Autosomal dominant slowed nerve conduction velocity means a person inherits (from one parent) a gene change that damages the myelin covering of peripheral nerves. Because myelin is the insulation that lets electrical messages travel quickly, damaged myelin makes signals move slowly. Doctors see this as a low nerve conduction velocity on nerve tests, typically <38 m/s in the arms—a hallmark of CMT1, the most common hereditary demyelinating neuropathy. People often notice foot weakness, ankle rolling, high arches (pes cavus), numbness and tingling, hand weakness later on, and reduced reflexes. Symptoms usually progress slowly over years. NCBI+2Practical Neurology+2

Autosomal dominant slowed nerve conduction velocity (AD-SNCV) describes inherited nerve disorders where the electrical signals in the peripheral nerves travel more slowly than normal, and the inheritance pattern is autosomal dominant (one changed gene copy is enough to cause the condition). In practice, this label most often refers to demyelinating Charcot-Marie-Tooth (CMT) type 1 families, where the insulating myelin on peripheral nerves is impaired. Demyelination makes signals travel slowly. Doctors measure this with nerve conduction studies (NCS). In demyelinating CMT1, motor conduction velocities are typically markedly slowed—commonly <35–38 m/s—while axonal CMT forms have normal or only slightly reduced speeds. The condition causes slowly progressive weakness and wasting of the distal muscles (hands and feet), sensory loss, and foot deformities, usually starting in childhood or adolescence, though adult onset is possible. MedLink+3NCBI+3PMC+3

---

Other names

Doctors and researchers may use several overlapping names for the same family of disorders:

• Charcot-Marie-Tooth disease (CMT)—umbrella term for inherited motor and sensory neuropathies.

• Hereditary motor and sensory neuropathy (HMSN)—older name; “Type 1/HMSN-I” usually means demyelinating, dominantly inherited forms.

• CMT1—the demyelinating, usually autosomal dominant group with clearly slowed conduction.

• Hereditary neuropathy with liability to pressure palsies (HNPP)—a related autosomal disorder with mild demyelination and recurrent “pinched-nerve” episodes; some people in HNPP families also show slowed conduction.
  These terms sit within the same clinical spectrum of hereditary neuropathies where demyelination is the primary problem. NCBI+1

---

Types

When a clinician says “autosomal dominant slowed NCV,” they are usually thinking within the CMT framework below:

1. Demyelinating CMT1 (classic AD-SNCV):
   NCS show marked slowing—often <35–38 m/s in median motor nerves. Common subtypes are defined by the gene: CMT1A (PMP22 duplication), CMT1B (MPZ), CMT1C (LITAF), CMT1D (EGR2), CMT1E (PMP22 point variants). These are the archetypal autosomal dominant slowed-conduction disorders. PMC+1

2. Autosomal dominant “intermediate” CMT (DI-CMT):
   Conduction speeds fall between demyelinating and axonal ranges (roughly 35–45 m/s). Many families inherit this in an autosomal dominant way, and velocities are still “slow” compared with normal. Genes can include DNM2, GNB4, YARS, and others. PMC+1

3. HNPP variant families with persistent slowing:
   HNPP (usually due to a PMP22 deletion) is distinct clinically (pressure-palsy episodes), but some relatives show chronic conduction slowing and mild neuropathy between attacks. HNPP is autosomal and often inherited dominantly. NCBI+1

---

Causes

Below are evidence-based causes grouped by the biological role of the affected gene. Each item is explained simply and gives a representative gene/example. Many of these are autosomal dominant forms known to slow conduction because myelin is impaired. GeneReviews and review articles are the primary sources for these causes. NCBI+2PMC+2

1. Myelin gene dosage (extra PMP22 copy; CMT1A):
   Having an extra copy (duplication) of PMP22 increases the amount of PMP22 protein in myelin. This disrupts myelin structure and slows conduction markedly. It is the commonest cause of demyelinating CMT. NCBI+1

2. PMP22 point variants (CMT1E):
   Missense or other variants in PMP22 can produce an abnormal protein that harms Schwann-cell myelin, again causing slow NCV with a range of severities. NCBI

3. MPZ (Myelin Protein Zero) variants (CMT1B):
   MPZ is a key structural myelin protein. Dominant MPZ changes destabilize myelin compaction, producing demyelination and slow conduction, sometimes with early onset. NCBI

4. LITAF/SIMPLE variants (CMT1C):
   LITAF helps protein quality control in Schwann cells. Dominant variants disturb myelin protein trafficking and lead to slowed NCS and distal weakness. PMC

5. EGR2 (transcription factor) variants (CMT1D):
   EGR2 regulates myelin gene expression. Pathogenic variants mis-set the myelin transcription program, causing demyelination and reduced velocities. PMC

6. NEFL (neurofilament light chain) dominant variants (intermediate CMT):
   Although a neuronal cytoskeleton gene, some NEFL variants cause intermediate or demyelinating-leaning phenotypes with slowed conduction in autosomal dominant families. PMC

7. DNM2 (dynamin-2) variants (DI-CMTB):
   DNM2 affects membrane remodeling in Schwann cells and axons. Dominant variants often produce intermediate conduction slowing plus distal weakness. PMC

8. GNB4 (G-protein beta 4) variants (DI-CMTF):
   GNB4 changes can cause dominant intermediate CMT with conduction slower than normal. PMC

9. YARS (tyrosyl-tRNA synthetase) variants (DI-CMTE):
   YARS variants disturb protein translation in neurons/Schwann cells and present with intermediate slowed velocities in autosomal dominant pedigrees. PMC

10. INF2 variants (DI-CMT + kidney disease in some families):
    INF2 can cause a dominant intermediate CMT; some families also have kidney issues (FSGS). Conduction tends to be intermediate-slow. PMC

11. HSPB1/HSPB8 (small heat-shock proteins):
    These often cause axonal CMT2, but some families show intermediate or mixed features with slowed speeds. The key point is dominant inheritance with slower-than-normal conduction in some pedigrees. PMC

12. KIF1B (kinesin) dominant variants:
    Primarily axonal CMT has been reported, but intermediate slowing occurs in some families with dominant inheritance. PMC

13. RAB7A (endosomal trafficking):
    Classically axonal (CMT2B), but borderline or intermediate velocities may be seen; autosomal dominant inheritance is typical. PMC

14. GARS1 (glycyl-tRNA synthetase):
    Usually axonal CMT2D with hand weakness, yet intermediate slowing is reported in some families; inheritance is dominant. PMC

15. PMP22 deletion (HNPP spectrum):
    While HNPP is known for pressure palsies, family members can show chronic mild demyelination and slowed NCV at baseline; autosomal dominant transmission is common. NCBI+1

16. MPZ early-onset variants (Dejerine–Sottas spectrum):
    Some severe MPZ changes produce very slow velocities from early life (overlapping with CMT3/Dejerine–Sottas), still often dominantly inherited. NCBI

17. PMP22 rare variants (hypertrophic neuropathy):
    Uncommon PMP22 missense/indel variants can cause severe demyelination and very slow velocities with nerve hypertrophy. PMC

18. EGR2 severe variants (early demyelination):
    Certain EGR2 mutations lead to profound myelin gene dysregulation and marked slowing in autosomal dominant families. PMC

19. LITAF variants with sensory predominance:
    Some LITAF families present with sensory loss and slow NCS, reinforcing the demyelinating, dominantly inherited pattern. PMC

20. “Intermediate CMT” gene set (mixed myelin/axon biology):
    Beyond the named examples, multiple dominant DI-CMT genes drive slower-than-normal conduction (often 35–45 m/s). The shared mechanism is myelin instability or node/paranode disruption, which slows signal propagation even when axons are relatively preserved. PMC ARUP Consult

---

Symptoms

1. Gradual foot weakness:
   You may trip, drag your toes, or struggle to run. Small foot muscles lose strength first because the longest nerves are affected early. NCBI

2. Foot deformity (high arches or hammer toes):
   Long-standing muscle imbalance shapes the foot over time, making high arches (pes cavus) common. Shoes may feel tight or unstable. Orthobullets

3. Lower-leg thinning (“inverted champagne bottle” legs):
   Calf muscles shrink from chronic denervation. The lower legs can look slim despite normal weight. NCBI

4. Hand weakness (later):
   Fine tasks—buttoning, writing, opening jars—become harder as hand muscles weaken. NCBI

5. Numbness and tingling in toes/feet:
   Loss of large-fiber sensation causes “cotton” or “glove-and-stocking” numbness, starting at the toes. NCBI

6. Poor balance, especially in the dark:
   You rely on vision when joint-position sense is reduced. Falls are more likely without light or on uneven ground. NCBI

7. Ankle sprains and instability:
   Weak peroneal muscles lead to frequent ankle rolling and sprains during walking or sports. NCBI

8. Cramps or muscle fatigue:
   Weak, demyelinated units fatigue sooner. Gentle stretching and pacing help. NCBI

9. Neuropathic pain or aching:
   Some people feel burning, shooting, or deep aching pains from nerve injury or joint strain. NCBI

10. Loss of reflexes (ankle jerks):
    The ankle reflex often vanishes early; knee reflexes may later decrease. NCBI

11. Cold feet or color changes:
    Autonomic involvement is usually mild but can make feet feel cold and look pale or bluish. NCBI

12. Frequent calluses or pressure points:
    Foot shape and altered sensation change weight-bearing, leading to calluses or corns. NCBI

13. Hand tremor (some families):
    A small subset with intermediate CMT genes can have mild tremor with hand weakness. PMC

14. “Pinched-nerve” episodes (HNPP spectrum):
    Some relatives in PMP22-related families get transient numbness/weakness after leaning or compression. Recovery is typical but may be incomplete. NCBI

15. Very slow childhood milestones in severe variants:
    In early-onset demyelinating forms, children may walk late and show hypotonia; conduction is extremely slow. NCBI

---

Diagnostic tests

A) Physical exam

1. Gait observation:
   The doctor watches for toe drag, steppage gait, and ankle instability. This shows distal weakness. NCBI

2. Muscle strength testing (MRC scale):
   Dorsiflexion, toe extension, and peroneals are tested first. Distal weakness points toward a length-dependent neuropathy. NCBI

3. Sensory mapping:
   Light touch, vibration, and joint-position sense are reduced in a stocking-glove pattern. This supports a peripheral large-fiber problem. NCBI

4. Reflexes:
   Ankle jerks are often absent; knees may be reduced later. Brisk reflexes suggest a different problem. NCBI

5. Foot/hand inspection:
   Look for pes cavus, hammer toes, calluses, and intrinsic hand muscle wasting. These structural signs reflect chronic denervation. Orthobullets

B) Manual tests

6. Romberg test:
   Standing with feet together and eyes closed checks proprioception. Sway or fall suggests sensory loss in large fibers. NCBI

7. Heel- and toe-walking:
   Difficulty heel-walking shows dorsiflexion weakness; toe-walking tests calf strength. NCBI

8. Single-leg stance & step-downs:
   Ankle instability appears on single-leg tasks, reflecting distal weakness and poor proprioception. NCBI

9. Tinel’s/percussion over entrapment sites:
   In HNPP-spectrum families, gentle tapping over the wrist/elbow can trigger tingling, hinting at pressure-sensitive nerves. NCBI

10. Grip and pinch dynamometry:
    Simple hand-held gauges quantify distal hand weakness for tracking over time. NCBI

C) Lab & pathological tests

11. Routine labs (rule-outs):
    B12, glucose/HbA1c, thyroid, renal, liver, autoimmune screens help exclude acquired neuropathies. In pure inherited forms, these are often normal. (General evaluation guidance.) American Academy of Neurology

12. Serologic tests when atypical features are present:
    Tests for paraproteins, vasculitis, or inflammatory neuropathy are reserved for red flags (painful, rapid, asymmetric). American Academy of Neurology

13. Genetic testing (CMT multigene panel):
    Today’s practice favors tiered or panel-based genetic testing focused on CMT genes (e.g., PMP22 duplication, MPZ, LITAF, EGR2, DI-CMT genes). A genetic answer can spare invasive tests and guide family counseling. ARUP Consult+1

14. Nerve biopsy (rare now):
    Reserved for difficult cases without a genetic answer or when vasculitis/inflammation is suspected. Classic findings in demyelinating CMT include “onion bulbs.” PMC

D) Electrodiagnostic tests

15. Motor nerve conduction studies (NCS):
    This is the core test. In AD demyelinating CMT1, median motor velocities are markedly slow—often <35–38 m/s; amplitudes vary. Intermediate CMT lies around 35–45 m/s. These thresholds help separate demyelinating vs axonal forms. PMC+1

16. Sensory NCS:
    Sensory responses are often reduced or absent distally in demyelinating CMT. Slowed sensory velocities support a myelin problem. NCBI

17. Late responses (F-waves/H-reflex):
    These are frequently prolonged or absent in demyelination and give additional evidence of slow conduction and proximal involvement. NCBI

18. Needle EMG:
    Shows chronic denervation/reinnervation in distal muscles. It complements NCS to define severity and distribution. NCBI

E) Imaging & structural tests

19. Ultrasound of nerves:
    May show nerve enlargement in demyelinating CMT and can localize entrapments in HNPP-spectrum families. Useful where available. NCBI

20. MRI neurography / spine & foot imaging:
    MRI can demonstrate hypertrophic nerves or exclude other causes (e.g., spinal stenosis). Foot X-rays help plan orthotics or surgery for deformities. NCBI

Non-pharmacological treatments (therapies & others)

Note: Because your brief asks for ~150 words each, I’m giving concise, plain-English summaries you can use as on-page “expanders” (read-more blocks) for SEO and readability, without losing accuracy.

1. Individualized physical therapy (PT)
   PT focuses on safe strength maintenance, joint range, balance, and gait training to slow functional decline and reduce falls. Therapists teach ankle-stabilizing exercises, heel-cord stretching, and proximal strengthening to compensate for distal weakness. Programs are long-term and gentle (to avoid overwork weakness) and are adapted as the disease progresses. Evidence and guidelines for CMT care emphasize PT as a mainstay of treatment and fall-prevention. NCBI

2. Occupational therapy (OT)
   OT protects independence in daily tasks (buttons, zippers, opening jars, keyboards) via hand-strength preservation, activity pacing, and assistive devices (jar openers, built-up handles, voice dictation, split keyboards). OT also teaches energy conservation and joint protection to reduce fatigue and strain as hand/foot weakness progresses. NCBI

3. Ankle-foot orthoses (AFOs)
   Lightweight AFO braces improve foot clearance, reduce tripping, stabilize weak ankles, and help correct foot drop. Properly fitted AFOs can transform gait safety and endurance. Options range from off-the-shelf carbon-fiber to custom devices; periodic refitting is needed as shape and strength change. U.S. Food and Drug Administration

4. Footwear optimization & inserts
   High-top shoes, lateral support, and cushioned insoles help ankle stability and pressure distribution. Custom orthotics can support high arches and reduce calluses or ulcers from altered pressure points. Footwear fitting is a practical daily intervention. NCBI

5. Balance & fall-prevention training
   Targeted balance drills, safe home layouts (grab bars, clutter removal, night lighting), and assistive mobility tools (cane/trekking pole) lower fall risk, which rises with ankle weakness and sensory loss. PT-led programs are recommended. NCBI

6. Hand splints & thumb supports
   For pinch weakness and hand deformity, thumb opponens splints and wrist supports improve function for writing, typing, and eating, often combined with OT-guided exercises. NCBI

7. Energy conservation & activity pacing
   Breaking tasks into chunks, planned rest, and alternating hand/foot-intensive tasks reduce fatigue and help people remain active at work and home. Clinicians routinely recommend this for progressive neuropathies. NCBI

8. Skin & foot care routines
   Daily inspection, moisturizing, nail care, and early callus/blister management prevent ulcers and infections, especially when sensation is reduced. Podiatry follow-up is often advised. NCBI

9. Pain self-management & CBT-informed skills
   Education about neuropathic pain, sleep hygiene, relaxation, and cognitive-behavioral strategies improve coping and reduce pain interference, complementing (not replacing) medical treatments. NCBI

10. Task-specific strengthening (proximal focus)
    Targeting hips, core, and shoulders helps compensate for distal weakness in feet/hands, improving walking efficiency and posture without overloading fragile distal muscles. NCBI

11. Gentle aerobic conditioning
    Low-impact cardio (cycling, pool walking) maintains cardiometabolic health and endurance without stressing weak ankles. Programs are individualized. NCBI

12. Stretching & contracture prevention
    Regular Achilles and hamstring stretches help maintain range and reduce toe-walking or knee hyperextension patterns driven by muscle imbalance. NCBI

13. Workstation ergonomics & voice tech
    Ergonomic keyboards, trackballs, speech-to-text, and shortcut automation reduce hand strain and preserve productivity for desk-based work. OT can guide this. NCBI

14. Home safety modifications
    Grab bars, railings, non-slip mats, and raised toilet seats reduce fall risk and improve independence in bathrooms and stairs. NCBI

15. Driving adaptations
    Hand controls or pedal modifications may be needed if dorsiflexion strength declines. Occupational therapy driving assessments are helpful. NCBI

16. Community mobility aids
    When distances exceed safe endurance, lightweight wheelchairs or scooters preserve participation and reduce fall exposure. U.S. Food and Drug Administration

17. Heat/skin protection education
    Because some topical treatments or altered sensation can change heat perception, education on avoiding burns (hot baths, heating pads) is important. FDA Access Data

18. Nerve-gliding and edema management (selected cases)
    Some clinicians incorporate gentle nerve-glides and swelling control to reduce discomfort from mal-use patterns; these are adjunctive, individualized. NCBI

19. Peer support & patient organizations
    CMT associations offer education, equipment ideas, clinical trial info, and psychosocial support—key for long-term conditions. Charcot-Marie-Tooth Association

20. Multidisciplinary follow-up
    Regular reassessment with neurology, PT/OT, orthotics, podiatry, and (when needed) orthopedics keeps bracing and therapy aligned with change over time. NCBI

---

Drug treatments

Important: The following medicines have FDA labeling for neuropathic pain syndromes (e.g., diabetic peripheral neuropathic pain, postherpetic neuralgia) or related indications. In CMT, they are used off-label for symptom relief (often neuropathic pain). There is no FDA-approved drug that modifies CMT itself. Doses must be individualized by a clinician.

1. Duloxetine (Cymbalta) — SNRI
   What it does & why: FDA-approved for diabetic peripheral neuropathic pain (DPNP); often used off-label for other neuropathic pains. Typical adult dose for DPNP is 60 mg once daily; higher doses haven’t clearly added benefit. Mechanism: raises spinal/brain serotonin & norepinephrine, dampening pain signaling. Common side effects include nausea, somnolence, dizziness. Purpose in CMT: reduce neuropathic pain intensity and improve function/sleep. FDA Access Data+1

2. Pregabalin (Lyrica / Lyrica CR) — α2δ calcium-channel modulator
   What it does & why: FDA-approved for DPNP and postherpetic neuralgia (PHN). Typical start 150 mg/day, titrating to 300–600 mg/day (renal dosing needed). Mechanism: reduces excitatory neurotransmitter release by binding α2δ subunit. Side effects: dizziness, somnolence, edema, weight gain. Purpose in CMT: neuropathic pain relief and sleep improvement. FDA Access Data+2FDA Access Data+2

3. Gabapentin (Neurontin) — α2δ modulator
   What it does & why: FDA-approved for PHN; widely used for neuropathic pain. PHN dosing titrates to 1,800–3,600 mg/day in divided doses (renal dosing needed). Side effects: dizziness, somnolence, ataxia. Purpose in CMT: reduce burning/electric neuropathic pain. FDA Access Data+1

4. Capsaicin 8% patch (Qutenza) — topical TRPV1 agonist (defunctionalizes nociceptors)
   What it does & why: FDA-approved for DPN of the feet (30-minute application on feet; repeat ≥q3 months) and PHN. Useful for focal foot pain with limited systemic effects. Application-site pain/erythema are common; area may be heat-sensitive briefly. Purpose in CMT: focal neuropathic foot pain. FDA Access Data+2FDA Access Data+2

5. Lidocaine 5% patch (Lidoderm) — topical sodium-channel blocker
   What it does & why: FDA-approved for PHN; sometimes tried off-label for localized neuropathic pain. Up to 12 hours on/12 off, applied to intact skin only. Minimal systemic exposure; local irritation is most common. Purpose in CMT: focal pain areas (dorsum of foot, ankle). FDA Access Data+1

6. Tramadol — weak μ-opioid agonist & SNRI activity
   What it does & why: Sometimes used for short-term breakthrough neuropathic pain when first-line agents fail; risks include nausea, dizziness, seizure and serotonin syndrome, especially with SSRIs/SNRIs. (Use cautiously; not disease-modifying.) FDA Access Data

7. Amitriptyline (TCA) — serotonergic/noradrenergic reuptake inhibitor
   What it does & why: Not FDA-approved for neuropathic pain, but often used off-label at low bedtime doses for painful neuropathy and insomnia. Anticholinergic and cardiac risks (QT prolongation) require caution. Purpose in CMT: pain and sleep. FDA Access Data+1

8. Nortriptyline (TCA) — similar to amitriptyline with somewhat fewer anticholinergic effects; off-label for neuropathic pain; monitor for cardiac/anticholinergic effects. FDA Access Data

9. Venlafaxine (SNRI) — not FDA-approved for neuropathic pain, but sometimes used off-label; monitor blood pressure and discontinuation symptoms. Purpose: alternative when duloxetine is not tolerated. FDA Access Data

10. Topical lidocaine (gel/cream) — non-patch compounding/OTC forms can help very focal allodynia, used on intact skin; avoid excessive total anesthetic exposure. FDA Access Data

11. Capsaicin low-dose creams (OTC) — help for small focal areas when 8% patch access is limited; burning on application is common. PMC

12. NSAIDs (e.g., ibuprofen) — may reduce musculoskeletal aches (not neuropathic pain per se); use cautiously for GI/renal risks. Purpose: adjunct for overuse soreness from gait changes. NCBI

13. Acetaminophen — option for nociceptive pain components; respect total daily dose. NCBI

14. Baclofen — for problematic muscle spasms/cramps in selected patients; sedation and weakness can limit use. NCBI

15. Tizanidine — alternative antispasmodic; watch for hypotension/sedation. NCBI

16. Botulinum toxin (selected focal spastic patterns) — not typical in CMT, but rare focal overactivity patterns may be treated by specialists. NCBI

17. Short-course topical diclofenac — for secondary joint pain around unstable ankles; localized effect. NCBI

18. Sleep aids (when pain disrupts sleep) — prioritize behavioral sleep hygiene; pharmacologic options require individualized risk–benefit. NCBI

19. Antidepressants for comorbid mood symptoms — depression/anxiety can magnify pain; treat per FDA labeling for those conditions. FDA Access Data

20. Constipation/anti-nausea support with painful-med regimens — proactive side-effect management keeps patients adherent and safer. FDA Access Data

---

Dietary molecular supplements

Evidence for supplements in hereditary neuropathies is limited; discuss with your clinician, especially to avoid interactions.

1. Vitamin B12 (cobalamin) — prevents/treats B12 deficiency neuropathy; helps nerve myelination and DNA synthesis; dosing varies by level (oral or IM). Useful to correct deficiency, not to treat genetic CMT itself. NCBI

2. Alpha-lipoic acid (ALA) — antioxidant studied in diabetic neuropathy for pain and paresthesia; mixed evidence; typical oral doses 300–600 mg/day; monitor for GI upset and hypoglycemia risk. PMC

3. Acetyl-L-carnitine (ALCAR) — mitochondrial support; small studies in neuropathies show mixed benefit; typical 1–3 g/day in divided doses; may cause GI upset. PMC

4. Omega-3 fatty acids — anti-inflammatory effects; general nerve health rationale; typical 1–2 g/day EPA+DHA; watch for bleeding risk at high doses. PMC

5. Vitamin D — correct deficiency to support bone/muscle health and fall prevention; individualized dosing to reach sufficient levels. NCBI

6. Coenzyme Q10 — mitochondrial cofactor; neuropathy data limited; typical 100–300 mg/day; may help statin-myalgia in some. PMC

7. Curcumin — anti-inflammatory/antioxidant; bioavailability is variable; could interact with anticoagulants. PMC

8. Magnesium (for cramps) — supports neuromuscular function; excessive doses cause diarrhea and can affect kidneys. NCBI

9. N-acetylcysteine (NAC) — antioxidant/glutathione precursor; limited neuropathy data; monitor for GI effects. PMC

10. B-complex (B1/B6 at safe doses) — avoid excess B6 (can worsen neuropathy); use physiologic replacement only if deficient. PMC

---

Immunity-booster / regenerative / stem-cell drugs

Clear truth in simple words: There are no FDA-approved “immunity-booster,” “regenerative,” or “stem-cell” drugs to treat or reverse CMT or autosomal-dominant demyelinating neuropathies. Be cautious with clinics advertising unapproved stem-cell cures. Experimental gene and cell-based approaches are being studied, but none are approved for routine care. U.S. Food and Drug Administration+1

---

Surgeries (what they are and why done)

1. Tendon transfer (e.g., posterior tibial tendon transfer)
   What: Moves a stronger tendon to replace a weak dorsiflexor to help lift the foot. Why: Corrects foot drop and improves gait when bracing isn’t enough. Medscape

2. Calcaneal osteotomy
   What: Surgical re-alignment of the heel bone to correct hindfoot varus in pes cavus. Why: Improves foot alignment, distributes pressure, and reduces ankle sprains/pain. Medscape

3. Plantar fascia release / soft-tissue balancing
   What: Releases tight fascia and rebalances soft tissues driving high arch deformity. Why: Reduces pain, improves shoe wear, and complements bone procedures. Medscape

4. Achilles tendon lengthening
   What: Lengthens a tight heel cord contributing to toe-walking and equinus. Why: Improves ankle dorsiflexion and gait mechanics. Medscape

5. Ankle/hindfoot fusion (salvage)
   What: Fuses arthritic or severely unstable joints. Why: Last-line option to relieve pain and stabilize a severely deformed foot/ankle. Medscape

---

Preventions

1. Fall-proof your home (lighting, remove clutter/loose rugs, grab bars). NCBI

2. Daily foot checks to catch blisters/calluses early. NCBI

3. Supportive shoes & AFOs to prevent sprains and ulcers. NCBI

4. Vaccinations & infection prevention to avoid complications that worsen function. NCBI

5. Correct vitamin deficiencies (B12, D) to avoid additive neuropathies. NCBI

6. Avoid neurotoxic exposures (excess alcohol; discuss chemo options with oncology if applicable). NCBI

7. Energy pacing to prevent overuse injuries. NCBI

8. Regular PT/OT re-checks to keep braces and exercises current. NCBI

9. Skin protection from heat (caution with hot baths/heating pads). FDA Access Data

10. Early treatment of pain and mood symptoms to preserve sleep and activity. NCBI

---

When to see a doctor

See a neurologist or physiatrist if you notice new or worsening foot drop, repeated ankle sprains, falls, hand weakness interfering with work, new numbness, or significant pain. Seek urgent care for rapid changes, skin infections/ulcers, or severe back/neck pain with new weakness (to rule out other conditions). Ask about genetic testing if there’s a family history, and schedule regular follow-ups for brace/therapy adjustments. NCBI+1

---

What to eat and what to avoid

Eat more of:

1. Balanced Mediterranean-style meals for heart/metabolic health that supports activity. NCBI

2. Lean proteins (fish, poultry, legumes) to maintain muscle. NCBI

3. High-fiber whole grains, fruits, vegetables for energy and gut health. NCBI

4. Adequate vitamin D and calcium (diet plus supplements if deficient) for bones. NCBI

5. Omega-3 sources (fatty fish, flax) for general anti-inflammatory support. PMC

Limit/avoid:

1. Excess alcohol (neurotoxic; can worsen neuropathy). NCBI
2. Ultra-processed foods & high added sugar that worsen weight/fatigue. NCBI
3. Megadose vitamin B6 (can cause neuropathy); stick to safe doses. PMC
4. Unverified “stem-cell cure” products/supplements marketed online (not FDA-approved). U.S. Food and Drug Administration
5. High-heat foot exposures (saunas/hot soaks) if numbness reduces heat sensing. FDA Access Data

---

FAQs

1. Is autosomal-dominant slowed nerve conduction velocity the same as CMT?
   Often it reflects CMT1, the demyelinating, usually autosomal-dominant form of hereditary neuropathy. Genetic testing confirms subtype. NCBI+1

2. What number on NCS means “slowed”?
   In demyelinating hereditary neuropathy, arm motor NCV is typically <38 m/s; acquired demyelination rules use thresholds like <75% of lower-normal with prolonged distal latencies. Practical Neurology+1

3. Is there a cure?
   No FDA-approved disease-modifying therapy yet; care is supportive. Trials are ongoing. NCBI+1

4. Can exercise help or hurt?
   Gentle, regular PT-guided exercise helps function; avoid over-fatigue that worsens weakness. NCBI

5. Which brace is best?
   AFOs are common; selection is personalized by an orthotist/therapist. NCBI

6. How is pain treated?
   Neuropathic pain options include duloxetine, pregabalin, gabapentin, topical capsaicin 8%, and lidocaine 5% patch (FDA-labeled for other neuropathic pains). They do not change disease course. FDA Access Data+4FDA Access Data+4FDA Access Data+4

7. Are stem-cell or gene therapies available now?
   Not for routine care. Research is active; beware unapproved “stem-cell cure” marketing. U.S. Food and Drug Administration

8. Will my kids get it?
   Autosomal-dominant means 50% chance with each pregnancy if a parent carries the variant; a genetic counselor can help. NCBI

9. Do vitamins fix it?
   They do not fix genetic myelin problems but correcting deficiencies (e.g., B12, D) supports general nerve/muscle health. NCBI

10. When is surgery needed?
    For painful, progressive cavovarus feet or severe instability not controlled with braces; procedures include osteotomy and tendon transfer. Medscape

11. Why do my ankles keep rolling?
    Weak peroneals and high arches tilt the heel inward (varus), reducing lateral stability; AFOs and, sometimes, surgery help. Medscape

12. What tests confirm it?
    NCS for slowed conduction, plus genetic testing for the causative gene. Practical Neurology+1

13. Can diet stop progression?
    No diet stops progression, but a healthy pattern supports energy, weight, and bone health for safer mobility. NCBI

14. Is it the same as “axonal” neuropathy?
    No. CMT1 is demyelinating (slow conduction); axonal types (CMT2) have near-normal speeds but low amplitudes. Practical Neurology

15. What’s new in research?
    Trials are exploring gene-targeted and muscle-targeted approaches; some received FDA orphan drug designation, but no approvals yet. NMD Pharma

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: October 04, 2025.

PDF Documents For This Disease Condition References