Strachan’s Disease

Strachan’s disease is a rare nerve and eye disorder. It mainly affects three systems at the same time. The eyes get a type of optic nerve damage that causes central, painless blurring. The peripheral nerves in the hands and feet get inflamed and damaged, which causes burning pain, tingling, and numbness. The skin and moist linings of the mouth and genitals can get sore, cracked, or inflamed. Some people also lose part of their hearing because the inner ear nerves are affected. Doctors call this mix of problems a triad: optic neuropathy, a painful sensory polyneuropathy, and sometimes orogenital dermatitis and sensorineural hearing loss. The pattern has been described since the late 1800s and has been seen most often in people who are under-nourished or who have gaps in key vitamins, especially the B-vitamins. The strongest suspects are riboflavin (vitamin B2) and vitamin B12, but other B-vitamins may also play a part. EyeWikiBMJ Paediatrics

Strachan’s disease—also called Strachan’s syndrome—is a toxico-nutritional neuropathy. That means nerves are damaged because the body is missing key nutrients (especially several B-vitamins) and sometimes also exposed to toxins (for example, from alcohol, tobacco, or poorly processed cassava). The condition typically causes painless, slowly progressive vision problems (a “nutritional optic neuropathy” with trouble seeing colors and central blurry spots) together with painful burning, tingling, or numbness in the feet and hands (a length-dependent peripheral neuropathy). Some people also notice hearing problems, plus mouth soreness (stomatitis), a smooth red tongue (glossitis), and dry/scaly skin—all classic clues of vitamin deficiency. It has been described historically in tropical settings and in populations with restricted or unbalanced diets, but it can occur anywhere if deficiencies and risk factors are present. The strongest links are with deficits in vitamin B12, folate, thiamine (B1), riboflavin (B2), and sometimes copper, often worsened by smoking and alcohol use; in some regions, cyanide exposure from inadequately processed cassava has also been implicated. Early identification and rapid nutritional repletion improve the chance of visual and neurologic recovery. NCBIBioMed CentralPMCResearchGate

The syndrome was first written up in 1887 by Henry Strachan in Jamaica. Later, very similar cases were noted in prisoners of war and in large clusters in Cuba and East Africa. These outbreaks pointed to poor diet and B-vitamin shortage as important drivers. Because another doctor named Madan also reported similar cases in the 1890s, some authors use the name “Strachan–Madan syndrome.” EyeWiki

Doctors also use the name “Strachan syndrome” in medical catalogs. You may also see the phrase “amblyopia, neuropathy, orogenital dermatitis syndrome,” which is a descriptive synonym for the same clinical picture. NCBI

Why it happens

The simplest way to understand this disease is to think of nerves as high-energy, vitamin-hungry cells. When the diet is poor, or the body cannot absorb or use vitamins well, the optic nerve and the long sensory nerves are some of the first to suffer. A low intake of B-vitamins, rapid weight loss, strict restrictive diets without proper supplements, or illnesses that reduce appetite and absorption can set the stage. In real life, cases often follow months of dietary restriction, illness, or weight loss. BMJ Paediatrics

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Types

Doctors do not use one official sub-type list, but for simple understanding it helps to group by what is most prominent and by the time course.

1. Optic-dominant type. The main problem is central, painless blurring in both eyes with color dulling (especially red) and trouble reading. Eye findings may look surprisingly normal at first, but vision tests show central scotomas. This tracks with “nutritional optic neuropathy.” WebEyeEyeWiki

2. Peripheral-painful type. The main problem is burning pain, tingling, numbness, and cramps in the feet and hands. People may be very sensitive to touch, and walking may be hard. Reflexes can be reduced. This matches the painful sensory polyneuropathy described in classic reports. EyeWiki

3. Mixed triad type (classic Strachan’s). Eye blurring, painful sensory neuropathy, and mucosal or skin soreness appear together. Some patients also notice gradual hearing loss. This is the full triad as described since the 19th century. EyeWikiBMJ Paediatrics

4. Auditory-prominent type. A smaller group has noticeable hearing decline along with pain and numbness, with or without major eye complaints. Case series report combined visual loss and deafness in some patients. PubMed

5. Subacute-onset type. Symptoms develop over weeks to a few months after illness, weight loss, or tight diet restriction. This tempo is typical in modern reports linked to nutritional deficiency. BMJ Paediatrics

6. Epidemic-linked type. Clusters in specific places and times have been tied to broad B-vitamin shortfalls in populations. These events strengthen the nutrition link. EyeWiki

7. Overlap with “tropical ataxic neuropathy.” Some people meet features that overlap with the older term “tropical ataxic neuropathy,” where malnutrition and optic involvement appear together. The names and boundaries have shifted historically, but the shared theme is nutritional stress on the nervous system. Wikipedia

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Causes

1) Riboflavin (vitamin B2) deficiency. Low B2 disrupts energy-making enzymes in nerves and eyes. Modern case reviews highlight B2 as a key suspect in Strachan’s syndrome. BMJ Paediatrics

2) Vitamin B12 deficiency. Low B12 damages myelin and axons and is linked to combined optic and peripheral neuropathy. Dietary restriction and malabsorption are common roots. BMJ Paediatrics

3) Thiamine (vitamin B1) deficiency. B1 is central to energy pathways. When it is low, nerves cannot keep up, and neuropathy can develop alongside other problems. EyeWiki

4) Folate (vitamin B9) deficiency. Folate helps DNA and repair. Shortage can worsen optic and nerve dysfunction, especially together with B12 or B2 gaps. EyeWiki

5) Niacin (vitamin B3) deficiency. Severe niacin shortage harms skin and nerves. It often travels with other B-vitamin gaps in poor diets. EyeWiki

6) General malnutrition and weight loss. Low total energy and protein over time make all B-vitamin gaps worse and starve nerves and the optic nerve. Historic clusters and prisoner-of-war reports point to this broad cause. EyeWiki

7) Strict vegan or highly restrictive diets without proper supplements. When animal products are fully removed without planned B12 and B2 intake, optic and peripheral neuropathies can appear. BMJ Paediatrics

8) Eating disorders or prolonged poor intake. Prolonged low intake can deplete vitamin stores and damage nerves. EyeWiki

9) Post-bariatric or other gut surgeries. Surgery can reduce absorption of B-vitamins, leading to optic and peripheral neuropathies if not supplemented. MDPI

10) Malabsorption from gut disease. Conditions like celiac disease or inflammatory bowel disease can reduce vitamin absorption and set up deficiencies. (This is a general mechanism supported across nutritional neuropathy literature.) EyeWiki

11) Chronic infection or systemic illness that reduces intake. Ongoing illness can lower appetite and absorption, tipping people into deficiency. BMJ Paediatrics

12) Alcohol misuse. Alcohol impairs nutrient absorption and use. It often coexists with poor diet and B-vitamin deficits. EyeWiki

13) Tobacco exposure with poor diet. Tobacco use is frequently reported in nutritional optic neuropathy cohorts and may worsen risk when diet is poor. MDPI

14) Food insecurity or famine. Community-wide shortages can produce clusters of cases, as seen in historical outbreaks. EyeWiki

15) Pregnancy or lactation with inadequate supplementation. Needs rise in these periods. Without support, deficiency risk grows. (General nutritional neuropathy principle.) EyeWiki

16) Older age with poor diet. Appetite and absorption can fall with age, increasing risk of B-vitamin shortage. EyeWiki

17) Vegan or vegetarian adolescents without guidance. Rapid growth plus restricted diet can strain vitamin status and has been linked to optic neuropathy patterns. MDPI

18) Poverty and limited food diversity. Monotonous diets low in animal protein and fresh foods are a recurring background factor in case series. EyeWiki

19) Over-reliance on starchy staples with little protein. Diets heavy in single staples without B-vitamin-rich foods can set the stage for deficiency-related neuropathies. Some overlap literature uses the term “tropical ataxic neuropathy” in such contexts. Wikipedia

20) Combined deficiencies rather than a single vitamin. Many patients show overlapping shortfalls (B2, B12, B1, folate), and the combined effect may be what drives the full triad. EyeWiki

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Symptoms

1) Central, painless blurring in both eyes. Reading and recognizing faces get hard. Colors, especially red, look dull. This is typical of nutritional optic neuropathy. WebEye

2) A central or centro-cecal blind spot. Visual field testing shows a hole near the center of vision in each eye. WebEye

3) Eye strain with near work. Small print becomes exhausting because of central vision loss. WebEye

4) Burning pain in feet and hands. This is often the earliest and most distressing nerve symptom. EyeWiki

5) Tingling, pins-and-needles, and numbness. Sensation fades in a “stocking-glove” pattern as peripheral nerves are affected. EyeWiki

6) Cramps and weakness. Muscles may cramp, and strength can feel reduced due to nerve dysfunction. EyeWiki

7) Unsteady gait. People may feel off-balance when walking because of sensory loss in the feet. Wikipedia

8) Reduced hearing or muffled sounds. Some patients notice hearing loss over weeks to months. BMJ Paediatrics

9) Sore mouth, tongue, or cracked lip corners. The mucosa can be inflamed; angular cracks or glossitis may be seen. Taber’s Medical Dictionary

10) Soreness or rash in the genital area. Orogenital dermatitis can occur and can be painful. Taber’s Medical Dictionary

11) Weight loss and low energy. Intake is often poor, and people feel fatigued. EyeWiki

12) Headache or eye ache from strain. This is secondary to visual effort, not usually from the optic nerve itself. WebEye

13) Light sensitivity. Bright light may feel harsh because central vision is impaired. WebEye

14) Mood changes or irritability. Chronic pain, poor nutrition, and vision loss can affect mood. (General principle in chronic neuropathy.) EyeWiki

15) Slow reflexes or reduced ankle jerks. Nerve damage can reduce deep tendon reflexes. EyeWiki

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Diagnostic tests

Doctors confirm the diagnosis by combining the story, the exam, vitamin studies, nerve and eye tests, and by ruling out other causes. Below are practical tests grouped by category. The mix chosen depends on the person.

A) Physical-exam–based

1) General nutrition exam. The doctor checks weight, body mass index, muscle wasting, and signs of vitamin lack. This helps show if poor intake or absorption is likely. Clues support a nutritional neuropathy picture. EyeWiki

2) Skin and mucosal inspection. The mouth corners, tongue, and genital skin are checked for inflammation or cracks that point to B-vitamin shortage. These findings were part of the original disease description. EyeWikiTaber’s Medical Dictionary

3) Neurologic sensory exam. Light touch, pinprick, vibration, and position sense are tested in the feet and hands. Length-dependent loss supports a peripheral neuropathy. EyeWiki

4) Reflex and gait testing. Doctors test ankle and knee reflexes and watch the patient walk. Reduced reflexes and an unsteady gait back up sensory nerve dysfunction. Wikipedia

5) Basic eye exam with pupil and fundus check. Visual behavior, pupils, and optic discs are examined. Early on, the optic nerve may look normal even when vision is reduced, which is typical for nutritional optic neuropathy. WebEye

B) Manual / bedside functional tests

6) Visual acuity testing (Snellen or similar). Measures central vision loss. Strachan’s pattern shows bilateral, symmetric acuity drop. WebEye

7) Color vision testing (e.g., Ishihara plates). Red color often fades first. Color testing is very sensitive for optic nerve dysfunction. WebEye

8) Contrast sensitivity testing (e.g., Pelli–Robson). People struggle with low-contrast letters early in optic neuropathy. This aligns with nutritional optic neuropathy physiology. MDPI

9) Visual field testing (automated perimetry). Typically shows a central or centro-cecal scotoma in both eyes. This helps separate optic nerve problems from retinal disease. WebEye

10) Bedside hearing tests (Rinne and Weber with tuning fork) and formal audiometry referral. These screen for sensorineural hearing loss, which can accompany the triad. EyeWiki

C) Laboratory and pathological tests

11) Vitamin B12 level with methylmalonic acid and homocysteine. B12 alone can look “low-normal.” Methylmalonic acid and homocysteine rise when B12 is inadequate, so they help confirm tissue-level deficiency. This is standard in nutritional optic neuropathy work-ups. MDPI

12) Riboflavin status by EGRAC (erythrocyte glutathione reductase activation coefficient). This functional blood test measures how much the riboflavin-dependent enzyme “wakes up” when fed extra cofactor in the lab. High EGRAC means riboflavin shortage. Public-health and clinical nutrition groups use it to gauge B2 status. King’s College LondonPubMed

13) Thiamine (B1) and folate (B9) levels. These identify other common gaps that can worsen neuropathy and optic nerve stress. EyeWiki

14) Complete blood count (CBC) with red cell indices. Macrocytosis can point to B12 or folate shortage; anemia also signals under-nutrition. EyeWiki

15) Metabolic and endocrine screen where indicated. Tests such as glucose (to exclude diabetic neuropathy), thyroid function, and liver tests help rule out other neuropathy causes that could mimic the picture. EyeWiki

16) Tests for malabsorption when history suggests it. Celiac serology or other GI work-ups are used if absorption problems are suspected. EyeWiki

D) Electrodiagnostic tests

17) Nerve conduction studies and EMG. These show reduced sensory nerve responses in a length-dependent pattern and help confirm a painful sensory polyneuropathy rather than a spinal cord or brain problem. EyeWiki

18) Evoked potentials (visual and brainstem auditory). Visual evoked potentials can confirm optic nerve conduction delay. Brainstem auditory evoked responses can detect sensorineural pathway dysfunction. These are helpful when standard tests are inconclusive. EyeWiki

E) Imaging and advanced ocular tests

19) Optical coherence tomography (OCT) of the retinal nerve fiber layer and ganglion cell layer. OCT can detect thinning in the papillomacular bundle and macular ganglion cell complex that matches central vision loss in nutritional optic neuropathy. OCT helps document damage and track recovery after re-nutrition. PMC+1

20) MRI of brain and orbits (with optic nerves). MRI is usually normal in purely nutritional cases but is important to rule out other causes such as compressive, demyelinating, or inflammatory optic neuropathies. PMC

Non-Pharmacological Treatments (therapies & others)

Each item includes a Description → Purpose → Mechanism in plain English.

1. Immediate balanced diet restoration → Reintroduce varied, energy-adequate meals with animal or fortified sources of B-vitamins (eggs, dairy, fish, meats or fortified cereals/plant foods). → Restores missing co-factors the nerves need for energy and myelin repair. PMC

2. Stop alcohol → Abstain completely during recovery. → Lowers direct neurotoxicity and improves nutrient absorption and utilization. MDPI

3. Stop tobacco → Quit smoking/chewing tobacco. → Reduces optic-nerve toxin exposure and improves oxygen/nutrient delivery. MDPI

4. Cassava safety (if cassava is eaten) → Use traditional detox steps: soak, ferment, and dry before cooking. → Removes cyanogenic compounds that can injure mitochondria and nerves. ResearchGate

5. Fortified foods & B-complex–rich choices → Choose fortified grains/cereals and B-rich foods daily. → Keeps B-vitamin levels steady while nerves heal. Office of Dietary Supplements

6. Low-vision rehabilitation → Get refraction, contrast-enhancing lighting, magnifiers, and orientation/mobility training if needed. → Maximizes remaining vision while the optic nerve recovers. EyeWiki

7. Color-vision & visual field training → Use simple home tasks and clinic-guided exercises to adapt to color/central field defects. → Improves functional vision and safety. EyeWiki

8. Physical therapy for neuropathy → Balance, strength, and gait work; desensitization for burning feet. → Improves walking confidence, reduces fall risk, and retrains sensation. Emergency Care BC

9. Occupational therapy → Home/work adaptations; footwear and fall-proofing. → Lowers injury risk and keeps daily life independent during recovery. Emergency Care BC

10. Foot care & protective footwear → Inspect feet daily; wear cushioned, closed-toe shoes. → Prevents ulcers/infections when sensation is reduced. Emergency Care BC

11. Pain coping skills (CBT/mindfulness pacing) → Learn non-drug pain management strategies. → Reduces pain distress and improves sleep/function. NCBI

12. Sleep hygiene → Regular sleep schedule, screen curfew, cool/dark room. → Poor sleep worsens pain perception; good sleep improves nerve repair milieu. NCBI

13. Treat mouth and skin changes → Gentle oral care, saline rinses; skin emollients and sun protection. → Helps stomatitis/glossitis and dermatitis linked to deficiency. BioMed Central

14. Address malabsorption → Work-up for causes (e.g., post-GI surgery, celiac, IBD) and treat them. → Ensures the gut can absorb the vitamins you reintroduce. PMC

15. Hearing support → Audiology evaluation; consider hearing aids. → Improves communication when auditory neuropathy is present. ASHA Apps

16. Avoid neurotoxins → Strictly avoid methanol-containing “illicit alcohol” and recreational nitrous oxide. → These can mimic or worsen B-12–related nerve injury. PMCNCBI

17. Hydration & general micronutrients → Regular fluids and balanced minerals (per clinician advice). → Supports overall metabolic recovery. PMC

18. Community nutrition & food security supports → Enroll in local food/fortification programs. → Sustains recovery and prevents relapse in at-risk settings. ResearchGate

19. Education & adherence coaching → Simple checklists and reminders for supplements and follow-ups. → Ensures consistent repletion during the months nerves need to heal. NCBI

20. Regular monitoring → Follow vision, color vision, fields, and nerve tests; check vitamin levels when appropriate. → Confirms recovery or flags relapses early. EyeWikiPMC

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Drug Treatments

(Doses are typical adult starting ranges; individual plans must be set by a clinician, especially with kidney/liver disease, pregnancy, or drug interactions.)

1. Vitamin B1 (Thiamine) – Vitamin (cofactor).
   Dose/Time: often 50–100 mg/day orally for weeks–months; severe deficiency may start 100 mg IV/IM then oral. Purpose: correct B1 deficit. Mechanism: restores carbohydrate metabolism enzymes and neuronal energy. Side effects: rare; occasional GI upset. Office of Dietary SupplementsMedscape Reference

2. Vitamin B2 (Riboflavin) – Vitamin (cofactor).
   Dose/Time: for deficiency, 6–30 mg/day (divided) until replete, then RDA maintenance. Purpose: restores flavoprotein reactions critical to mitochondrial function. Mechanism: supports oxidative metabolism and antioxidant recycling. Side effects: harmless bright-yellow urine. MedscapeMayo Clinic

3. Vitamin B12 (Cyanocobalamin or Hydroxocobalamin) – Vitamin (cofactor).
   Dose/Time: common approach: 1 mg IM weekly × 8, then 1 mg monthly or 1 mg/day oral in selected patients; duration depends on cause (sometimes lifelong). Purpose: fix B12 deficit driving optic and peripheral neuropathy. Mechanism: restores myelin methylation and mitochondrial pathways. Side effects: rare; watch for hypokalemia in severe anemia as marrow recovers. Journal of Optometric EducationPMC

4. Folic Acid (Vitamin B9) – Vitamin (cofactor).
   Dose/Time: 1–5 mg/day until deficiency is corrected; avoid high-dose folate if B12 deficiency is uncorrected (can mask anemia while neuropathy worsens). Purpose/Mechanism: cofactor for DNA synthesis and methylation needed for nerve repair. Side effects: generally well tolerated. NCBI

5. Copper (if deficient) – Trace element replacement.
   Dose/Time: typical elemental 2–4 mg/day orally (or parenteral if severe), with careful monitoring. Purpose/Mechanism: corrects copper-related myeloneuropathy/optic neuropathy. Side effects: GI upset; excess zinc lowers copper—avoid high-dose zinc. ScienceDirect+1

6. Gabapentin – Anticonvulsant for neuropathic pain.
   Dose/Time: start 100–300 mg at night, titrate toward 300 mg t.i.d. (or higher as tolerated/indicated). Purpose: reduce burning/tingling pain. Mechanism: α2δ calcium-channel modulation dampens aberrant nerve firing. Side effects: dizziness, somnolence; adjust in renal disease. NICESouth East London ICS

7. Pregabalin – Anticonvulsant for neuropathic pain.
   Dose/Time: typical start 75 mg b.i.d., titrate to 150 mg b.i.d. if needed. Purpose/Mechanism: similar to gabapentin; often faster titration. Side effects: edema, weight gain, sedation; dependence potential noted in guidance. NICEniformulary.hscni.net

8. Amitriptyline – Tricyclic antidepressant (neuropathic pain).
   Dose/Time: start 10–25 mg at night, titrate cautiously (e.g., to 50–75 mg). Purpose: first-line for nerve pain in many guidelines. Mechanism: modulates descending inhibitory pathways (serotonin/norepinephrine). Side effects: dry mouth, constipation, drowsiness; avoid in some cardiac conditions. NICEPrescqipp

9. Duloxetine – SNRI antidepressant (neuropathic pain).
   Dose/Time: 30–60 mg/day; in diabetic neuropathy, 60–120 mg/day may be used. Purpose/Mechanism: boosts descending pain inhibition via serotonin/norepinephrine reuptake blockade. Side effects: nausea, dry mouth, insomnia; watch BP and drug interactions. GMMMGNICE

10. Topical Capsaicin 8% (clinic-applied patch) or low-dose cream – Topical analgesic.
    Dose/Time: single 8% patch application in clinic (can repeat at intervals) or OTC lower-dose cream applied regularly. Purpose: reduces localized neuropathic pain. Mechanism: TRPV1 desensitization of pain fibers. Side effects: burning at application site. (Adjunct—not a substitute for vitamin repletion.) NCBI

Important: Strachan’s disease should not be treated with corticosteroids as “optic neuritis” unless another inflammatory cause is proven—this entity is nutritional/toxico-nutritional, and steroids don’t treat the root problem. Urgent vitamin repletion and exposure removal are the pillars of care. NCBI

Dietary Molecular Supplements

(These support general nerve health; strongest evidence for alpha-lipoic acid is in diabetic neuropathy—not specifically Strachan’s disease. Use only with your clinician.)

1. Alpha-lipoic acid (ALA) 600 mg/day → antioxidant; may lessen neuropathic symptoms in diabetes; mixed but generally favorable evidence in meta-analyses. MDPIPMC

2. Acetyl-L-carnitine (ALC) 500–1000 mg twice daily → supports mitochondrial function; evidence mixed (benefit in some chemo-induced neuropathies; other guidance discourages for prevention). PMCASCO Publications

3. Omega-3 fatty acids (EPA+DHA) 1–2 g/day → membrane support/anti-inflammatory; modest analgesic benefit in some neuropathic conditions. (Adjunctive). Frontiers

4. Coenzyme Q10 100–200 mg/day → mitochondrial antioxidant; limited neuropathy data but biologically plausible. (Adjunctive.) PMC

5. Vitamin D₃ 1000–2000 IU/day if low → supports neuromuscular health; correct deficiency per labs. (Adjunctive.) NCBI

6. Magnesium 200–400 mg/day (avoid if renal failure) → muscle/nerve support; modest general benefits; check interactions. NCBI

7. B-complex (maintenance doses) as labeled after initial high-dose repletion → keeps B-vitamin stores stable. PMC

8. N-acetylcysteine (NAC) 600 mg 1–2×/day → antioxidant; limited neuropathy data; consider only as adjunct. MedRxiv

9. Probiotics/fermented foods (dietary, not pills necessarily) → may help gut absorption in some settings; adjunctive. NCBI

10. Zinc: avoid high doses unless deficient → high zinc can worsen copper deficiency; discuss with your clinician. ScienceDirect

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Regenerative / stem-cell” drugs

There are no approved immune-booster or stem-cell drugs that repair the optic nerve or peripheral nerves in Strachan’s disease. Research in optic nerve regeneration (gene therapy, growth-factor cocktails, mesenchymal stem cells) is experimental; early studies and meta-analyses suggest possible benefit in selected optic neuropathies, but clinical use is not established, and professional groups caution against commercial stem-cell clinics. If you see these offered for this condition, consider them experimental and seek tertiary-center advice or clinical trial enrollment. Safer “regenerative” steps are exactly what you read above: rapid vitamin repletion, exposure removal, and rehabilitation. PMCGlaucoma Research FoundationNational Eye Institute

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Surgeries

Surgery does not treat Strachan’s disease itself. Procedures are considered only for complications managed by specialists:

1. Cochlear implant (if profound hearing loss from auditory neuropathy and hearing aids fail) → can improve access to sound for some patients, although outcomes vary. SpringerOpenPMC

2. Spinal cord stimulation for refractory neuropathic pain after conservative therapy → specialist pain service decision per NICE technology appraisals. NCBI

3. Intrathecal drug delivery systems (rare) for intractable neuropathic pain → specialist-only after exhausting safer options. NCBI

4. Dental/ENT procedures for severe, non-healing stomatitis or secondary infections → symptomatic relief while deficiencies are corrected. BioMed Central

5. Cataract or other ocular surgeries only for unrelated co-existing eye disease—not for the nutritional optic neuropathy itself. NCBI

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Preventions

1. Eat a balanced, energy-adequate diet with reliable B-vitamin sources or fortified alternatives daily. PMC

2. Do not smoke; avoid alcohol (or keep within medical guidance). MDPI

3. Detoxify cassava before eating (soak, ferment, dry). ResearchGate

4. Use a daily B-complex if your diet is restricted (e.g., strict vegan) or if you’ve had bariatric/intestinal surgery. PMC

5. Regular health checks for B12, folate, thiamine, and copper if you have risk factors. NCBI

6. Treat malabsorption disorders promptly (celiac/IBD/low stomach acid). PMC

7. Avoid methanol and recreational nitrous oxide entirely. NCBI

8. Vaccinations and general health maintenance to reduce illness-related malnutrition. NCBI

9. Food-security/fortification programs where available. ResearchGate

10. Education about early symptoms (color vision loss, central blur, burning feet) and fast medical access. NCBI

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When to see a doctor (red flags)

• Any new, painless, both-eyes vision decline, trouble seeing colors, or central/cecocentral blind spots. NCBI

• Burning or numb feet/hands that are new or worsening. Emergency Care BC

• Mouth soreness, smooth red tongue, weight loss, or dietary restriction with fatigue/tingling. BioMed Central

• After bariatric/GI surgery or strict vegan diets without reliable B12 intake. PMC

• Any exposure to methanol or nitrous oxide with neurologic symptoms. NCBI

What to eat — and what to avoid

Eat more of:

1. Eggs, milk, yogurt, cheese (B2, B12, protein). Office of Dietary Supplements

2. Fish, poultry, lean meats (B12, B3, protein). PMC

3. Legumes, lentils, leafy greens, citrus (folate) + fortified grains/cereals (B-complex). NCBI

4. Nuts and seeds (supportive nutrients). PMC

5. Plenty of water (general recovery). NCBI

Avoid or limit:

1. Alcohol (nerve toxin, depletes vitamins). MDPI
2. Tobacco (optic-nerve toxin). MDPI
3. Illicit/unsafe alcohol (methanol risk). PMC
4. Recreational nitrous oxide (inactivates B12). NCBI
5. Poorly processed cassava; if you eat cassava, always soak/ferment/dry before cooking. ResearchGate

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Frequently Asked Questions

1) Is Strachan’s disease the same as “nutritional optic neuropathy”?
Strachan’s disease includes nutritional optic neuropathy plus peripheral (and sometimes auditory) neuropathy due to deficiencies and exposures; nutritional optic neuropathy is the eye part of that broader picture. NCBI

2) How fast can vision improve after vitamins?
If caught early and causes are removed, some people improve over weeks to months; others stabilize with partial deficits if damage was longstanding. Continuous repletion and follow-up matter. NCBI

3) Which vitamins are most important?
B12, folate, thiamine (B1), and riboflavin (B2) are the key players; your clinician may also check copper. NCBI

4) Do I need injections or pills for B12?
Either can work; many protocols start with IM injections then switch to oral maintenance if absorption is adequate and adherence is good. Journal of Optometric EducationPMC

5) Can I just take a multivitamin?
Multivitamins help prevent relapse, but therapeutic doses of specific vitamins are usually needed first to correct deficiencies. Follow lab-guided, clinician-directed dosing. PMC

6) Are painkillers like paracetamol or NSAIDs helpful for burning feet?
They’re often not very effective for neuropathic pain. First-line medicines are amitriptyline, duloxetine, gabapentin, or pregabalin, chosen and titrated by your clinician. NICE

7) Can stem cells or “immune boosters” cure this?
No approved stem-cell or immune-booster drugs exist for this disease; such therapies remain experimental. Focus on rapid vitamin repletion, exposure removal, and rehab. Glaucoma Research FoundationPMC

8) I’m vegan—how do I prevent this?
Use reliable B12 sources (fortified foods or supplements) and ensure overall energy/B-vitamin intake. Get periodic B12/folate checks. PMC

9) I had bariatric surgery—am I at risk?
Yes; malabsorption can lead to B12 and other deficiencies. Routine supplementation and lab monitoring are important. PMC

10) What tests confirm the diagnosis?
Eye tests (color vision, visual fields, OCT), nerve tests (NCS/EMG), and blood tests for B12, folate, thiamine, riboflavin status, and copper; MRI may rule out other causes. EyeWikiPMC

11) Why is cassava mentioned so often?
Improperly processed cassava can contain cyanide compounds; traditional methods (soak/ferment/dry) remove them and lower risk. ResearchGate

12) Can nitrous oxide (laughing gas) really hurt nerves if my B12 blood test is normal?
Yes. Nitrous oxide can inactivate B12 function even when serum B12 looks normal; clinicians often check methylmalonic acid and homocysteine in that scenario. RACGP

13) How long do I need supplements?
Often months; sometimes lifelong if the cause persists (e.g., malabsorption). Your clinician will tailor the plan to labs and recovery. PMC

14) Will my vision fully recover?
Many improve, especially if treated early; some have partial, permanent deficits if treatment is delayed. Low-vision rehabilitation can maximize function either way. NCBI

15) What’s the single most important step right now?
Start vitamin repletion promptly and remove exposures (alcohol, tobacco, nitrous oxide, unsafe cassava). Early action improves outcomes. NCBI

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 26, 2025.