Visual Symptoms of Parkinson’s Disease

Visual symptoms of Parkinson’s disease are problems with how the eyes move, how comfortable the eyes feel, and how the brain handles visual information. They can include dry eyes, blurry vision, double vision, trouble reading, difficulty seeing in low light or low contrast, problems with depth perception, color vision changes, slower visual processing, and visual hallucinations (seeing things that are not actually there). These changes happen because Parkinson’s affects dopamine—a chemical that helps control movement—in several places: the retina (the “film” at the back of the eye), the brain circuits that guide eye movements, and the brain networks that interpret what we see. As Parkinson’s progresses, these visual issues can become more noticeable and can affect daily tasks like reading, walking safely, recognizing faces, and driving. Research shows that dry eye is very common in Parkinson’s, that the retina can thin on specialized scans, and that visual hallucinations can appear, especially later in the disease or when certain medicines are used. Parkinson’s FoundationPMC+2PMC+2

Visual symptoms of Parkinson’s disease (PD) are problems with seeing and using vision that happen because PD affects not only movement but also the eyes, retina, eye movements, and brain’s visual networks. People with PD can have blurry or fluctuating clarity, reduced contrast (things look “washed out”), color changes (especially blue–yellow), double vision (often up-close while reading), dry, irritated eyes, eyelid spasms or trouble opening the lids, trouble tracking or shifting gaze, reading slowdowns, glare and light sensitivity, depth-perception errors (steps, curbs), and visual illusions or hallucinations.

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Types

1) Ocular surface problems (the front of the eye)

• Dry eye: People with Parkinson’s blink less, so tears evaporate faster. This makes the eyes feel gritty, sore, and watery and can blur vision. It can also make light feel harsh. Parkinson’s FoundationPMC

2) Ocular motor problems (how the eyes move)

• Convergence insufficiency: The eyes struggle to turn inward for near tasks. Result: double vision at near and eye strain while reading.

• Saccadic hypometria: Your quick eye jumps are too short, so reading lines or shifting gaze is harder.

• Smooth pursuit impairment: The eyes don’t track a moving target smoothly, so moving scenes feel jumpy. PMC+1

3) Pupillary and focusing problems

• Subtle changes in pupil reactions and accommodation (near focus) can add to blur or slow refocusing, especially with age and autonomic changes in Parkinson’s. (These are less prominent than other features but can contribute.)

4) Retinal/contrast and color vision problems

• The retina, which has dopamine-sensitive cells, may thin on OCT scans. People can have reduced contrast sensitivity (harder to see in dim light or fog) and color vision changes. PMC+1

5) Visual processing problems (how the brain interprets images)

• Slower visual processing and visuospatial problems: judging distance, navigating clutter, and recognizing faces can become difficult, especially in complex environments. PubMed

6) Visual hallucinations and illusions

• Minor hallucinations (a sense that someone is passing by, or brief “corner-of-the-eye” images) and formed visual hallucinations (seeing people, animals, or objects) are common as the disease advances or with certain drugs. Hallucinations can start mildly and become more frequent over time. PMC

7) Medication-related visual issues

• Some Parkinson’s medicines (especially anticholinergics and, in some people, dopamine agonists or amantadine) can worsen blurry vision or trigger hallucinations. Parkinson’s Foundation

8) Device-related changes

• After deep brain stimulation (DBS), convergence problems may appear or worsen in some people, especially at certain settings, leading to near double vision. Parkinson’s Foundation

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Causes

1. Reduced blinking – Parkinson’s lowers blink rate, so tears evaporate faster, causing dry eye and blurry vision. Parkinson’s FoundationPMC

2. Meibomian gland dysfunction – The oily layer of tears can be poor, making the tear film unstable and vision fluctuate.

3. Dopamine loss in the retina – Dopamine helps retinal cells signal contrast and color. Loss can reduce contrast sensitivity and color discrimination. PMC

4. Retinal thinning – Measurable thinning of the retinal nerve fiber layer (RNFL) or ganglion cell layer on OCT relates to visual performance and may track disease severity. PMC

5. Saccadic hypometria – Eye “jumps” undershoot targets, making reading and scanning slower. PMC

6. Smooth pursuit impairment – Following moving objects is less smooth, so motion feels jerky or uncomfortable. PMC

7. Convergence insufficiency – Eyes don’t turn inward well for near tasks, causing near double vision and eye strain. PMC

8. Accommodation problems – Focusing up close can be slower or weaker, adding to blur and reading fatigue, especially with age and autonomic changes.

9. Pupillary changes – Subtle changes in pupil reactions can contribute to glare and focus problems.

10. Visual processing slowdown – The brain takes longer to process complex scenes, so cluttered places or fast visual changes feel overwhelming. PubMed

11. Visuospatial difficulties – Judging distances (e.g., stairs, curbs), navigating in low light, and recognizing faces can be hard.

12. Hallucinations from disease progression – As Parkinson’s advances, visual hallucinations may appear due to changes in brain networks that integrate vision, attention, and memory. PMC

13. Medication-induced hallucinations – Dopamine agonists, anticholinergics, or amantadine can trigger or worsen hallucinations in susceptible people. Clinical guidance recommends reducing culprit medications first if possible. NICE

14. Parkinson’s disease dementia (PDD)/Lewy body pathology – Cognitive changes and specific Lewy body patterns increase the risk of hallucinations and misperceptions. PMC

15. Coexisting eye disease – Cataract, glaucoma, macular degeneration, or uncorrected refractive error can add blur, glare, and distortion, complicating Parkinson’s-related vision issues.

16. Autonomic dysfunction – Tear production and pupil control rely on the autonomic nervous system; Parkinson’s can affect these pathways.

17. Post-DBS changes – Some visual issues (especially convergence) can appear or worsen with certain DBS parameters. Adjustments may help. Parkinson’s Foundation

18. Poor lighting and low contrast environments – Because contrast sensitivity is commonly reduced, dim or shadowed areas make seeing details harder. PubMed

19. Sleep and fatigue effects – Tiredness and poor sleep can worsen hallucinations and visual discomfort. Parkinson’s UK

20. Orthostatic hypotension (drop in blood pressure on standing) – Can cause brief graying or blurring of vision and unsteadiness when getting up quickly (common in Parkinson’s with autonomic involvement).

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Symptoms

1. Dry, gritty, or burning eyes – Eyes feel uncomfortable; vision may blur between blinks.

2. Watery eyes – Reflex tearing can happen because the surface is actually dry; tears don’t stay stable.

3. Blurry vision – From dry eye, focusing problems, or coexisting eye disease; often worse later in the day.

4. Double vision – Especially at near (reading), due to convergence insufficiency; sometimes at distance. Parkinson’s Foundation

5. Eye strain and headaches with reading – The visual system works harder to keep text single and clear.

6. Difficulty tracking moving objects – Sports on TV, busy streets, or scrolling screens feel jumpy.

7. Trouble in low light or low contrast – Dim restaurants, dusk, fog, or patterned floors are hard to navigate. PubMed

8. Glare and light sensitivity – Bright light or oncoming headlights bother the eyes.

9. Faded colors – Colors look less vibrant; distinguishing shades (especially blues) is harder. PubMed

10. Slow refocusing – Shifting between near and far (phone ↔ TV) feels slow.

11. Depth-perception problems – Misjudging curbs, steps, or reaching for objects; spills or stumbles can happen.

12. Reading difficulties – Losing place on the page, skipping words or lines, reading fatigue.

13. Visual misperceptions – Shadows look like people or animals; patterned carpets look like obstacles.

14. Visual hallucinations – Seeing figures, animals, or shapes that aren’t there; can start mild and become more formed over time. PMC

15. Fluctuating vision – Good moments and bad moments; stress, fatigue, or medication timing can change how well you see.

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Diagnostic tests

Below are common tests grouped into Physical Exam, Manual Tests, Lab/Pathological Tests, Electrodiagnostic Tests, and Imaging Tests. Not everyone needs all tests. Clinicians choose based on your symptoms and safety needs.

A) Physical Exam (what the clinician observes directly)

1. External eye and eyelid exam
   The clinician looks for redness, lid margin inflammation, blepharitis (eyelid oil-gland irritation), and incomplete blinking. They observe blink rate because a low blink rate suggests dry eye risk in Parkinson’s. PMC

2. Tear film evaluation at the slit lamp
   A microscope light (slit lamp) shows whether the tear film is smooth or breaks up quickly. Rapid tear film breakup supports dry eye as a cause of blur or discomfort. PMC

3. Cranial nerve and ocular alignment check
   The clinician checks eye positions, alignment, and extraocular muscle function—important to detect convergence insufficiency or subtle strabismus (eye misalignment) that causes double vision. Parkinson’s Foundation

4. Ocular motility exam (saccades and pursuit at bedside)
   They ask you to look quickly between two targets (saccades) and follow a moving target (smooth pursuit). Short saccades (hypometria) and jerky pursuit suggest Parkinsonian ocular motor involvement. PMC+1

5. Pupil exam and light responses
   They look for abnormal pupil size or slow light responses that could add glare or focus difficulties (often mild but worth noting).

B) Manual tests (simple tools done in the clinic)

6. Near point of convergence (NPC)
   A small target is brought closer to your nose to see where double vision appears. A remote NPC supports convergence insufficiency—a key cause of near blur/diplopia in Parkinson’s. PMC

7. Cover–uncover and alternate cover tests
   Covering one eye at a time reveals hidden misalignment. This identifies small deviations that may cause intermittent double vision, especially when tired.

8. Reading acuity and speed assessment
   Timed reading passages reveal visual fatigue, line skipping, or slowed tracking, common in convergence and saccadic problems.

9. Contrast sensitivity testing
   Charts with faint gray stripes measure contrast sensitivity—often reduced in Parkinson’s—even when standard visual acuity (the “20/20” chart) looks okay. PubMed

10. Color vision testing
    Ishihara or Farnsworth tests check color discrimination, which can be subtly impaired in Parkinson’s. PubMed

11. Amsler grid
    A simple square grid screens for distortion or missing areas in central vision, helping rule out macular disease that could be adding to Parkinson’s-related problems.

12. Schirmer test / tear meniscus assessment
    Filter paper measures tear production (Schirmer), and clinicians can also judge tear volume at the slit lamp; Parkinson’s often shows shorter tear breakup time and lower secretion. Nature

C) Lab and pathological tests (to exclude other causes that can worsen vision or cause hallucinations)

13. Basic blood tests
    Complete blood count, electrolytes, kidney and liver function can rule out metabolic problems or infection that may worsen confusion or hallucinations.

14. Vitamin B12 and thyroid tests
    Low B12 or thyroid imbalance can affect cognition, fatigue, and visual comfort; treating them can reduce overlapping symptoms.

15. Urinalysis and infection screens
    Infections (like urinary tract infections) can trigger sudden confusion or hallucinations in older adults with Parkinson’s; checking and treating them helps stabilize vision-related complaints.

16. Medication review (structured)
    While not a “lab,” a systematic review of current medications is essential to spot drugs that worsen blur or hallucinations (e.g., anticholinergics, some dopamine agonists, amantadine). Guidelines recommend reducing the culprit if safe. NICE

D) Electrodiagnostic tests (measure electrical activity of the eyes/visual system)

17. Electroretinography (ERG)
    ERG measures the retina’s electrical response to light. Changes can reflect dopamine-related retinal dysfunction and correlate with contrast or color issues in Parkinson’s.

18. Visual evoked potentials (VEP)
    VEP tracks the brain’s response to visual stimuli and can show slowed conduction or processing delays that align with subjective complaints in Parkinson’s.

19. Instrumented eye movement recording (video-oculography)
    Infrared cameras objectively measure saccades, pursuit, and convergence, quantifying the Parkinsonian patterns (e.g., short saccades, pursuit deficits). PMC

E) Imaging tests (picture-based tests)

20. Optical coherence tomography (OCT)
    OCT is a painless scan that measures retinal nerve fiber layer (RNFL) and ganglion cell thickness. Studies show thinning in Parkinson’s and links to disease severity; OCT can also rule out macular disease. PMC

Non-pharmacological treatments (therapies & practical fixes)

(Each includes description → purpose → mechanism of help)

1. Comprehensive eye exam + PD-aware refraction → find correct glasses, screen other eye disease → reduces blur by fixing optical issues and tailoring lenses to CI.

2. Task lighting & contrast boosts (brighter, even light; high-contrast labels, bold fonts, dark-on-light) → clearer edges → extra photons + stronger signal offsets low contrast. PMC

3. Prism lenses (often base-in for near) → align images in CI → bends light so both eyes see one image. Parkinson’s FoundationAPDA Parkinson

4. Convergence exercises (pencil push-ups, Brock string, vectograms) → strengthen near alignment → repeated vergence practice improves fusional reserves. PMC

5. Reading strategy reset (single-vision reading glasses, larger print, line guide; avoid progressives for prolonged near) → steadier near focus → decreases lens-induced image jump and CI strain. Journal of Optometric Education

6. Low-vision rehab (occupational therapy, magnifiers, e-readers) → independence → magnification and task redesign raise effective retinal signal.

7. Blink training + 20-20-20 breaks → wetter surface → restores tear film spread disrupted by low blink rate. PMC

8. Lid hygiene & warm compress (blepharitis care) → smoother tear lipids → less evaporation, clearer optics.

9. Humidify, hydrate, screen ergonomics → kinder micro-climate → reduces evaporation strain on the tear film.

10. Glare control (anti-glare lenses, hats, visors) → comfort, contrast → lowers stray light and veiling glare.

11. Home contrast cues (bold stair-edge tape, bigger clock faces, matte finishes) → safer mobility → enhances edge detection/depth cues.

12. Simplify visual clutter (organized shelves, color-coding) → faster finding → trims visual crowding load.

13. Cueing for “freezing” (floor stripes, metronome, laser canes) → smoother gait → strong visual cues bypass impaired internal timing.

14. Sleep hygiene / brighter daytime light → fewer illusions at dusk, steadier attention → improves circadian stability.

15. Care-partner education (reassurance scripts for hallucinations) → calmer episodes → reduces arousal, uses reality-orientation. Oxford Academic

16. Driving re-evaluation & route tweaks (daytime only, low-traffic routes) → safety → matches demand to reliable visual windows.

17. Falls-proofing with vision in mind (non-slip, contrast bathroom fixtures) → prevents injuries → reduces missteps from depth errors.

18. Task pacing (“ON” time scheduling) → schedule reading/screening during best motor/attention windows → leverages medication peaks.

19. Exercise that trains eyes & body together (tai chi, dance with gaze shifts) → steadier eye–head coordination → neuroplasticity and vestibulo-ocular practice.

20. Regular follow-ups with optometry/ophthalmology + neurology → early adjustments → keeps prisms, exercises, lighting, and meds optimized as PD evolves.

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Drug treatments

Always individualized by your clinician. Typical adult doses shown; your doctor may choose differently.

1. Carbidopa/Levodopa (dopamine replacement; DOPA precursor)
   Dose: often divided doses totaling ~300–1,000 mg levodopa/day.
   Purpose: may improve some eye-movement control and attention, indirectly helping reading/CI symptoms during “ON” periods.
   Mechanism: restores central dopaminergic tone. Side effects: nausea, dyskinesia, hallucinations in some.

2. Pimavanserin 34 mg once daily (5-HT2A inverse agonist)
   Purpose: treats hallucinations/delusions in PD psychosis without blocking dopamine.
   Mechanism: modulates cortical 5-HT2A signaling; does not worsen motor symptoms.
   Common effects: edema, nausea, QT prolongation risk. Evidence: FDA-approved at 34 mg based on randomized trials. FDA Access Data+1PMC

3. Clozapine (atypical antipsychotic; very low dose e.g., 12.5–50 mg/day)
   Purpose: gold-standard efficacy for PD psychosis when monitored.
   Mechanism: multi-receptor; minimal D2 blockade at low dose.
   Side effects: agranulocytosis risk → mandatory blood counts, sedation, orthostasis. Evidence: randomized trials show benefit without worsening motor function. New England Journal of MedicinePMC

4. Quetiapine (atypical antipsychotic; off-label, e.g., 12.5–50 mg hs)
   Purpose: alternative when clozapine monitoring not feasible; evidence mixed.
   Mechanism: 5-HT2A/D2 antagonism at low potency.
   Side effects: sedation, orthostasis; may not help everyone. Lippincott Journals

5. Rivastigmine (cholinesterase inhibitor; 1.5–6 mg bid or patch 4.6–13.3 mg/24 h)
   Purpose: for PD dementia; may reduce hallucinations/attention lapses that worsen visual symptoms.
   Mechanism: boosts cortical acetylcholine. Side effects: GI upset, bradycardia.

6. Melatonin (3–10 mg at night)
   Purpose: improves REM sleep behavior and nighttime visual phenomena for some.
   Mechanism: stabilizes circadian rhythms; Side effects: morning sleepiness.

7. Artificial tears (carboxymethylcellulose/glycerin; 1 drop up to qid+)
   Purpose: relieves dry eye blur/irritation.
   Mechanism: supplements tear film; Effects: transient blur, rare allergy. PMC

8. Topical cyclosporine 0.05% or lifitegrast 5%
   Purpose: chronic dry eye with inflammation.
   Mechanism: tames ocular surface inflammation; Effects: stinging, slow onset (weeks).

9. Botulinum toxin A (specialist-injected units, q3–4 months)
   Purpose: blepharospasm or eyelid-opening apraxia affecting vision.
   Mechanism: weakens overactive orbicularis muscle to open sightline.
   Effects: temporary ptosis/dry eye if spread. Evidence: first-line for blepharospasm; helpful for lid-opening issues. American Academy of OphthalmologyMedscapeScienceDirect

10. Lubricating gel/ointment at bedtime
    Purpose: night comfort, morning clarity.
    Mechanism: longer-lasting tear protection; Effects: temporary blur on application.

Medication note: doctors often first remove or reduce drugs that trigger psychosis (e.g., anticholinergics, some dopamine agonists) before adding antipsychotics. Parkinson’s Foundation

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Dietary “molecular” supplements*

None of these is a cure; most have limited or mixed evidence for PD visual symptoms. Discuss with your clinician (interactions are possible). Typical doses are common practice ranges, not personal advice.

1. Omega-3 (EPA+DHA 1 g/day) → anti-inflammatory tear film support; may ease dry eye quality.

2. Lutein 10 mg + Zeaxanthin 2 mg/day → macular pigment support; potential contrast help in general eye health.

3. Vitamin D3 (1,000–2,000 IU/day) → widespread deficiency in PD; supports neuromuscular/immune function.

4. Vitamin B12 (≈1,000 µg/day if low) → helps prevent optic neuropathy-like symptoms from deficiency.

5. CoQ10 (100–300 mg 2–3×/day) → antioxidant; did not show disease-modifying benefit in PD trials, but some use for fatigue.

6. Curcumin (≈500 mg 1–2×/day with pepper/optimized forms) → anti-inflammatory; limited human PD data.

7. Resveratrol (100–250 mg/day) → antioxidant; limited PD data.

8. N-acetylcysteine (600–1,200 mg/day) → glutathione precursor; research ongoing.

9. Caffeine (1–2 cups coffee/day if tolerated) → may modestly help alertness/motor function; can worsen tremor/anxiety.

10. Magnesium glycinate (100–200 mg at night) → may aid sleep/eyelid spasm comfort in some; GI caution.

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Regenerative / stem-cell” approaches

These are research/clinical-trial directions, not approved treatments for PD visual symptoms. No self-dosing—participation is protocol-based.

1. Anti-α-synuclein antibodies (e.g., prasinezumab) — aim to clear toxic protein; trials ongoing; uncertain clinical benefit.

2. Gene therapy (e.g., AAV2-AADC) — boosts dopamine-making enzymes; motor-focused; visual impact unknown.

3. GDNF/NRTN neurotrophic delivery — mixed results historically; still experimental.

4. iPSC-derived dopaminergic neuron grafts — early human studies; long-term safety/benefit being evaluated.

5. Adaptive/next-gen DBS — motor-focused; indirect visual effects vary; still being optimized.

6. Microglia/immune-modulating agents — theoretical neuroprotection; not standard care.

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Procedures/surgeries

1. Deep Brain Stimulation (STN/GPi) — for motor fluctuations/dyskinesia, not a direct vision surgery. Hallucinations can improve, persist, or (rarely) appear; careful candidate selection is crucial. PubMed+1The Journal of Neuroscience

2. Cataract extraction — if cataract is present, clearing the cloudy lens improves brightness, contrast, and safety; PD itself isn’t a barrier with good planning. PMCPubMed

3. Blepharospasm surgery (myectomy) ± botulinum toxin — for severe, refractory eyelid closure preventing vision. PubMed

4. Punctal occlusion (plugs) — helps severe dry eye by reducing tear drainage when drops are not enough.

5. Strabismus surgery — rare, for stable, large misalignment not correctable with prisms/therapy. Semantic Scholar

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Practical preventions

1. Yearly (or sooner) eye exams with PD-aware clinician.

2. Bright, even lighting at home; night-lights in halls/ bathrooms.

3. High-contrast edges on stairs/steps and in bathrooms.

4. Regular blink breaks during screens; humidifier use.

5. Use single-vision readers + line guides for long reading sessions. Journal of Optometric Education

6. Keep glasses current; consider prism for near diplopia. Parkinson’s Foundation

7. Declutter visual spaces; label shelves with bold print.

8. Schedule visually demanding tasks during “ON” times.

9. Review meds with your doctor for hallucination risk. Parkinson’s Foundation

10. Exercise, sleep regularity, hydration to support attention and tear film.

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When to see a doctor

Seek urgent care now if you have: sudden vision loss, painful red eye, new continuous double vision, sudden dense floaters/flashes, or rapidly worsening hallucinations with unsafe behavior.
See your eye doctor soon for: new near diplopia, persistent blur or glare, gritty burning, trouble reading despite glasses, eyelid squeezing/opening trouble, or recurrent visual illusions.
See neurology promptly if hallucinations start or escalate, reading/freezing worsens, or vision issues clearly track medication changes (may need dose or drug adjustments). Parkinson’s Foundation

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What to eat — and what to avoid

To eat (most days):

1. Leafy greens (spinach, kale) — lutein/zeaxanthin for macular health.

2. Colored veggies (peppers, carrots) — carotenoids for glare/contrast support.

3. Oily fish (salmon, sardines 2×/wk) — omega-3 for tears and anti-inflammation.

4. Berries/citrus — flavonoids for vessel/antioxidant support.

5. Nuts/seeds — vitamin E and healthy fats.

6. Whole grains/legumes — steady energy for reading sessions.

7. Adequate water — tear film stability.

8. Coffee/tea in moderation — alertness (if tolerated).

9. Probiotic foods — general gut–brain support.

10. Bright-colored fruits/veg at dinner — evening vision comfort.

To limit/avoid:

1. Very high-protein at levodopa times (can interfere; many patients use “protein redistribution”—ask your doctor).

2. Alcohol excess (blurs, worsens balance).

3. Heavy evening caffeine (sleep disruption → more illusions).

4. Ultra-processed, high-sugar foods (energy crashes).

5. Trans fats (inflammation).

6. Very spicy/salty snacks if they worsen dry eye symptoms.

7. Mega-dose vitamin A (optic toxicity risk).

8. Unvetted supplements that interact with PD meds.

9. Dehydration (worse tear film).

10. Grapefruit if on interacting meds (ask your clinician/pharmacist).

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FAQs

1) Are vision problems part of PD?
Yes—retina, eye movements, and brain networks are involved, so vision can be affected in many ways. PMC+1

2) Why do I see double when I read?
Often convergence insufficiency; prisms and exercises help. PMC+1

3) Why are things “washed out”?
Reduced contrast sensitivity from retinal dopamine changes. PMC

4) Why do I get blurry/watery eyes?
Low blink rate → dry eye; drops, lid care, humidifiers help. PMC

5) What about hallucinations—am I “losing my mind”?
Visual hallucinations are a known PD symptom; talk to your doctor—effective treatments exist. Oxford Academic

6) Which antipsychotics are safest in PD?
Pimavanserin (34 mg daily) is FDA-approved; clozapine is very effective with blood monitoring; quetiapine has mixed evidence. FDA Access DataNew England Journal of MedicineLippincott Journals

7) Can DBS fix vision symptoms?
DBS is for motor issues. Visual symptoms may improve, persist, or rarely worsen; selection and counseling matter. PubMed+1

8) Do progressive lenses make reading harder?
They can in PD with CI; single-vision readers often work better for long reading. Journal of Optometric Education

9) Are eye exercises real?
For CI, orthoptic exercises have structured programs that can help. PMC

10) Are prisms a permanent solution?
They help symptoms and can be adjusted as PD changes. Parkinson’s Foundation

11) Should I change my home for safety?
Yes—contrast strips, brighter light, declutter reduce falls and visual confusion.

12) Do supplements cure PD vision problems?
No. Some support eye comfort/health; evidence is limited—discuss with your clinician.

13) Can my medications be causing hallucinations?
Sometimes. Doctors often reduce offending PD meds before adding antipsychotics. Parkinson’s Foundation

14) Why is reading slow?
PD can cause longer fixations and more regressions; magnification and pacing help. PMC

15) How often should I get eye checks?
At least yearly (sooner with new symptoms or treatment changes).

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 30, 2025.