Neurotrophic keratitis is an eye surface disease caused by poor corneal nerve function. The clear front window of the eye is called the cornea. The cornea needs a healthy nerve supply from the trigeminal nerve to stay alive and to heal after tiny injuries. These nerves send feeling to the cornea, and they also release growth signals that keep the corneal surface healthy. When the nerves are damaged or weak, the cornea becomes numb or less sensitive. A numb cornea does not feel pain well. A numb cornea also does not heal well. The surface cells break down easily, and small defects can become ulcers. Because the cornea is numb, people may have fewer symptoms even when the surface is injured. This is why neurotrophic keratitis is tricky and dangerous. A painless defect can grow into a deep ulcer, thinning, or even a hole in the cornea if not treated.
Neurotrophic keratitis (NK) is a corneal healing disorder caused by damage to the eye’s sensory nerve (the trigeminal nerve). When this nerve does not work properly, the cornea loses feeling and the surface stops repairing itself. That leads to fragile skin on the eye (the epithelium), non-healing defects, infections, thinning, ulcers, and—if untreated—perforation. Doctors often grade NK in three stages (Mackie classification) from early surface changes (stage 1) to a non-healing defect (stage 2) to a deep ulcer or melting/perforation (stage 3). NCBIScienceDirect
Neurotrophic keratitis means the cornea can no longer “sense” the world properly because its nerve supply is damaged. Sensation is not just for pain—corneal nerves release “growth” signals that keep the surface moist, stable, and quick to heal. Without those signals, the surface dries out, tiny scratches do not heal, bigger defects form, germs can invade more easily, and the tissue can thin or even perforate. People with NK often do not feel much pain, even when the eye looks very irritated or badly damaged. That “quiet” pain response is a hallmark of NK and an important reason it can be missed until it is advanced. NCBI
Corneal nerves do three important jobs. First, they tell you to blink when something touches your eye. Blinking spreads tears and protects the surface. Second, they trigger reflex tears when the eye is dry or irritated. Reflex tears wash and nourish the cornea. Third, the nerves release chemical messengers, such as growth factors, that help the surface cells grow, stick together, and repair damage. When nerves are lost or weak, all three jobs fail. Blinks are slower. Tears are fewer. Healing is poor. The corneal surface dries, breaks down, and gets infected more easily. That is the core problem in neurotrophic keratitis.
Types
Doctors often describe NK by severity. This helps plan care.
Stage 1 (Mild surface disease):
The corneal surface looks rough and dry. There are small punctate spots that stain with dye. The cornea may look dull. There is usually reduced feeling when gently tested. Healing is slower than normal, but there is no open defect yet.Stage 2 (Persistent epithelial defect):
There is an actual open area on the corneal surface that does not heal in the usual time. The edges of the defect may look rolled or loose. The base looks smooth and does not show healthy healing tissue. This stage needs careful protection and support to prevent deeper damage.Stage 3 (Ulcer, thinning, or perforation):
The defect goes deeper into the corneal stroma. The cornea may thin. There can be melting of tissue from enzymes and inflammation. In worst cases, a tiny hole forms and fluid leaks from the eye. This is an emergency because it can threaten vision and the eye’s structure.
Congenital vs acquired: present from birth (rare) or developed later in life.
Peripheral nerve, ganglion, or brainstem origin: the injury can be in the cornea itself, in the ophthalmic branch (V1), at the trigeminal ganglion, or in the brainstem where corneal nerves connect.
Transient vs chronic: sometimes the nerve loss is temporary after surgery; sometimes it is long-term due to disease.
Causes of Neurotrophic Keratitis
Herpes simplex virus (HSV) infection:
HSV can damage corneal nerves during active infection or from repeated inflammation. The nerve loss can persist even when the infection looks quiet.Herpes zoster ophthalmicus (shingles involving the eye):
Varicella zoster virus can injure the ophthalmic branch of the trigeminal nerve. This reduces corneal feeling for months or permanently.Diabetes mellitus:
Diabetes can cause small-fiber neuropathy in many places, including the cornea. Corneal nerve density drops, corneal feeling falls, and healing slows.Surgery for trigeminal neuralgia (nerve ablation or alcohol injection):
Procedures that cut, compress, or chemically injure the trigeminal nerve can reduce corneal sensation as an unintended effect.Brainstem stroke or demyelinating disease affecting trigeminal pathways:
Lesions in the pons or medulla can interrupt corneal sensory signals, leading to NK.Skull base tumors (meningioma, schwannoma) compressing the trigeminal nerve or ganglion:
Pressure on the nerve reduces nerve traffic to the cornea and causes loss of feeling.Vestibular schwannoma (acoustic neuroma) surgery:
Skull base surgery near the trigeminal nerve can injure sensory fibers and reduce corneal sensation.Orbital or facial trauma affecting the ophthalmic branch (V1) or ciliary nerves:
Fractures, lacerations, or surgical scars can harm the small nerves that feed the cornea.Chemical burns (especially alkali burns):
Strong chemicals destroy corneal epithelium and nerves. Healing after a burn is slow, and nerve recovery can take a long time.Thermal or radiation injury to the cornea or orbit:
Heat or radiation can damage delicate nerve fibers and reduce corneal feeling.Long-term contact lens overuse or misuse:
Chronic mechanical stress and reduced oxygen can lower corneal sensitivity over time.Chronic abuse of topical anesthetic eye drops:
Frequent numbing drops are toxic to the cornea and its nerves. They stop pain but block healing and can cause severe, painless ulcers.Toxicity from frequent preserved eye drops (for example, long-term benzalkonium chloride exposure):
Some preservatives irritate the ocular surface and can harm nerves with heavy, long-term use.Refractive surgery (LASIK, PRK):
These procedures cut corneal nerves. Sensation usually improves over months, but some patients have longer-lasting reduction.Corneal transplant (keratoplasty):
Graft surgery severs nerves. Nerve regrowth is slow, and sensation may remain low, especially at the graft-host junction.Phototherapeutic keratectomy (PTK):
Laser polishing of the corneal surface can also reduce nerve density for a period.Corneal cross-linking:
This strengthens corneal collagen but can temporarily reduce nerve fibers until regeneration occurs.Leprosy (Hansen disease):
The bacterium can involve cranial nerves and cause corneal anesthesia.Congenital corneal anesthesia (isolated or with syndromes):
Rare conditions at birth cause very poor or absent corneal sensation. Children may rub their eyes and cause damage because they do not feel pain.Systemic neuropathies and deficiencies (for example, severe alcoholism-related neuropathy or advanced B-vitamin deficiency):
Widespread nerve damage can include the small fibers that serve the cornea.
Symptoms
A key feature of neurotrophic keratitis is less pain than expected. Many symptoms are mild or even absent despite serious surface damage. Here are 15 possible symptoms in simple words:
Reduced or absent eye pain even with injury:
You may not feel the usual pain from a corneal scratch or ulcer.Mild redness that does not match the severity of the problem:
The eye can look only slightly red even when the surface is quite unhealthy.Blurred or fluctuating vision:
A rough or open surface scatters light and reduces clarity.Dry or gritty feeling may be less than expected:
Because nerves are weak, the dry feeling may be muted or absent.Mild tearing or sometimes fewer reflex tears:
Reflex tear production is blunted, so the eye may actually water less.Light sensitivity can be mild or variable:
Photophobia may be present, but it is often less than in other corneal diseases.Foreign body sensation may be faint:
Even with debris or a defect, the eye may not “feel” it strongly.Stringy or mucous discharge:
A stressed surface makes unstable tear film and mucous strands.Feeling of “filmy” or foggy vision in the morning:
The surface can dry overnight and blur vision on waking.Slow recovery after minor irritations:
Small scratches take a long time to heal and may reopen.Recurrent erosions but oddly little pain:
The surface can break open repeatedly with less discomfort.Contact lens intolerance or poor comfort:
The surface cannot tolerate lenses well and becomes unstable.Worsening vision without dramatic symptoms:
Vision can slowly decline even though the eye “doesn’t hurt.”Poor healing after eye surgery:
Post-operative epithelial defects may persist longer than expected.In advanced disease, sudden drop in vision due to ulcer or thinning:
A painless ulcer can deepen and quickly affect sight.
Diagnostic Tests
Below are 20 tests grouped by category. Each test has a plain-English explanation of what it checks and why it matters for NK.
A. Physical Exam
1) Visual acuity testing (distance and near):
This is the basic eye chart test. It tells how clearly you can see. In NK, vision often drops because the corneal surface is rough or open. Tracking acuity over time helps show if the surface is improving or getting worse.
2) External exam of eyelids and blink rate:
The doctor watches how often you blink and whether your eyelids close fully. A slow blink or incomplete closure dries the cornea and worsens NK. Identifying poor blinking helps the doctor add treatments like lubrication or eyelid support.
3) Inspection of the tear meniscus and conjunctival redness:
The doctor looks at the ridge of tears along the lower lid and checks for redness in the white of the eye. Reduced tears and dryness raise concern in NK because a numb cornea does not trigger reflex tearing well. Subtle redness may hide serious surface disease.
4) Cranial nerve exam for facial and corneal sensation (light touch on forehead, cheeks, jaw):
The trigeminal nerve has three branches to the face. Testing sensation on the skin can show if there is a wider nerve problem, not just the cornea. Reduced feeling in the forehead (V1) can support the diagnosis of trigeminal dysfunction affecting the eye.
5) Corneal reflex (blink reflex) at the slit lamp:
A gentle stimulus near the cornea should cause a blink. In NK, this reflex may be weak or absent. Loss of this reflex means the eye is less protected and the surface is at higher risk.
B. Manual Tests
6) Cochet–Bonnet aesthesiometry (quantitative corneal sensitivity):
This is a thin nylon filament test. The doctor touches the cornea with a very fine thread and changes its length to measure how sensitive the cornea is. A longer filament is a gentler touch. If you do not feel even gentle touches, your corneal sensitivity is low. This is the hallmark of NK.
7) Cotton wisp corneal sensitivity (qualitative test):
A tiny wisp of cotton is brushed toward the cornea. In a healthy eye, this causes instant blink and discomfort. In NK, there may be little or no response. This simple test is helpful when specialized tools are not available.
8) Fluorescein staining and Seidel test for leaks:
A yellow dye called fluorescein shows surface defects under blue light. In NK, it can outline punctate staining or larger persistent defects. The Seidel test uses fluorescein to detect fluid leakage if there is a corneal hole. This is critical in advanced NK.
9) Lissamine green or rose bengal staining:
These dyes color dead or unprotected cells on the eye surface. In NK, the pattern often shows dry, damaged cells and mucous strands. It helps map the true extent of surface disease beyond what you can see with white light.
10) Tear breakup time (TBUT):
After fluorescein is placed, the doctor measures how long the tear film stays smooth before it breaks into dry spots. A short TBUT means the surface dries quickly. In NK, poor reflex tears and blinking cause early breakup.
11) Schirmer test (with or without anesthesia):
A small paper strip under the eyelid measures tear production over a few minutes. NK often shows reduced reflex tearing. If reflex tearing is low, the surface is at higher risk and needs more lubrication.
12) Non-contact gas aesthesiometry (if available):
Some clinics use a gentle puff of air at different intensities to measure corneal sensitivity without touching the eye. It gives a precise threshold number. Very high thresholds or no response confirm reduced sensitivity.
C. Lab and Pathological Tests
13) Corneal scraping for culture and microscopy (if infection suspected):
NK eyes are prone to infection because the surface barrier is weak. If there is an ulcer or infiltrate, the doctor gently scrapes the edge and base to check for bacteria, fungi, or amoebae. Pinpointing the organism guides targeted treatment and improves healing.
14) PCR testing for herpes viruses (HSV/VZV) on corneal or tear samples (when indicated):
If the pattern suggests a herpetic cause, polymerase chain reaction can detect viral DNA. A positive result supports the cause of nerve damage and can guide antiviral therapy.
15) Tear osmolarity or inflammatory marker testing:
These tests look at saltiness and inflammation in your tears. High osmolarity means the tear film is unstable and concentrated. In NK, poor reflex tearing often raises osmolarity, which harms cells and slows healing.
16) Impression cytology of the ocular surface:
A small filter paper gently touches the surface to collect cells. Under the microscope, the lab studies cell shape, goblet cell numbers, and signs of surface stress. In NK, the epithelium often looks unhealthy and shows squamous changes.
D. Electrodiagnostic Tests
17) Blink reflex study (electrophysiology of trigeminal–facial pathway):
This test measures the early (R1) and late (R2) blink responses after an electrical stimulus to the trigeminal nerve area. Delayed or absent waves point to a lesion along the corneal reflex arc. It helps localize whether the problem is in the peripheral nerve, ganglion, or brainstem.
18) Trigeminal somatosensory-evoked potentials (SSEPs):
This test tracks electrical signals from trigeminal stimulation up to the brain. Abnormal results show impaired sensory conduction. It is useful when MRI is normal but nerve function is clearly reduced.
E. Imaging Tests
19) In vivo confocal microscopy (IVCM) of the cornea:
This is a special microscope that looks at living corneal layers cell by cell. It can directly count and photograph the tiny nerve fibers in the sub-basal nerve plexus. In NK, nerve fibers are fewer, thinner, or absent. IVCM provides objective proof of nerve loss and can track regrowth over time.
20) Anterior segment OCT and brain/orbit MRI (two complementary studies):
Anterior segment optical coherence tomography (AS-OCT) gives high-resolution cross-sections of the cornea. It measures defect depth and thinning and helps watch healing. MRI of the brain and orbits follows the trigeminal nerve from the brainstem to the orbit. MRI can reveal tumors, inflammation, or compression along the nerve that explain the NK. Together, AS-OCT and MRI give both local and central views of the disease.
Non-pharmacological treatments
Goal: protect the surface, restore a healthy environment, and remove anything toxic while the cornea regrows.
Patient education and “no-numbing-drops” rule. Never use topical anesthetic at home; it worsens NK. EyeWikiReview of Optometry
Preservative-free care. Switch to preservative-free tears and avoid benzalkonium chloride (BAK) when possible to reduce toxicity. PMCEyeWiki
Aggressive lubrication schedule. Frequent non-medicated, preservative-free tears by day plus thick ointment at night to keep the defect moist.
Eyelid taping or sleep shields if lids don’t close fully.
Moisture-chamber goggles / humidifiers to cut evaporation at work and during sleep.
Blink training and “20-20-20” screen breaks to fight exposure from reduced blink.
Warm compresses & lid hygiene if blepharitis is present to stabilize the tear film.
Bandage contact lens (BCL)—a soft, sterile protective lens that reduces friction so the epithelium can regrow; used with antibiotic cover. PMCAAO
Scleral lens / PROSE device—a fluid-filled vault over the cornea that protects, hydrates, and often improves vision dramatically. PMCIOVS
Temporary “protective ptosis” with botulinum toxin—a small injection into the levator muscle makes the upper lid droop on purpose for weeks, shielding the cornea without suturing the lids. PubMed
Punctal plugs to keep more tears on the eye (non-surgical, removable).
Manage systemic triggers (tighten diabetes control; treat neuropathies).
Stop toxic surface meds (limit or replace preserved drops, avoid chronic vasoconstrictors). EyeWiki
Protective eyewear outdoors (wind/sun/dust protection).
Treat exposure problems (e.g., tape at night, moisture shields, consider ptosis or tarsorrhaphy if needed later).
Amniotic membrane (sutureless device like PROKERA®) placed in-office to supply growth factors and anti-inflammatory matrix that speeds epithelial closure. Annals of Eye SciencePubMed
Nutritional optimization (protein, vitamins A/C/D, zinc, omega-3s) to support wound healing (details in “What to eat”).
Avoid contact lens wear for vision only unless it is a medical BCL or scleral lens fit by a specialist.
Treat eyelid closure problems from facial palsy (taping, weights, or surgery if needed) to prevent exposure keratopathy.
Early referral for advanced care (amniotic membrane, cenegermin, neurotization) in stage 2–3 disease; early action prevents scarring. NCBI
Drug treatments
Always use preservative-free versions whenever possible in NK.
Cenegermin (OXERVATE®) – recombinant human nerve growth factor (rhNGF).
Class/Purpose: Regenerative biologic that restores corneal nerve signaling and promotes healing.
Dose & time: 1 drop, 6 times daily, about every 2 hours for 8 weeks (both eyes if needed). Space from viscous drops by ≥15 minutes.
Mechanism: Replaces NGF to stimulate epithelial cell survival, nerve regrowth, and tear reflex.
Common side effects: Eye pain, redness, foreign-body sensation, increased tearing.
Evidence: Pivotal trials led to approval; label specifies dosing above. FDA Access Data+1NCBI
Preservative-free artificial tears/gel/ointment.
Class: Lubricants.
Dose: Tears as often as needed (typically 6–10×/day); gel/ointment at night.
Purpose/Mechanism: Restores moisture and reduces friction while healing; no pharmacologic action; aim is constant surface protection.
Notes: Choose BAK-free formulas to avoid toxicity in NK. PMC
Autologous serum tears (20–50%, up to 100%).
Class: Patient-derived biologic drops rich in growth factors (vitamin A, EGF, fibronectin).
Dose: Typical 1 drop 6–8×/day; higher frequency during active defects.
Purpose/Mechanism: Mimics natural tear components that promote epithelial migration and adhesion.
Evidence: Long clinical experience and studies in persistent epithelial defects and NK show faster closure. PMC+1ScienceDirect
Platelet-rich plasma (PRP) eye drops.
Class: Blood-derived biologic (high in PDGF, TGF-β).
Dose: Often 4–8×/day.
Purpose/Mechanism: Supplies concentrated growth factors to accelerate epithelial healing and reduce inflammation; used when serum alone is not enough.
Evidence: Case series/observational data support benefit in PEDs. (Overview in ocular surface literature.)
Topical antibiotic prophylaxis (e.g., moxifloxacin 0.5%).
Class: Fluoroquinolone antibiotic.
Dose: 3–4×/day while the epithelium is open and any bandage/scleral lens is in place.
Purpose/Mechanism: Prevents secondary infection in a non-healing defect.
Evidence/Note: Standard when using BCLs and for open epithelial defects. AAOjournalofmedicaloptometry.com
Oral doxycycline (100 mg twice daily initially, then 50–100 mg daily).
Class: Tetracycline antibiotic with MMP-inhibiting and anti-inflammatory effects.
Purpose/Mechanism: Slows collagen breakdown (anti-collagenase) to reduce melting; helps the epithelium re-adhere.
Side effects: GI upset, photosensitivity; avoid in pregnancy/young children.
Evidence: Human/animal data support MMP inhibition and improved corneal healing in melting disorders. PMCWiley Online Library
Topical cyclosporine (0.05%–0.1%).
Class: Immunomodulator for ocular surface inflammation.
Dose: 1 drop twice daily.
Purpose/Mechanism: Calms surface inflammation, improves tear film quality, and may indirectly support nerve/epithelium recovery; recent work suggests benefit in herpetic-related NK.
Evidence: Early clinical data show reduced defects and better tear parameters in NK secondary to HSV. PubMedClinical Therapeutics
Topical insulin (off-label; compounded).
Class: Regenerative/epithelial trophic agent.
Dose: Commonly ~1 unit/mL, 3–4×/day, used 6–12 weeks; some reports use higher concentration more frequently.
Purpose/Mechanism: Stimulates epithelial cell migration and adhesion via insulin receptors.
Evidence: Small studies and recent reviews show promising epithelial closure in NK; still investigational. MDPIPMCNature
Anti-collagenase mucolytic support (topical N-acetylcysteine 5–10%).
Class: Mucolytic/anti-oxidant.
Dose: Typically 4×/day (compounded).
Purpose/Mechanism: Reduces mucus filaments and may blunt MMP activity; helpful when filamentary keratitis complicates NK.
Evidence: Case-based and review evidence support use in filamentary keratitis. PubMedScienceDirect
Vitamin C (ascorbic acid) supplementation (oral).
Class: Nutritional cofactor in collagen synthesis.
Dose: Typical safe range 500–1000 mg/day short term; avoid megadoses >2 g/day long term.
Purpose/Mechanism: Supports stromal collagen remodeling and reduces risk of melt.
Evidence: Clinical studies and lab data link adequate vitamin C with better corneal repair; avoid excessive dosing. PMC+1EyeWiki
Important: Topical corticosteroids are used cautiously (if at all) in NK; they can slow epithelial healing and increase thinning risk. Your specialist will decide case-by-case.
Dietary molecular supplements
These can support healing and nerve health but do not replace medical/surgical treatment. Discuss with your clinician—some interact with medications or are unsafe in pregnancy.
Omega-3 fatty acids (EPA+DHA 1000–2000 mg/day): Improve tear lipid layer, reduce surface inflammation, and support nerve membranes.
Vitamin A (prefer beta-carotene sources; if supplementing retinol, keep to RDA unless medically supervised): Critical for epithelial differentiation and mucin production.
Vitamin C (500–1000 mg/day short term): Collagen cross-linking and antioxidant support during repair. PMC
Vitamin D3 (1000–2000 IU/day if deficient): Immune modulation; low D is linked with worse ocular surface symptoms.
Zinc (10–20 mg/day for a limited course): Cofactor in epithelial repair and immunity; avoid long-term high doses.
Vitamin B12 (1000 mcg/day oral or as directed if deficient): Supports peripheral nerve health and myelination.
Alpha-lipoic acid (ALA 600 mg/day): Antioxidant used in diabetic neuropathy; may help nerve health.
L-carnitine (1–2 g/day): Mitochondrial energy support; sometimes used in neuropathic conditions.
Curcumin (500–1000 mg/day with bioavailability enhancer): Anti-inflammatory/antioxidant; limited ocular-specific data.
Lutein + Zeaxanthin (10 mg + 2 mg/day): Antioxidant carotenoids that support ocular tissues and tear film quality.
Regenerative / “hard immunity-booster” / stem-cell–related options (
These focus on regeneration and biologic repair. Some are established, others are still emerging.
Cenegermin (rhNGF; see above): FDA-approved regenerative drop that replaces missing nerve growth signals; standard regimen is 6×/day for 8 weeks. FDA Access Data
Autologous serum tears (20–100%) or PRP drops: Patient-derived growth factors (EGF, fibronectin, PDGF) promote epithelial migration and adhesion; dose typically 6–8×/day. PMC
Umbilical cord serum drops (allogeneic; where available): Higher growth-factor content than adult serum; used 6–8×/day in specialized centers when personal serum is not possible (investigational in many regions).
Thymosin β4 (RGN-259; investigational): A naturally occurring peptide with pro-healing, anti-inflammatory actions; early studies in neurotrophic PEDs reported rapid re-epithelialization in small cohorts. Frontiers
Topical insulin (compounded; off-label): 1 U/mL, 3–4×/day is common in studies; stimulates epithelial migration via insulin receptors; promising but not yet standard of care. MDPI
Mesenchymal stem-cell secretome / conditioned media (investigational): Delivers paracrine growth factors and anti-inflammatory cytokines to enhance epithelial healing; currently limited to trials/experimental protocols.
Surgeries
Tarsorrhaphy (temporary or permanent)
What: Partially sewing the eyelids together (or creating a temporary droop with botulinum) to physically shield the cornea.
Why: Reduces exposure and evaporation so the defect can close; often used for stage 2–3 or when other measures fail. (Protective ptosis via botulinum can be a non-sutured alternative.) PubMed
Amniotic membrane transplantation (AMT)
What: Sutured or sutureless (e.g., PROKERA®) placement of cryopreserved amniotic membrane over the cornea.
Why: The membrane provides a biologic scaffold with growth factors that speeds epithelial closure and dampens inflammation/pain. Lippincott JournalsAnnals of Eye Science
Punctal cautery (surgical tear-drain closure)
What: Thermally sealing the tear drains to keep more natural and applied tears on the eye permanently (or long-term).
Why: For severe aqueous tear deficiency or repeated plug loss; improves surface hydration and lowers risk of melt. PMC+1
Conjunctival (Gundersen) flap
What: Sliding a thin, living conjunctival flap over the cornea.
Why: Covers and nourishes a dangerously thin, non-healing cornea to prevent perforation and calm inflammation; vision is blurred while flap is in place but the globe is saved. PMCAnnals of Eye Science
Corneal neurotization
What: Microsurgery that brings a healthy sensory nerve (often supraorbital/supratrochlear via graft, e.g., sural nerve) to the cornea.
Why: Addresses the root cause—lost innervation—so sensation and blink reflex can return over months; a durable option for advanced, recurrent NK, especially in younger patients or post-surgery nerve injuries. PubMedLippincott Journals
Emergency “rescue” surgery: If perforation occurs, tectonic keratoplasty (emergency corneal transplant) may be required to restore globe integrity; this is vision-saving, not cosmetic, and carries higher risks than elective grafts. PMC
Prevention tips
Treat herpetic eye disease quickly and take antivirals as prescribed to limit nerve damage.
Control blood sugar if you have diabetes (nerve-protective).
Avoid home use of numbing drops and limit preserved drops; ask for preservative-free. PMC
Manage eyelid closure—tape at night or use moisture shields if lids don’t close fully.
Follow safe contact-lens habits or avoid lenses during active disease.
Use humidifiers and moisture-chamber glasses in dry/windy environments.
Blink breaks during screen time (conscious full blinks every few minutes).
Wear protective eyewear in dusty/UV-intense settings.
Stop smoking and limit alcohol (both worsen surface dryness and healing).
Vaccinate for shingles (age-appropriate) to reduce zoster-related corneal nerve damage risk.
When to see a doctor—urgently vs. soon
Call urgently (same day) if you notice a new persistent open spot, sudden vision drop, a white spot/ulcer, increasing redness with discharge, trauma/chemical exposure, or suspected perforation (sharp pain at first, then less pain, fluid leakage, or a visible hole).
Schedule soon if your eye looks worse than it feels, dryness never settles, or you have recurrent “scratches” that don’t heal. This mismatch between bad signs and low pain is classic for NK and should never be ignored. (Clinical guidance emphasizes early, aggressive management.) Johns Hopkins CME
What to eat” and “what to avoid”
Eat more of:
Lean protein (egg, fish, pulses) to supply building blocks for repair.
Fatty fish/flax/chia (omega-3s) for anti-inflammatory tear support.
Orange/yellow vegetables (carrots, squash) and leafy greens for vitamin A and lutein/zeaxanthin.
Citrus/berries/peppers for vitamin C to support collagen. PMC
Nuts and seeds (zinc, vitamin E).
Dairy or fortified alternatives (vitamin D and calcium).
Whole grains & legumes for B-vitamins (including B12 if fortified).
Hydration—water regularly through the day.
Olive oil & avocados (healthy fats for cell membranes).
Foods rich in B12 (fish, dairy, fortified foods) if you are plant-based and at risk of deficiency.
Limit or avoid:
Smoking and vaping (surface toxicity and poor healing).
Heavy alcohol (dehydration and poor nutrition).
Ultra-processed, very salty snacks (worsen dryness/dehydration).
Excess sugar spikes (worse diabetes control and neuropathy).
High-dose vitamin A supplements without medical supervision (toxicity).
Mega-doses of vitamin C long term (>2 g/day) unless prescribed. EyeWiki
Energy drinks/caffeine excess if they replace water (dehydration).
Allergens that trigger eye rubbing or inflammation.
Over-the-counter redness drops with vasoconstrictors (rebound, irritation).
Unvetted herbal remedies that could interact with eye meds.
FAQs
1) Is neurotrophic keratitis the same as “dry eye”?
No. Many people with NK look dry, but the problem is nerve damage, not just tear quality. NK needs special protection and often regenerative therapy (e.g., cenegermin). NCBI
2) Why does my eye look bad but not hurt?
Because the pain-sensing nerve is impaired. Low pain in a sick-looking eye is a warning sign of NK. NCBI
3) Can NK heal completely?
Yes—especially stages 1–2—if treated early with lubrication, protection, biologic drops, and sometimes cenegermin or amniotic membrane. Severe stage 3 often heals but may leave scars that reduce vision.
4) How long does healing take?
Small defects can close in days to weeks; larger ulcers can take weeks to months, especially if scarring or thinning occurred. Cenegermin courses are 8 weeks. FDA Access Data
5) Is cenegermin safe?
Most patients tolerate it. The label lists eye pain, redness, tearing, and foreign-body sensation as common side effects; dosing is 1 drop 6×/day for 8 weeks. FDA Access Data
6) Are autologous serum or PRP drops “better” than artificial tears?
They contain natural growth factors and often work better than simple lubricants for non-healing defects; many specialists add them when a defect persists. PMC
7) Can a special contact lens really help?
Yes. Bandage and scleral/PROSE lenses physically protect and hydrate the cornea, often improving vision and comfort while healing. They are paired with antibiotic cover and strict hygiene. PMC
8) Do I need surgery?
Not always. Surgery is for protection (tarsorrhaphy), biologic healing (AMT), tear retention (punctal cautery), or rescue (keratoplasty). Corneal neurotization can restore sensation longer-term in selected patients. Lippincott Journals
9) Is NK contagious?
No. But some causes (like herpes viruses) are infections; your doctor will treat those appropriately.
10) Can NK come back?
Yes, if the underlying nerve problem persists. Ongoing surface care and trigger control reduce recurrences.
11) Can I keep wearing my usual contact lenses?
During active NK, no—unless your doctor prescribes a medical BCL or scleral lens with close follow-up. Regular lenses can worsen defects.
12) Are numbing drops okay if my eye hurts?
Never at home. They damage the cornea and can cause or worsen NK. Use oral pain meds or doctor-given nerve blocks instead. EyeWiki
13) What about cyclosporine (or lifitegrast) for NK?
Cyclosporine can calm surface inflammation and support tear quality; recent studies suggest benefit in herpetic-related NK as an adjunct, not a standalone cure. PubMed
14) Is topical insulin a real option?
It’s off-label but promising in small studies; still not a substitute for approved therapy like cenegermin. MDPI
15) What’s the most advanced option to restore feeling?
Corneal neurotization surgery—it reroutes a healthy sensory nerve to the cornea and can bring back sensation over months, reducing relapses. 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.
