).
    These check for myasthenia gravis, a treatable cause of droopy lids and diplopia that can coexist with ALS or mimic it.

13. Thyroid function (TSH, free T4).
    Helps find thyroid eye disease, a common cause of double vision that is separate from ALS.

14. Diabetes screening (fasting glucose, HbA1c).
    Finds microvascular risk that can cause true cranial nerve palsies and diplopia.

15. B12 and folate.
    Checks for nutritional or neurologic contributors that can blur vision or cause neuropathy.

D) Electrodiagnostic Tests

16. Video-oculography (VOG) or infrared eye tracking.
    This instrument measures saccade speed, latency, pursuit gain, and fixation stability with precision. Research shows measurable oculomotor differences in ALS that may track disease involvement. FrontiersTaylor & Francis Online

17. Visual evoked potentials (VEP).
    Measures the brain’s response to visual patterns. It helps if optic pathway disease is suspected. In ALS, VEP is often normal; abnormal results push doctors to look for another cause.

18. Electroretinography (ERG).
    Records retinal electrical responses. It helps when OCT or symptoms suggest a retinal disorder not directly caused by ALS.

E) Imaging / Structural Tests

19. Optical coherence tomography (OCT).
    Takes cross-section scans of the retina and optic nerve layers. Research results in ALS are mixed, so OCT is supportive rather than diagnostic on its own. PMC

20. MRI brain and brainstem.
    Looks for other causes of eye movement problems and shows disease patterns that support ALS diagnosis in the right context (for example, corticospinal tract signal changes). It mainly rules out mimics. EyeWiki

21. High-resolution orbital imaging (selected cases).
    If true diplopia is persistent, imaging of the orbits can exclude thyroid eye disease or muscle inflammation.

22. Diffusion tensor imaging (research setting).
    Assesses white-matter tracts and may show network involvement related to eye control, but not used routinely.

23. Fundus photography.
    Documents the retina and optic nerve head to track any non-ALS eye disease that could be driving symptoms.

Non-pharmacological treatments

1. Artificial tears (preservative-free) often: Soothe dryness, improve comfort and clarity; simply replace the missing tear layer.

2. Nighttime ointment: Thicker gel protects the surface during sleep when blink is absent.

3. Moisture-chamber glasses or humidifier: Traps humidity around the eyes or in the room so tears don’t evaporate as fast.

4. Blink “hygiene”: Gentle blink exercises, timed “blink breaks,” and conscious blinking while reading/screening keep the surface wet.

5. Warm compresses + lid hygiene: Melts thick oils in meibomian glands and cleans lids; improves tear quality and reduces burning.

6. Blue-light filtering and glare control: Tinted lenses, hats, and screen settings ease light sensitivity from dry eye and fixation fatigue.

7. Large-print, high-contrast reading setups: Bigger fonts and good contrast reduce effort when saccades are a bit inaccurate.

8. Reading strategies: Line guides or e-readers with auto-scroll allow smaller eye jumps and less fatigue.

9. Prism readers (case-by-case): Small prisms can ease near-work alignment strain if diplopia or convergence insufficiency appears.

10. Eyelid taping at night (short term): A gentle tape strip helps full closure if the lids don’t seal during sleep, preventing exposure keratopathy.

11. Punctal occlusion (clinic procedure, non-systemic): Tiny plugs or cautery reduce tear drainage; more tears stay on the eye.

12. Occupational therapy for access: Optimizes reading stands, lighting, bed positioning, and switch placement to minimize head and eye strain.

13. Physical therapy & neck support (“dropped head”): A soft or semi-rigid collar helps hold eyes in a comfortable reading/gaze zone.

14. Speech-language pathology (SLP) for AAC: Trains efficient eye-gaze communication and selects the right interface for fatigue-resistant typing. PMC

15. Eye-tracking computers: Let you type and control devices using gaze; newer systems add predictive text to reduce keystrokes. Nature

16. Brain–computer interfaces (research/clinical trials): Some centers can decode attempted or even “inner” speech to restore faster communication—promising but still specialized. Nature

17. Non-invasive ventilation (NIV) when breathing weakens: Better oxygenation and sleep can improve daytime stamina for reading/communication and overall quality of life. PubMed

18. Sleep hygiene: Regular sleep, head-of-bed elevation, and avoiding late caffeine reduce eye fatigue and morning irritation.

19. Hydration & room air care: Frequent sips of water and avoiding smoke or strong air-conditioning vents keep the ocular surface healthier.

20. Multidisciplinary clinic follow-up: Regular check-ins with neurology, neuro-ophthalmology, SLP, OT, PT, and respiratory therapy coordinate care and reduce complications. PubMed

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Drug treatments

Always follow your clinician’s advice; many of these are prescription-only and require monitoring.

1. Riluzole (glutamate modulator; disease-slowing)
   Dose/Timing: 50 mg by mouth every 12 hours; take on an empty stomach.
   Purpose/Mechanism: Modestly slows ALS progression by reducing glutamate-related excitotoxicity.
   Side effects: Nausea, fatigue; monitor liver enzymes. FDA Access Datarestasis.com

2. Edaravone (IV or oral) (free-radical scavenger; disease-slowing)
   Dose/Timing: IV 60 mg daily in cycles (14 days on, 14 off first cycle; then 10 days on out of 14, followed by 14 off). Oral (Radicava ORS) 105 mg once daily mornings on the same cycle pattern, fasting.
   Purpose/Mechanism: Limits oxidative stress-related neuronal injury; benefits shown in early ALS subsets.
   Side effects: Bruising, gait disturbance, headache; hypersensitivity is possible. FDA Access DataMayo Clinic

3. Tofersen (Qalsody) (antisense oligonucleotide; gene-targeted for SOD1-ALS only)
   Dose/Timing: 100 mg intrathecal injection: 3 loading doses every 14 days, then 100 mg every 28 days.
   Purpose/Mechanism: Lowers mutant SOD1 protein and neurofilament markers; accelerated approval for SOD1-ALS.
   Side effects: Procedure-related headache/back pain, CSF abnormalities; requires specialist care. FDA Access DataU.S. Food and Drug Administration

4. Dextromethorphan/Quinidine (Nuedexta) (NMDA/sigma-1 modulator + CYP2D6 inhibitor; for pseudobulbar affect, PBA)
   Dose/Timing: 20 mg/10 mg capsule once daily for 7 days, then twice daily.
   Purpose/Mechanism: Reduces uncontrolled laughing/crying that can interfere with eye-tracking communication and care.
   Side effects: Dizziness, diarrhea; QT prolongation risk and drug interactions—screen carefully. nuedexta.comnuedextahcp.com

5. Glycopyrrolate (peripheral anticholinergic; for sialorrhea/drooling)
   Dose/Timing: Often 1–2 mg orally, 2–3×/day (titrate to effect).
   Purpose/Mechanism: Blocks salivary gland muscarinic receptors to reduce drooling that can blur vision, soil eye-tracking cameras, and cause skin irritation.
   Side effects: Dry mouth, constipation, possible blurred vision; fewer brain effects than older anticholinergics. PMC

6. Scopolamine transdermal patch (anticholinergic; sialorrhea)
   Dose/Timing: 1 patch behind the ear every 72 h.
   Purpose/Mechanism: Sustained muscarinic blockade reduces saliva.
   Side effects: Dry eye, blurred vision, confusion in sensitive patients—monitor for ocular effects. PMC

7. Atropine 1% ophthalmic drops used sublingually (off-label) (sialorrhea)
   Dose/Timing: Commonly 1–2 drops under the tongue up to 3–4×/day, titrated cautiously.
   Purpose/Mechanism: Rapid saliva reduction via local antimuscarinic effect.
   Side effects: Dry eyes, blurred near vision, tachycardia; use carefully and avoid overdosing. The ALS Associationsurreyccg.res-systems.net

8. Botulinum toxin injections to salivary glands (procedure-delivered drug; sialorrhea refractory to pills)
   Dose/Timing: Given by ENT/neurologist every ~3–4 months.
   Purpose/Mechanism: Temporarily blocks acetylcholine release in salivary glands; reduces drooling without systemic side effects.
   Side effects: Thickened saliva, mild swallowing change; ultrasound guidance improves safety. PMC

9. Preservative-free lubricating eye drops/gel (ocular surface support)
   Dose/Timing: Drops 4–8×/day; gel/ointment at bedtime.
   Purpose/Mechanism: Replaces the water or oil layer of tears, easing dryness from reduced blink.
   Side effects: Temporary blur (gel/ointment), rarely allergy.

10. Topical anti-inflammatories for dry eye (e.g., cyclosporine 0.05%, lifitegrast 5%)
    Dose/Timing: Cyclosporine 1 drop twice daily; Lifitegrast 1 drop twice daily.
    Purpose/Mechanism: Calms ocular surface inflammation to improve natural tear production over weeks.
    Side effects: Burning on instillation, dysgeusia (lifitegrast). PMCPubMed

Important update about AMX0035 (sodium phenylbutyrate/taurursodiol): This medicine (brand RELYVRIO) was voluntarily withdrawn from the U.S. and Canadian markets in 2024 after a phase 3 trial did not confirm benefit. If you see references online, know that it is no longer marketed in those regions. Drugs.com

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Dietary molecular supplements

No supplement has proven to stop ALS. Think of these as adjuncts for general nerve, eye-surface, or overall health. Discuss each with your clinician for safety and interactions.

1. Omega-3 (EPA/DHA) — 1–2 g/day combined EPA+DHA with food.
   Function: anti-inflammatory support; may help meibomian oil quality for dry eye. Mechanism: membrane and eicosanoid effects. (Observational data suggest higher omega-3 intake may relate to slower progression, but trials are mixed.) FDA Access Data

2. Vitamin D3 — 1000–2000 IU/day, individualized to labs.
   Function: bone, immune, and muscle support; prevents deficiency common in limited mobility. Mechanism: nuclear receptor-mediated gene regulation.

3. B-complex with B12 (standard oral doses unless prescribed high-dose IM)
   Function: supports neuronal metabolism; corrects deficiency that can worsen neuropathy. Mechanism: co-factors in methylation and energy pathways.

4. Magnesium glycinate — 200–400 mg at night.
   Function: helps cramps and sleep quality; may ease eyelid twitching. Mechanism: neuromuscular membrane stabilization.

5. N-acetylcysteine (NAC) — 600–1200 mg/day.
   Function: antioxidant precursor to glutathione; conceptual support against oxidative stress.

6. Alpha-lipoic acid — 300–600 mg/day with food.
   Function: antioxidant; studied in neuropathy; ocular surface oxidative balance.

7. Coenzyme Q10 (ubiquinone or ubiquinol) — 100–300 mg/day with fat.
   Function: mitochondrial co-factor; ALS trials have not shown benefit, so use only as general support if desired. American Academy of Neurology

8. Creatine monohydrate — 3–5 g/day.
   Function: cellular energy buffer; ALS trials showed no clear benefit—use only if tolerated for general muscle energy. amylyx.com

9. Curcumin (with piperine/formulation for absorption) — 500–1000 mg/day.
   Function: anti-inflammatory and antioxidant; may help dry-eye symptoms in some people.

10. Lutein/Zeaxanthin — 10 mg/2 mg daily.
    Function: macular pigment support; filters blue light and may improve glare/contrast on screens.

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Regenerative / immune-modulating” drugs

These are not “hard immunity boosters.” They are experimental or specialized. None is a cure; many require trials or specific mutations.

1. High-dose methylcobalamin (vitamin B12, injectable) — 50 mg IM twice weekly studied in Japan for early ALS. Some benefits reported in early-stage patients, but it is not globally approved and requires physician oversight. Mechanism: axonal support and methylation. investors.medicinova.com

2. Tofersen (SOD1 antisense) — Approved for SOD1-ALS only; reduces a proven molecular driver in that subtype. Mechanism: gene silencing in CSF. FDA Access Data

3. Ibudilast (MN-166; PDE4/10 inhibitor) — being tested for neuroinflammation modulation; data mixed and investigational. Frontiers

4. Masitinib (tyrosine-kinase inhibitor) — targets mast cell/microglial signaling; phase 2/3 data suggest possible benefit in subgroups but remains investigational. PMC

5. Stem-cell approaches (e.g., autologous mesenchymal stem cells, NurOwn) — multiple trials; no FDA approval to date; the FDA issued a Complete Response Letter in 2024 after earlier negative advisory committee feedback. Consider only in regulated trials. Neurology live

6. Brain–computer interface (BCI) neuroprostheses — not disease-modifying, but regenerative in function by restoring communication speed. Several centers show real-time speech decoding in paralysis; still limited to trials/specialized programs. Nature

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Procedures/surgeries

1. Punctal plug insertion (clinic procedure): For stubborn dry eye, tiny plugs in tear drains keep tears on the eye longer—quick, reversible, no general anesthesia.

2. Temporary or permanent tarsorrhaphy (minor eyelid surgery): Partially closes the eyelids to protect the cornea if exposure keratopathy threatens vision; used when taping/ointment fail.

3. Botulinum toxin injections to parotid/submandibular glands: Technically a procedure, not an operation; it sharply reduces drooling that interferes with communication devices and skin care. PMC

4. Salivary-gland radiotherapy (select refractory cases): Small doses aimed at glands can reduce saliva when medicines and Botox fail; used cautiously with specialist guidance. radicava.com

5. Ptosis or eyelid-opening surgery (rare, case-by-case): If eyelid disorders severely block vision and conservative measures fail, oculoplastic surgery may be considered after careful neuro-ophthalmic evaluation.

Major ALS procedures like PEG or tracheostomy are crucial for nutrition and breathing but are outside this eye-focused guide.

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Prevention tips

1. Blink early, blink often during screens and reading.

2. Use preservative-free tears before long tasks; don’t wait for burning.

3. Humidify your space and avoid direct fans/vents on your face.

4. Protect from glare with caps, filters, and indoor tints.

5. Night protection with ointment and (if needed) gentle lid taping.

6. Treat lid inflammation (warm compress/lid hygiene) to prevent tear-film breakdown.

7. Stay hydrated and manage medications that worsen dryness (with your doctor).

8. Plan ergonomics: good lighting, proper reading distance, and head/neck support.

9. Check devices early (eye-tracking calibration when energy is best).

10. See neuro-ophthalmology regularly to catch problems early.

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When to see a doctor urgently or promptly

• Urgent: sudden painful red eye, sudden vision loss, new double vision, light sensitivity with severe tearing, or corneal scratch feeling—these can be emergencies.

• Prompt: persistent dryness unrelieved by drops, eyelids not closing fully at night, frequent eye fatigue that blocks communication, new difficulty opening eyelids, or any new eye-movement change.

• ALS clinic triggers: more choking or drooling, worse sleep or morning headaches (possible hypoventilation), or mood swings/cry-laugh spells (possible PBA)—these affect eye care and communication plans. PubMed

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What to eat and what to avoid

1. Eat enough calories and protein: weight loss worsens outcomes in ALS; work with a dietitian early.

2. Prefer moist, soft foods if swallowing tires you—add sauces, broths, or gravies to reduce eye-watering cough fits.

3. Frequent small meals to match energy and reduce fatigue.

4. Omega-3-rich foods (fish like salmon/sardines, walnuts) support general anti-inflammatory balance.

5. Colorful produce (greens/orange/yellow) supplies lutein, zeaxanthin, and antioxidants for the ocular surface.

6. Stay well-hydrated (water, broths); dehydration worsens dry eye.

7. Limit alcohol (dries mucous membranes, disturbs sleep).

8. Limit very spicy, acidic, or crumbly foods if they trigger cough/choking or reflux.

9. Watch caffeine at night (sleep matters for eye comfort).

10. Discuss thickeners for liquids with SLP if thin fluids cause coughing.

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Frequently asked questions

1) Are the eyes “spared” in ALS?
Mostly at the beginning. Many people keep full eye movements for a long time. With progression or cognitive involvement, subtle control problems—like fixation instability or slightly inaccurate saccades—can appear. Dry eye from less blinking is common and very treatable. EyeWiki

2) Can eye problems predict how fast ALS will progress?
Not reliably for an individual. Eye-movement metrics and OCT changes are being studied as biomarkers, but results are mixed and mainly useful in research for now. PMC+1

3) Why are my eyes so dry even though I make tears?
Blinking spreads and renews tears. When blinking slows or lids don’t close fully, tears evaporate and the surface dries. Fixing blink habits and adding lubricants usually helps quickly.

4) My reading is slower—am I losing vision?
Often it’s control, not eyesight. Small saccadic inaccuracies or fatigue slow scanning. Bigger fonts, better contrast, and line guides help, along with artificial tears.

5) Can I keep using eye-tracking to communicate as ALS advances?
Usually yes. Calibrating when you’re rested, optimizing lighting and positioning, and combining prediction tools can keep typing efficient. If standard eye-tracking becomes hard, some centers offer visual BCI options; investigational BCIs can even decode attempted or “inner” speech. FrontiersNature

6) Is there any cure?
No cure yet. Riluzole and edaravone modestly slow disease for some; tofersen helps only SOD1-ALS. Many other agents are under study. restasis.comFDA Access Data+1

7) I heard about AMX0035 (RELYVRIO). Should I take it?
It was withdrawn from the U.S. and Canadian markets in 2024 after a trial failed to confirm benefit. Ask your clinician about current options in your region. Drugs.com

8) Will anticholinergic drooling medicines hurt my eyes?
They can worsen dryness or blur near vision. Glycopyrrolate tends to have fewer brain effects; dosing must be individualized. If pills cause problems, Botox to salivary glands avoids whole-body side effects. PMC+1

9) Do nutrition and hydration really change eye comfort?
Yes. Adequate fluids and balanced fats (including omega-3s) support tear film quality; dehydration and alcohol worsen dryness. FDA Access Data

10) Does NIV help only breathing, or overall quality of life too?
NIV clearly improves sleep-related symptoms and quality of life and can extend survival, especially when bulbar function is relatively preserved. Better rest helps you sustain reading and eye-tracking sessions. PubMed

11) Can retinal scans diagnose ALS?
No. OCT findings vary and are not diagnostic. They are research tools that may one day help track disease. PMC

12) Are there exercises to “strengthen” the eyes?
You can’t strengthen nerves damaged by ALS, but practical strategies—blink routines, reading ergonomics, lighting, and lubricants—make a big difference.

13) Is double vision part of ALS?
It’s uncommon. If it appears, your doctor will also look for other causes. Temporary prisms can help selected cases.

14) Will I need eye surgery?
Usually not. Most problems are managed with drops, devices, or small procedures like punctal plugs; protective eyelid surgery is reserved for severe exposure.

15) Who should be on my team?
Neurologist (ALS clinic), neuro-ophthalmologist, SLP (AAC), OT/PT, respiratory therapy, dietitian, and social work—coordinating care reduces complications and helps you communicate better. PubMed

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Safe, practical care plan you can start discussing today

• Schedule a neuro-ophthalmology visit to baseline your eye movements, blink, and ocular surface.

• Build an eye-comfort routine: preservative-free tears by day, gel at night, warm compresses, humidifier, and regular blink breaks.

• Optimize your communication setup: early SLP/OT involvement for eye-tracking, seating, screen angle, and lighting. PMC

• Discuss disease-modifying therapy eligibility: riluzole/edaravone for most; genetic testing if family history or early onset to see if tofersen applies. U.S. Food and Drug Administration

• Manage drooling early to protect skin and devices (glycopyrrolate → scopolamine → Botox if needed). PMC

• Plan respiratory care (NIV) and nutrition sooner rather than later; these improve stamina for communication and daily life. PubMed

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 15, 2025.

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