Neuropathy Hereditary Motor and Sensory Type 1C

Neuropathy hereditary motor and sensory type 1C is usually called Charcot–Marie–Tooth disease type 1C (CMT1C). It is a rare, inherited nerve disease that mainly damages the long nerves of the legs and arms. It is a demyelinating neuropathy, which means the insulation (myelin) around the nerves is hurt, so signals travel more slowly. Most people have slowly increasing weakness and thinning of muscles in the feet and lower legs, with problems walking and loss of feeling in feet and hands. CMT1C is caused by a disease change (mutation) in a gene called LITAF and is passed in an autosomal dominant way, so one changed copy of the gene is enough to cause the disease. National Organization for Rare Disorders+4PMC+4Orpha+4

Hereditary motor and sensory neuropathy type 1C is also called Charcot-Marie-Tooth disease type 1C (CMT1C). It is a rare genetic nerve disease where changes (mutations) in the LITAF/SIMPLE gene damage the myelin sheath, the “insulation” around peripheral nerves. This damage slows down nerve signals, especially to the feet and hands, and slowly causes weakness, muscle wasting, loss of feeling, and problems with balance and walking. PMC+2PMC+2

CMT1C usually starts in childhood or teenage years and progresses slowly over life. Most people develop high-arched feet, hammertoes, ankle instability and difficulty running, then later need braces, special shoes or sometimes surgery. At the moment there is no cure that fixes the gene or fully stops the disease, so treatment focuses on keeping muscles strong, joints flexible, feet well aligned, pain controlled, and life as active and independent as possible. PMC+1

Other names

Doctors and books use many different names for this same disease. Some common names are: Charcot–Marie–Tooth disease type 1C, Charcot–Marie–Tooth neuropathy type 1C, hereditary motor and sensory neuropathy type 1C (HMSN 1C), neuropathy, hereditary motor and sensory, type IC, and CMT, slow nerve conduction type C. Older articles may simply say “demyelinating Charcot–Marie–Tooth disease due to LITAF mutation.” All these names describe the same condition: a dominantly inherited demyelinating motor and sensory neuropathy linked to the LITAF gene. NCBI+3MalaCards+3MIPS Helmholtz München+3

Types

1. Classic childhood-onset CMT1C
   In the classic form, symptoms start in late childhood or teenage years. Children may have frequent tripping, weak ankles, high-arched feet and reduced feeling in the feet. Weakness and numbness slowly spread upward in the legs and later to the hands, but many people remain able to walk for life. Orpha+2Genetic & Rare Diseases Center+2

2. Predominantly sensory, milder CMT1C
   Some people have a milder form where sensory symptoms are more obvious than weakness. They may complain of tingling, pins-and-needles, burning pain or reduced feeling in hands or feet, but have little or no clear loss of muscle power for many years. Walking can be fairly normal for a long time. Orpha+2Genetic & Rare Diseases Center+2

3. Late-onset adult CMT1C
   In a few families, symptoms start later, in mid-adult life. People may first notice foot pain, cramps, imbalance or hand clumsiness. Because the onset is late and the course is slow, this form can be mistaken for other causes of neuropathy unless a detailed family history and genetic test are done. PMC+2PubMed+2

4. CMT1C with extra features (such as tremor)
   Some individuals with CMT1C have extra signs like hand tremor, more striking foot deformities (very high arches, hammertoes) or stronger sensory loss than weakness. These differences are part of the phenotypic spectrum, meaning that the same LITAF gene change can look slightly different in each person. Springer+3Genetic & Rare Diseases Center+3MalaCards+3

Causes and contributing factors

Important: In medical research, the main true cause of CMT1C is a disease-causing mutation in the LITAF gene. The list below breaks this cause into detailed parts and also mentions factors that can influence severity or make symptoms worse, but these extra factors do not cause CMT1C by themselves. PMC+2MalaCards+2

1. Pathogenic mutation in the LITAF gene
   A harmful change in the LITAF (lipopolysaccharide-induced TNF factor) gene changes the LITAF protein in nerve Schwann cells. This faulty protein interferes with normal myelin maintenance and starts the disease process in CMT1C. PMC+2MalaCards+2

2. Autosomal dominant inheritance pattern
   CMT1C is usually autosomal dominant, meaning one changed copy of LITAF (from either mother or father) is enough. Each child of an affected parent has about a 50% chance to inherit the mutated gene and therefore the disease. NCBI+3Orpha+3Genetic & Rare Diseases Center+3

3. Abnormal LITAF protein handling in cells
   Mutant LITAF protein may be mis-folded and sent to the wrong place inside the cell. Studies show it can be trapped in certain cell compartments and broken down more quickly, disturbing protein quality control pathways that are important for Schwann cell health. PMC+2MalaCards+2

4. Dysfunction of endolysosomal pathways
   LITAF is involved in endolysosomal trafficking, which helps cells recycle membrane proteins. In CMT1C, this pathway may not work well, leading to build-up or loss of key proteins in myelin, which contributes to nerve demyelination and slow nerve conduction. PMC+2Springer+2

5. Segmental demyelination of peripheral nerves
   The disease process causes repeated episodes where small segments of myelin are lost and then partly repaired. Over time this segmental demyelination and remyelination leads to “onion bulb” formations, a classic microscopic feature of demyelinating CMT. NCBI+3MalaCards+3NCBI+3

6. Loss of large myelinated axons over time
   With repeated myelin damage, some large nerve fibers (axons) are lost. This axonal loss is a direct cause of permanent weakness, wasting and sensory loss, especially in the longest nerves to the feet and hands. PMC+2Monarch Initiative+2

7. Length-dependent vulnerability of long nerves
   Longer nerves are more fragile in demyelinating neuropathies. In CMT1C, the longest nerves to the feet are affected earliest, which is why symptoms start in the toes and ankles before they appear in the hands. Monarch Initiative+2NCBI+2

8. Family history of Charcot–Marie–Tooth disease
   Having blood relatives with CMT or hereditary motor and sensory neuropathy strongly increases the chance of carrying the same LITAF mutation and thus “explains” why the disease appears in a family line. MedlinePlus+2NCBI+2

9. De novo (new) mutation in LITAF
   In some rare cases, a person with CMT1C has no affected parent. A new mutation may have occurred in the sperm, egg or very early embryo. This is still a genetic cause, but it starts in that person for the first time in the family. NCBI+2Monarch Initiative+2

10. Genetic modifiers affecting severity
    Other genes can slightly change how severe the neuropathy is. While they do not cause CMT1C alone, they may influence age at onset, strength of symptoms or how quickly disability progresses in someone who already has the LITAF mutation. PubMed+2Monarch Initiative+2

11. Co-existing diabetes adding extra nerve damage
    If a person with CMT1C also develops diabetes, the high blood sugar can cause diabetic neuropathy on top of CMT. This extra nerve injury can make numbness, pain and weakness worse, even though it is not the original cause of CMT1C. Mayo Clinic+2Best Practice+2

12. Vitamin B12 or folate deficiency
    Low vitamin B12 or folate can cause a separate neuropathy. In a person with CMT1C, this deficiency can worsen nerve symptoms and speed disability. Treating the vitamin problem does not cure CMT1C, but it may remove this extra stress on the nerves. NCBI+2PMC+2

13. Exposure to neurotoxic medicines (for example vincristine)
    Some chemotherapy drugs are known to damage peripheral nerves. In people with CMT, especially demyelinating types, these medicines can cause sudden, severe worsening because the nerves are already fragile. Doctors try to avoid such drugs when CMT is known. NCBI+2Best Practice+2

14. Heavy or long-term alcohol use
    Alcohol abuse can cause a separate toxic neuropathy. When it happens in someone with CMT1C, there is “double injury” to the same nerves, which can increase weakness and sensory loss even more. NCBI+2Wikipedia+2

15. Chronic kidney disease or thyroid disease
    Kidney failure and low thyroid function are well-known causes of acquired neuropathy. If these conditions occur in a person with CMT1C, they can add to nerve problems, although they do not create CMT1C by themselves. NCBI+2Best Practice+2

16. Mechanical stress and ankle sprains
    Because the ankles are weak and unstable, people with CMT1C often twist or sprain them. Repeated trauma and joint instability can further harm already thin muscles and may indirectly increase nerve irritation or compression. National Organization for Rare Disorders+2Mayo Clinic+2

17. Poorly fitting or rigid shoes
    Tight or hard shoes can press on high-arched, deformed feet and irritated nerves. In CMT, this pressure can worsen pain, calluses and ulcers, which may later damage local nerves more. Proper footwear is important to avoid this secondary harm. Mayo Clinic+2Charcot-Marie-Tooth Association+2

18. Spinal or joint deformities causing nerve compression
    Some people with CMT develop scoliosis or joint deformities that may compress nerve roots or peripheral nerves. This compression can add extra weakness or pain on top of the genetic neuropathy. Monarch Initiative+2Radiopaedia+2

19. Lack of physical activity and muscle disuse
    Because of fatigue and weakness, some patients avoid exercise. When muscles are not used, they shrink faster, and joints become stiff. This disuse does not cause the neuropathy, but it increases disability and makes walking harder. NCBI+2National Organization for Rare Disorders+2

20. Aging and lifelong disease progression
    CMT1C is slowly progressive. Over many years, repeated demyelination, remyelination and axonal loss build up. Aging itself also weakens nerves and muscles, so older adults with CMT1C may show more clear disability than they did earlier in life. Monarch Initiative+2NCBI+2

Symptoms

1. Distal leg weakness (especially around ankles)
   One of the first signs is weakness in the muscles that lift the foot and ankle. People may drag the front of the foot (foot drop), have trouble climbing stairs, or feel that their ankles “give way” easily on uneven ground. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

2. Muscle wasting in feet and lower legs
   Over time, the small muscles of the feet and calves become thin because the weak nerves cannot fully activate them. The lower legs can look like an “inverted champagne bottle,” with thinner calves and relatively normal thighs. MalaCards+2Monarch Initiative+2

3. High-arched feet (pes cavus) and hammertoes
   Many people with CMT1C develop high arches and curled toes. These deformities happen because some foot muscles are weaker than others, pulling the bones into abnormal positions. Pes cavus is a common physical clue to inherited neuropathy. Radiopaedia+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

4. Walking and balance problems
   Weak ankles, foot deformities and reduced sensation make walking on uneven ground difficult. People may walk with a high steppage gait (lifting knees more) to avoid tripping, and they can lose balance in the dark because they cannot feel where their feet are. Genetic & Rare Diseases Center+2Mayo Clinic+2

5. Numbness and reduced feeling in feet
   Loss of sensation, especially to vibration and touch in the toes and soles, is common. People may not feel small injuries, hot water or tight shoes, which raises the risk of unnoticed wounds or ulcers on the feet. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

6. Pins-and-needles, tingling or burning pain
   Abnormal nerve signals can cause paresthesias, such as tingling, buzzing, or burning feelings in the feet and sometimes hands. These sensations can be mild or very bothersome and may worsen with fatigue or at night. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

7. Loss of vibration and joint position sense
   People often have trouble feeling a tuning fork vibration on their toes or knowing exactly where their toes are without looking. This loss of proprioception makes it harder for the brain to control balance and fine foot placement when walking. Genetic & Rare Diseases Center+2Monarch Initiative+2

8. Weakness and wasting in hands
   As the disease progresses upward, small muscles in the hands can weaken and shrink. People may find it hard to do tasks like buttoning clothes, writing for a long time, opening jars or typing quickly. MedlinePlus+3National Organization for Rare Disorders+3Monarch Initiative+3

9. Hand tremor in some patients
   A fine tremor of the hands can appear in certain forms of CMT1, including CMT1C. Tremor may be seen when holding the hands out or during movement and can make tasks like drinking from a full cup or using tools more challenging. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

10. Reduced or absent tendon reflexes
    When the doctor taps the Achilles or knee tendon, the normal “jerk” may be very weak or absent because the reflex loop uses damaged peripheral nerves. Loss of reflexes is a common sign on neurologic exam in demyelinating CMT. NCBI+3MalaCards+3NCBI+3

11. Foot and leg cramps
    Muscle cramps and tightness, especially at night or after walking, are common and relate to unstable nerve signals and weak, overworked muscles. Cramps can be painful but are not dangerous; they add to discomfort and disturbed sleep. National Organization for Rare Disorders+2Mayo Clinic+2

12. Fatigue and reduced stamina
    Because walking and standing demand more effort when muscles are weak and balance is poor, people with CMT1C tire more easily. Even simple activities like shopping or climbing stairs can cause early fatigue and require rest breaks. National Organization for Rare Disorders+2Mayo Clinic+2

13. Frequent tripping or falls
    Foot drop, poor balance and numbness make it easier to catch the toes on small obstacles. People often report tripping on uneven surfaces or stairs and may have bruises or sprains from falls, especially before diagnosis. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

14. Mild scoliosis or posture changes
    In some patients, long-term muscle imbalance in the trunk and lower limbs leads to curvature of the spine (scoliosis) or other posture changes. These can be mild but may cause back discomfort or further affect balance. Monarch Initiative+2Radiopaedia+2

15. Psychological impact (anxiety, low mood)
    Living with a chronic, hereditary, slowly progressive disease can affect mental health. Worry about future disability or children’s risk, and frustration with physical limits, may cause anxiety or low mood, so emotional support is important. National Organization for Rare Disorders+2NCBI+2

Diagnostic tests

Doctors diagnose CMT1C by combining history, physical exam, nerve tests and genetic tests. Most tests check how damaged the nerves are and then a genetic test looks for a LITAF mutation. NCBI+4PMC+4Charcot-Marie-Tooth Association+4

Physical exam

1. Full neurologic examination
   The neurologist looks at muscle bulk, strength, tone, reflexes and sensation in all limbs. Typical findings in CMT1C are distal muscle wasting, weakness around ankles and hands, reduced or absent reflexes and reduced vibration and pinprick sensation in feet. PMC+2Genetic & Rare Diseases Center+2

2. Gait and balance assessment
   The doctor watches how the person walks, including heel-walking, toe-walking and walking in a straight line. A high steppage gait, ankle instability and difficulty walking on heels are common signs of distal weakness in demyelinating CMT. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

3. Inspection of feet and hands
   The shape of the feet (high arches, hammertoes, calluses) and hands (thin muscles, clawing) gives clues to long-term neuropathy. These visible changes help the doctor suspect a hereditary neuropathy rather than a short-term nerve problem. NCBI+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

4. Reflex testing with a hammer
   Tendon reflexes at the ankle and knee are checked with a small rubber hammer. In CMT1C, these reflexes are often very weak or absent because the nerve pathways in the legs are demyelinated and conduct signals poorly. MalaCards+2Monarch Initiative+2

Manual tests at the bedside

5. Manual muscle strength testing (MRC scale)
   The doctor asks the patient to move joints against resistance (for example, dorsiflex the foot) and grades strength from 0 to 5. In CMT1C, distal muscles score lower than proximal muscles, showing the typical pattern of a length-dependent neuropathy. PMC+2Monarch Initiative+2

6. Simple sensory tests to touch and pinprick
   Using cotton, a fingertip or a blunt pin, the examiner checks if the patient feels light touch and sharp/dull on toes, feet and hands. Reduced sensation in a stocking-and-glove pattern supports a diagnosis of peripheral sensory neuropathy. MedlinePlus+3Genetic & Rare Diseases Center+3National Organization for Rare Disorders+3

7. Vibration testing with a tuning fork
   A vibrating tuning fork is placed on bony points like the big toe. In CMT1C, patients often feel vibration poorly or only for a short time compared with normal controls, reflecting loss of large myelinated sensory fibers. Genetic & Rare Diseases Center+2Monarch Initiative+2

8. Proprioception and Romberg test
   The doctor gently moves the toes up or down and asks the patient to say the direction with eyes closed, and may perform a Romberg test (standing with feet together, eyes closed). Increased sway or wrong answers show loss of joint position sense. Genetic & Rare Diseases Center+2Monarch Initiative+2

Lab and pathological tests

9. Targeted genetic test for LITAF
   If clinical and nerve tests suggest demyelinating CMT1, a blood sample can be analyzed for mutations in the LITAF gene. Finding a known disease-causing variant confirms CMT1C and helps with genetic counseling for the family. Orpha+3PMC+3MalaCards+3

10. CMT multigene panel or exome sequencing
    Often doctors order a panel that tests many CMT genes (PMP22, MPZ, GJB1, MFN2, LITAF and others) or use exome sequencing. This approach is efficient because more than 100 genes can cause inherited neuropathy, and CMT1C is rare. PubMed+2Monarch Initiative+2

11. Basic blood tests to rule out acquired causes
    Blood glucose, HbA1c, vitamin B12, folate, thyroid-stimulating hormone and kidney function are often checked. Normal results support a hereditary cause, while abnormal values might explain or add to neuropathy from non-genetic reasons. NCBI+2Best Practice+2

12. Serum protein electrophoresis
    This test looks for abnormal proteins in the blood that can be seen in diseases like monoclonal gammopathy or myeloma, which can cause different types of neuropathy. A normal result helps to exclude these acquired neuropathies in someone suspected of having CMT1C. NCBI+2Best Practice+2

13. Nerve biopsy (usually sural nerve) in unclear cases
    A small piece of a sensory nerve in the ankle may be removed and studied under the microscope. In demyelinating CMT, doctors can see segmental demyelination, remyelination and onion bulb formations. Today this is used less often because genetic tests are widely available. NCBI+3PMC+3NCBI+3

14. Family genetic counseling and pedigree analysis
    A genetics specialist may draw a family tree showing who is affected. An autosomal dominant pattern (vertical transmission across generations) supports CMT1C and guides which relatives should consider genetic testing and monitoring. NCBI+2Monarch Initiative+2

Electrodiagnostic tests

15. Nerve conduction studies (NCS)
    NCS measure how fast and how strong signals travel along motor and sensory nerves. In CMT1C, conduction velocities are markedly slowed (demyelinating range, usually below about 38 m/s), while response sizes may be moderately reduced. This pattern strongly supports a diagnosis of demyelinating CMT1. Best Practice+4PMC+4Charcot-Marie-Tooth Association+4

16. Electromyography (EMG)
    EMG uses a fine needle electrode in muscles to record electrical activity at rest and during contraction. In CMT1C, EMG may show signs of chronic denervation and reinnervation in distal muscles, confirming a long-standing neuropathy rather than a muscle disease. PMC+2Monarch Initiative+2

17. F-wave and H-reflex studies
    These special parts of NCS assess the entire length of motor pathways and reflex arcs. In CMT1C, F-wave latencies may be prolonged and H-reflexes absent or delayed, reflecting global demyelination of motor and sensory fibers in the legs. PMC+2Monarch Initiative+2

18. Quantitative sensory testing (QST)
    QST uses controlled devices to measure thresholds for feeling vibration, cold, warm and pain. It provides a more detailed picture of sensory function and can be useful in research or in following changes over time in people with hereditary neuropathy. PMC+2NCBI+2

Imaging tests

19. Peripheral nerve ultrasound
    High-resolution ultrasound can show thickened peripheral nerves in demyelinating CMT, including CMT1C. Studies have described characteristic patterns of enlarged nerve cross-sectional area and changes in echotexture, which may help distinguish CMT subtypes and support the diagnosis. MDPI+3PubMed+3Wiley Online Library+3

20. MRI of spine or limb in selected cases
    Magnetic resonance imaging can show muscle wasting patterns and exclude other causes such as spinal cord compression. MRI is not required to diagnose CMT1C but can be helpful when the clinical picture is confusing or when surgeons plan orthopedic procedures. Radiopaedia+2Monarch Initiative+2

Non-Pharmacological Treatments

These “non-drug” treatments are the core of CMT1C care. Medicines help, but rehab and bracing protect function day by day. PMC+1

1. Individualized Physiotherapy Program
   A physiotherapist designs a personal exercise plan to keep muscles strong and joints flexible. It usually includes stretching, strengthening, gait training and postural exercises. The aim is to slow muscle wasting, improve walking pattern, reduce fatigue and keep you independent in daily life for as long as possible. Physiopedia+1

2. Daily Stretching to Prevent Contractures
   Gentle, regular stretching of calves, hamstrings, toes and fingers helps keep the joints moving and slows down the development of fixed deformities like tight Achilles tendons and clawed toes. Passive and static stretches lengthen stiff muscles and tendons, reduce stiffness, and make walking, standing and shoe-wear more comfortable. Pod NMD+2Therapies for Inherited Neuropathies+2

3. Balance and Gait Training
   Special exercises train your balance system: standing on different surfaces, stepping tasks, and safe turning. The therapist also works on heel-to-toe walking, correcting foot drop and improving speed. This training lowers fall risk and makes moving around in real-life environments safer and more confident. PMC+1

4. Aerobic (Cardio) Conditioning
   Low-impact cardio like cycling, swimming or brisk walking is used to improve heart fitness and reduce fatigue. In CMT, supervised aerobic training has been shown to increase work capacity and reduce tiredness without harming weak muscles when done carefully. The goal is better stamina so daily tasks feel easier. Pod NMD+1

5. Targeted Resistance Training
   Light weight or band exercises are used to train muscles that still have strength, while avoiding overworking very weak ones. Research shows resistance training can improve function when it is carefully dosed and watched by a therapist. It helps you stand up, climb stairs and lift objects with less effort. Pod NMD+1

6. Occupational Therapy for Hands and Daily Tasks
   An occupational therapist focuses on fine motor skills, hand splints and adaptive tools like bigger-grip pens, button hooks, special cutlery and bath aids. They also teach energy-conservation and work-simplification techniques. The aim is to keep you independent with dressing, eating, writing, phone use and school or work tasks. Charcot-Marie-Tooth Disease+1

7. Orthoses (Braces) for Feet and Ankles
   Ankle-foot orthoses (AFOs) and silicone AFOs (SAFOs) support weak ankles, lift the toes to fix foot drop, and improve heel-to-toe walking. Studies show AFOs can increase walking speed, stride length, balance and reduce energy cost of walking in CMT. Good bracing can delay or reduce the need for surgery. Dorset Orthopaedic+4Charcot-Marie-Tooth Association+4PMC+4

8. Special Footwear and Custom Insoles
   Shoes with good heel support, wide toe boxes and firm soles help stabilize the foot, while custom insoles correct high arches or cavovarus deformity. For milder CMT, in-shoe orthoses can reduce pain and improve balance before needing full AFOs. The goal is comfort, stability and fewer falls. The Foundation for Peripheral Neuropathy+2Custom Orthotic+2

9. Assistive Devices for Mobility
   Canes, trekking poles, walkers or wheelchairs may be used in different situations, such as longer distances or rough ground. Using these tools is not “giving up”; they save energy, reduce fall risk and protect joints from repeated trauma. Many people with CMT switch between devices depending on the day. Charcot-Marie-Tooth News+1

10. Core and Postural Training
    Weak trunk muscles and poor posture can worsen balance and back pain. Core strengthening, breathing exercises and postural retraining make standing and walking more stable and also help with transfers, like getting up from a chair or bed. This indirectly protects the feet and ankles from extra strain. PMC+1

11. Pain Self-Management Skills
    Therapists and pain specialists can teach simple tools like heat/cold, gentle massage, pacing activities, relaxation, breathing exercises and distraction methods. These strategies are often combined with medicines and can reduce the total dose of pain drugs required. They also give you more sense of control over symptoms. PMC+1

12. Fall-Prevention and Home Modifications
    Simple changes at home—removing loose rugs, adding grab bars, using non-slip mats and good lighting—reduce falls. An OT may visit home to suggest safer layouts and equipment. This is essential because people with CMT have higher fall risk due to foot drop, numbness and ankle instability. Charcot-Marie-Tooth Disease+1

13. Hand Splints and Night Bracing
    Custom splints can keep fingers and wrists in functional positions, reduce pain and improve grip. Soft night splints for ankles or toes may also hold joints near neutral to reduce morning stiffness and slow deformity. These supports are adjusted over time as the condition changes. Charcot-Marie-Tooth Disease+1

14. Ergonomic and School/Workplace Adaptations
    Adjusting desk height, using ergonomic keyboards or voice-to-text, and modifying schedules can make studying or working much easier. Good ergonomics reduce strain on weak muscles and joints, and help you stay in education or employment longer. Applebaum+2Charcot-Marie-Tooth Association+2

15. Psychological Support and Counseling
    Living with a lifelong genetic neuropathy can cause worry, sadness or anxiety. Counseling, cognitive-behavioral therapy (CBT), and peer-support groups help you cope, build resilience and plan for the future in a realistic but hopeful way. Good mental health improves pain tolerance and motivation for rehab. PMC+1

16. Weight Management and Nutrition Guidance
    Extra body weight puts more stress on weak feet and ankles and can worsen mobility. A balanced diet rich in fruits, vegetables, lean protein and whole grains, while limiting sugar, salt and unhealthy fats, is recommended for people with CMT. Keeping weight in a healthy range supports joints, energy and overall health. Charcot-Marie-Tooth Association+1

17. Sleep Hygiene Strategies
    Pain, cramps and worry can disturb sleep, which then worsens pain and fatigue. Simple rules—regular bedtimes, limiting screens before sleep, relaxing routines, comfortable temperature and good pain control—can improve sleep quality. Better sleep helps nerve pain feel less overwhelming the next day. PMC

18. Education for Patient and Family
    Learning about CMT1C, realistic expectations and treatment options helps the whole family make good decisions. Written guides and specialist websites for CMT give evidence-based advice about exercise, bracing, surgery and research trials. Knowing the facts reduces fear and misinformation. Charcot-Marie-Tooth Association+1

19. Aquatic Therapy (Hydrotherapy)
    Exercising in warm water supports the body, reduces joint load and allows safer practice of walking, balance and strengthening. Many people with CMT find they can move more freely in water than on land, which is good for confidence and conditioning. PMC+1

20. Technology-Assisted Rehabilitation
    Some centers use treadmills with partial body-weight support, video games, or virtual-reality systems to make balance and gait training more intensive and fun. These tools can increase practice time and give instant feedback on movements. They are still being studied but look promising for long-term rehab in CMT. PMC+1

Drug Treatments

There is no medicine yet that cures or stops the gene problem in CMT1C. Medicines mainly treat:

• neuropathic pain (burning, shooting, electric shocks)

• musculoskeletal pain from deformities

• muscle stiffness or cramps

• mood or sleep problems related to chronic illness

Most pain medicines used in CMT are approved by the FDA for other neuropathic pain conditions (like diabetic neuropathy or post-herpetic neuralgia), not specifically for CMT1C, so use is often off-label under specialist supervision. FDA Access Data+3NCBI+3FDA Access Data+3

⚠️ Doses below are typical adult doses from FDA labeling. Many are not approved for children or teens. Your own safe dose can be very different. Always follow your neurologist’s advice.

1. Pregabalin (Lyrica)
   Pregabalin is an anti-seizure medicine widely used for neuropathic pain, such as diabetic neuropathy and spinal cord injury pain. Typical adult dosing for neuropathic pain starts at 75 mg twice daily (150 mg/day) and may be slowly increased to 300–600 mg/day if needed and tolerated. It reduces nerve pain by blocking calcium channels in overactive nerves. Common side effects include dizziness, sleepiness, weight gain and swelling in the legs. FDA Access Data+2FDA Access Data+2

2. Gabapentin (Neurontin and others)
   Gabapentin is another anti-seizure drug used for neuropathic pain, especially post-herpetic neuralgia. Adult doses are usually built up gradually from 300 mg once daily to 300 mg three times daily or more, depending on kidney function and response. It calms nerve firing by affecting calcium channels in the central nervous system. Side effects often include dizziness, sleepiness, and sometimes swelling or weight gain. FDA Access Data+2FDA Access Data+2

3. Duloxetine (Cymbalta, Drizalma Sprinkle)
   Duloxetine is an SNRI antidepressant approved for diabetic peripheral neuropathic pain and other chronic pain conditions. Adults often use 60 mg once daily, sometimes starting at 30 mg to improve tolerance. It increases serotonin and noradrenaline in pain pathways in the brain and spinal cord, which can dampen pain signals and help mood. Common side effects include nausea, dry mouth, constipation, sweating and sleep changes. FDA Access Data+2FDA Access Data+2

4. Amitriptyline (Elavil and generics)
   Amitriptyline is a tricyclic antidepressant used in low doses at night for neuropathic pain and poor sleep, although its label focuses on depression. Adult pain doses are typically 10–25 mg at bedtime, slowly increased as needed up to about 75–100 mg, under careful monitoring. It blocks re-uptake of serotonin and noradrenaline and also stabilizes nerve membranes. Side effects include dry mouth, constipation, blurred vision, weight gain and daytime sleepiness, and it must be used cautiously in young people. FDA Access Data+2FDA Access Data+2

5. Venlafaxine Extended-Release (Effexor XR)
   Venlafaxine XR is an SNRI antidepressant sometimes used off-label for neuropathic pain when duloxetine or TCAs are not suitable. Labelled adult dosing for depression and anxiety ranges from 75–225 mg/day in a single daily dose. By boosting serotonin and noradrenaline, it may reduce pain sensitivity while also improving mood. Side effects can include nausea, sweating, increased blood pressure and withdrawal symptoms if stopped suddenly. FDA Access Data+1

6. Topical Lidocaine 5% Patch (Lidoderm)
   Lidocaine patches deliver local anesthetic directly through the skin and are FDA-approved for post-herpetic neuralgia. For adults, up to three patches may be applied once daily over painful areas for up to 12 hours on, then 12 hours off. In CMT, similar local use (if doctor agrees) can calm small areas of burning pain with minimal systemic absorption. Side effects are usually mild skin reactions, but overdose from too many patches can be dangerous. FDA Access Data+3FDA Access Data+3FDA Access Data+3

7. Capsaicin 8% Patch (Qutenza)
   Qutenza is a high-strength capsaicin patch used in clinics for neuropathic pain in adults. It is applied by trained staff for 30–60 minutes, and a single treatment can reduce pain for weeks by desensitizing pain fibers (TRPV1 receptors) in the skin. In CMT, it might be considered for severe localized foot pain in specialized centers. Side effects include intense burning during application and temporary increased sensitivity. FDA Access Data+4FDA Access Data+4FDA Access Data+4

8. Naproxen (Naprosyn, Aleve, Naprelan)
   Naproxen is an NSAID pain reliever used for joint and muscle pain but does not treat nerve damage itself. Adult dosing depends on the product; Naprosyn tablets are often 250–500 mg twice daily with food, while OTC naproxen sodium (Aleve) is lower dose. It reduces pain and inflammation by blocking COX enzymes and prostaglandin production. Side effects include stomach irritation, ulcers, kidney strain and increased cardiovascular risk with long-term use. FDA Access Data+3FDA Access Data+3FDA Access Data+3

9. Topical Diclofenac 1% Gel (Voltaren Gel and generics)
   Diclofenac gel is an NSAID applied to the skin over painful joints, such as ankles or toes affected by deformity. Adults apply a measured amount several times daily as directed on the label. It reduces local inflammation with much lower blood levels than oral NSAIDs, which may lower systemic risks. Skin irritation and rare systemic NSAID side effects are the main concerns. FDA Access Data+4FDA Access Data+4FDA Access Data+4

10. Tramadol (Ultram, Ultram ER)
    Tramadol is a weak opioid with additional serotonin and noradrenaline effects, used for moderate to severe pain when safer options are not enough. Adult immediate-release dosing often starts at 50 mg every 4–6 hours as needed, with careful maximum daily limits; extended-release forms are taken once daily. Because of addiction risk, seizures and serotonin syndrome, tramadol is usually used at the lowest dose for the shortest time. It is often avoided in younger people unless absolutely necessary. FDA Access Data+5FDA Access Data+5FDA Access Data+5

11. Acetaminophen (Paracetamol)
    Acetaminophen is a common pain and fever reducer often used as a base medicine for mild musculoskeletal discomfort from CMT-related deformities or after surgery. It does not treat nerve pain directly but can be combined with other agents. When used within recommended daily limits and with healthy liver function, it is generally considered safe, but overdose can cause serious liver damage. (Dose and approval details depend on the specific brand and country labelling.)

12. Short-Acting Opioids (e.g., Morphine) – Rarely Used
    Strong opioids may be used in hospital or after major foot surgery for short periods. They bind opioid receptors in the brain and spinal cord to block pain perception. Because of high risks—addiction, constipation, drowsiness, breathing depression—they are not a routine choice for chronic CMT nerve pain and should be tightly controlled by specialists. FDA Access Data+1

13. Baclofen (tablets, liquids)
    Baclofen is a muscle relaxant used for spasticity and severe cramps. Adult doses are usually started low (e.g., 5 mg three times daily) and increased gradually, watching for drowsiness and weakness. It works by activating GABA-B receptors in the spinal cord to reduce overactive muscle reflexes. Side effects include sleepiness, dizziness and, if stopped suddenly after high doses, serious withdrawal symptoms. FDA Access Data+3FDA Access Data+3FDA Access Data+3

14. Botulinum Toxin Type A (for Focal Spasticity or Deformity)
    In some neuromuscular disorders, botulinum toxin injections are used to weaken over-active muscles (such as toe flexors) contributing to deformity or pain. It blocks acetylcholine release at the neuromuscular junction, temporarily relaxing the targeted muscle for 3–4 months. Evidence in CMT is limited and it must be done by experienced specialists, as over-weakening muscles can worsen function. PMC

15. Low-Dose Benzodiazepines (e.g., Clonazepam) – With Caution
    Sometimes small doses of clonazepam are used for severe nocturnal cramps, tremor or anxiety that is not controlled by other methods. These drugs enhance GABA activity in the brain, which calms nerve firing and muscle activity. However, they carry risks of dependence, sedation and breathing depression and are usually avoided or used for very short periods, especially in young patients. PMC

16. SSRIs (e.g., Sertraline) for Depression/Anxiety
    Selective serotonin reuptake inhibitors are standard treatments for depression and anxiety, which are common in people with chronic neurological diseases. By normalizing serotonin levels, they improve mood and can indirectly reduce pain perception and improve participation in rehab. Choice of SSRI and dose depends on age, other medicines and side-effect profile, so it must be personalized. PMC+1

17. Sleep-Targeted Medicines (e.g., Low-Dose Trazodone or Certain Antihistamines)
    When pain, worry or restless legs disturb sleep, doctors sometimes use low doses of sedating antidepressants or antihistamines. These medicines make it easier to fall asleep and stay asleep, which can moderate pain and fatigue the next day. They must be carefully chosen to avoid worsening balance, heart rhythm or breathing, especially in teenagers. PMC

18. Vitamin D Supplementation (When Deficient)
    Vitamin D is technically a nutrient but is prescribed like a drug when blood levels are low. Adequate vitamin D supports bone health and muscle function, which is important because people with CMT may be less active and more fracture-prone after falls. Doses depend on blood levels and local guidelines; overdose can cause high calcium and kidney problems. Charcot-Marie-Tooth Association+1

19. Short Courses of Corticosteroids (For Other Diagnoses, Not Pure CMT1C)
    Steroids do not treat hereditary demyelinating neuropathy, but they may be used if doctors suspect an additional immune neuropathy or after surgery to reduce inflammation. They work by powerfully suppressing immune responses and swelling. Long-term steroid use has many side effects (weight gain, bone loss, diabetes, infection risk), so they are not a routine CMT1C treatment. PMC

20. Clinical-Trial Medicines (Gene or Nerve-Protective Therapies)
    Around the world, researchers are testing gene-targeted therapies, neuroprotective drugs and other experimental agents for hereditary neuropathies, including some CMT subtypes. These treatments aim to correct the genetic defect or protect myelin and axons, but most are still in early trials. They should only be used inside regulated clinical trials with close safety monitoring. PMC+1

Dietary Molecular Supplements

Evidence for supplements in CMT1C is much weaker than for exercise, bracing and standard pain medicines. Most data come from diabetic or other peripheral neuropathies, not from hereditary CMT. Always talk to your neurologist before starting any supplement, especially in high doses. Bioscientifica+4PubMed+4PMC+4

1. Alpha-Lipoic Acid (ALA)
   ALA is an antioxidant that has shown benefit in some studies of diabetic neuropathy by reducing oxidative stress and improving nerve blood flow. Typical research doses are 600–1,800 mg/day in adults, often in divided doses. It may modestly reduce burning pain and numbness, but long-term benefits and safety in CMT1C are unknown. Side effects can include stomach upset and low blood sugar in some patients. MedRxiv+5PubMed+5MDPI+5

2. Acetyl-L-Carnitine (ALC)
   ALC supports mitochondrial energy production and may protect nerves. Clinical trials in various painful peripheral neuropathies suggest moderate pain relief and improved nerve tests at doses around 1,000–3,000 mg/day in adults. In theory it could help fatigued, energy-hungry nerve cells in CMT, but specific trials are lacking. Side effects are usually mild stomach upset or restlessness. RMJ+5PMC+5PLOS+5

3. Coenzyme Q10 (CoQ10)
   CoQ10 is a key antioxidant and electron carrier in mitochondria. It is used in some mitochondrial diseases to support energy production and reduce oxidative damage, typically at doses of 100–300 mg/day or more in adults. Reviews suggest it can promote nerve regeneration and protect against neuroinflammation in peripheral nerve disorders, but it is not proven for CMT1C specifically. It is generally well tolerated but can cause digestive upset in some people. JAMA Network+4PubMed+4ScienceDirect+4

4. Omega-3 Fatty Acids (Fish Oil, Algal Oil)
   Omega-3 fats (EPA/DHA) may reduce inflammation and support cell membrane health. Typical supplemental doses are 1–3 grams/day of combined EPA/DHA in adults. While they do not repair myelin directly, they may support overall nerve and cardiovascular health, which is useful in long-term chronic conditions. Side effects include fishy aftertaste and, at high doses, higher bleeding risk. Charcot-Marie-Tooth Association

5. B-Complex Vitamins (Especially B1, B6, B12)
   These vitamins are important for normal nerve function. In deficiency states, replacing them can dramatically improve neuropathy, but in hereditary neuropathies they will not cure the underlying gene problem. Typical supplement doses are in the range of standard multivitamins or under medical supervision for higher therapeutic doses. Too much B6 for long periods can itself cause nerve damage, so dosing must be controlled. MedRxiv+1

6. Vitamin D (If Low)
   Vitamin D helps with calcium balance, bone strength and muscle function. For people with low levels, doctors may prescribe high doses for a short time, then maintenance doses (for example, 800–2,000 IU/day in adults, but this varies). In CMT, maintaining bone strength is important because falls and reduced activity increase fracture risk. Overdose can cause high calcium, kidney stones and confusion. Charcot-Marie-Tooth Association+1

7. Magnesium (For Cramps, If Deficient)
   Magnesium helps muscle relaxation and nerve conduction. In people with low magnesium levels, replacement can reduce cramps and twitching. Typical adult doses range from 200–400 mg/day, but high doses can cause diarrhea and, in kidney disease, dangerous high magnesium levels. There is little direct evidence for CMT1C, but correcting deficiency is sensible. Charcot-Marie-Tooth Association

8. Gamma-Linolenic Acid (GLA – e.g., Evening Primrose Oil)
   GLA is a fatty acid that has been compared with alpha-lipoic acid in diabetic neuropathy studies, where it showed some pain-relieving effects. Doses in trials vary but often range around several hundred mg/day of GLA in adults. Mechanisms include anti-inflammatory effects and supporting nerve membrane lipids. It can cause stomach upset and should be used cautiously with blood-thinning drugs. E-DMJ

9. Antioxidant Mixes (Vitamin C, E and Others)
   Some people use combinations of antioxidants hoping to protect nerves from oxidative stress. Small studies in other conditions suggest theoretical benefits, but robust evidence for hereditary neuropathy is limited. Standard doses should not be exceeded, as very high antioxidant doses sometimes have paradoxical effects or interact with treatments. PubMed+1

10. Probiotics and Gut-Support Nutrients
    A healthy gut microbiome may influence inflammation, immunity and even pain processing. Probiotics and prebiotic fibers aim to support a healthier gut environment. Evidence is mostly indirect, but they may help overall well-being and tolerance of medicines. Doses depend on the specific product and should be chosen with a healthcare professional. Charcot-Marie-Tooth Association+1

Immune-Booster, Regenerative and Stem-Cell-Related Drugs

For hereditary motor and sensory neuropathy type 1C, there are no FDA-approved immune booster, regenerative or stem-cell drugs that specifically treat the disease today. Research is ongoing in related neuromuscular and mitochondrial diseases. These examples are mainly to explain the direction of science, not treatments you can simply start. Live Science+7PMC+7PMC+7

1. Gene-Replacement or Gene-Editing Therapies (Experimental)
   For some genetic neuromuscular disorders, such as spinal muscular atrophy, gene-replacement therapies have been approved. For CMT1C, scientists are exploring similar ideas—using viral vectors or editing tools (like CRISPR-based approaches) to correct the LITAF/SIMPLE mutation. These therapies are still in lab or very early clinical trial stages and are only available inside research protocols.

2. Neurotrophic-Factor-Based Therapies
   Experimental drugs that mimic nerve growth factors (like BDNF or NGF analogues) aim to protect or regrow damaged nerves. So far, clinical trials in other neuropathies have had mixed results, and none is approved for CMT. The idea is to support survival of myelinating Schwann cells and axons, but safety and long-term effects need more study.

3. CoQ10 Pathway Modulators (For Mitochondrial Disorders)
   In rare mitochondrial diseases linked to CoQ10 deficiency, experimental molecules that help the body make CoQ10 better have shown dramatic improvement in single case reports, including recovery of walking ability in a severely affected child. These treatments remain highly experimental and disease-specific, not general CMT therapies, but they show how targeting energy pathways may help certain genetic neuropathies in the future. Live Science+5PubMed+5PNAS+5

4. Stem-Cell Transplantation Approaches
   Researchers are studying whether certain stem cells can support nerve repair by releasing growth factors or even becoming Schwann-like cells. Most work is in animals or very early human trials for other neuropathies. At this time, stem-cell “clinics” offering unproven treatments outside trials are risky and should be avoided. Proper stem-cell therapies for CMT1C must go through controlled clinical trials first. PMC+1

5. Immunomodulatory Drugs (Only for Immune Neuropathies)
   Treatments like IVIG, plasma exchange or steroids are effective in autoimmune neuropathies such as CIDP, but CMT1C is not an immune disease. In rare situations where doctors suspect both hereditary and immune processes, these drugs may be tried. They work by calming abnormal immune attacks on myelin. Routine use in pure CMT1C is not recommended. PMC+1

6. Combination “Neuro-Recovery” Programs in Clinical Trials
   Some trials combine intensive rehab, advanced bracing and experimental neuroprotective drugs. The idea is that drugs may prepare the nerve for recovery, while exercise provides the necessary activity signals for repair. These are only available inside trial centers and are not yet standard care. PMC+1

Surgical Treatments (Procedures and Why They Are Done)

Surgery in CMT1C does not fix the nerve disease, but it can correct foot deformities and improve walking and pain when bracing and therapy are not enough. CU School of Medicine+6PubMed+6NMD Journal+6

1. Soft-Tissue Procedures (Achilles Tendon Lengthening, Plantar Fascia Release)
   Tight calf muscles and plantar fascia can pull the heel up and arch high, causing cavus feet and toe-walking. Lengthening these structures can allow the heel to touch the ground and the arch to flatten slightly, improving posture and making brace fitting easier.

2. Tendon Transfers (e.g., Peroneus or Extensor Tendon Transfers)
   In tendon transfer surgery, a stronger or less-important tendon is moved to help a weak movement, such as lifting the foot or stabilizing the ankle. For example, the Jones procedure transfers the extensor hallucis longus tendon to improve dorsiflexion in cavus feet. The goal is a more balanced foot and less foot drop. PubMed+2ENMC+2

3. Osteotomies (Bone Cuts and Re-Shaping)
   When the bones of the foot are twisted or tilted, surgeons can cut and reposition them (for example, calcaneal or first metatarsal osteotomy). This corrects cavovarus alignment and spreads pressure more evenly across the foot. It can improve shoe fit, reduce pressure sores, and make walking less painful. Orthobullets+3PubMed+3www.elsevier.com+3

4. Toe Straightening Procedures
   Hammertoes and claw toes can cause painful corns, shoe difficulty and ulcer risk. Straightening the toes (sometimes with tendon releases, joint work or small fusions) can reduce pain and make footwear more comfortable. Better toe position also improves push-off during walking. Charcot-Marie-Tooth Disease+1

5. Joint Fusions (Arthrodesis) – Reserved for Severe Cases
   In very advanced deformity or arthritis, surgeons may fuse one or more joints in the foot or ankle to create a stable, plantigrade foot. This sacrifices some movement but can greatly reduce pain and improve stability. Because it increases stress on nearby joints, surgeons now try to reserve fusion for specific severe situations. ENMC+2Wiley Online Library+2

Preventions

You cannot “prevent” the genetic cause of CMT1C, but you can reduce complications and slow secondary damage.

1. Keep a regular physiotherapy and stretching program to maintain strength and flexibility. Physiopedia+2Pod NMD+2

2. Use recommended braces and footwear consistently to stabilize feet and ankles and prevent repeated sprains. Charcot-Marie-Tooth Association+2The Foundation for Peripheral Neuropathy+2

3. Avoid very high-impact sports (like long-distance running or jumping) that might overload weak joints. Charcot-Marie-Tooth Association+1

4. Treat any foot sores, blisters or infections quickly to prevent ulcers and bone infection. CU School of Medicine

5. Keep body weight in a healthy range to reduce load on feet and ankles. Charcot-Marie-Tooth Association+1

6. Manage mood and stress early, as depression and anxiety can worsen pain and reduce activity. PMC+1

7. Avoid smoking and excess alcohol, which can further damage nerves and blood vessels. Charcot-Marie-Tooth Association+1

8. Use fall-prevention strategies at home and outside, including good lighting and appropriate walking aids. Charcot-Marie-Tooth Disease+1

9. Keep vaccinations up to date and treat infections promptly to avoid extra weakness and bed rest. PMC

10. Attend regular follow-up with your neurologist, therapist and orthotist to adjust braces and programs as your body changes. PMC+2Charcot-Marie-Tooth Association+2

When to See Doctors

You should see your neurologist or specialist team regularly, but especially if:

• you notice a sudden change in strength, sensation or walking that feels different from your slow usual progression

• you start falling more often or feel unsafe when walking

• braces or shoes suddenly become painful or no longer fit

• you develop open wounds, ulcers or infections on your feet or ankles

• pain becomes severe, keeps you from sleeping, or does not respond to usual measures

• you notice new symptoms like severe back pain, bowel or bladder problems, or rapid weight loss

• your mood is low most days, you lose interest in things, or you have thoughts of hopelessness

For any emergency (such as serious injury, high fever with weakness, or chest pain), seek immediate medical help. PMC+2CU School of Medicine+2

What to Eat and What to Avoid

Food cannot cure hereditary motor and sensory neuropathy type 1C, but the right eating pattern supports energy, bone health, weight control and possibly nerve health. MedRxiv+3Charcot-Marie-Tooth Association+3European CMT Federation+3

1. Eat plenty of colorful fruits and vegetables – they provide antioxidants and vitamins that support general tissue health.

2. Choose lean proteins (fish, poultry, beans, lentils, tofu) to support muscles, especially when you are exercising.

3. Use whole grains (brown rice, oats, whole-wheat bread) instead of refined flour to keep energy levels stable.

4. Include healthy fats like olive oil, nuts and seeds, and, if you eat it, fatty fish for omega-3s.

5. Limit sugary drinks and sweets, which add calories without nutrition and can worsen weight gain and blood sugar control.

6. Avoid very salty and highly processed foods, which can increase blood pressure and water retention and make swelling worse.

7. Keep caffeine moderate, especially if it worsens tremor, sleep problems or anxiety.

8. Avoid heavy alcohol use, as alcohol itself can damage peripheral nerves and interact with many medicines.

9. Drink enough water during the day to prevent cramps, constipation and low blood pressure on standing.

10. Work with a dietitian if you are underweight, overweight, or have other conditions like diabetes or celiac disease that affect nutrition choices.

Frequently Asked Questions

1. Is hereditary motor and sensory neuropathy type 1C the same as Charcot-Marie-Tooth disease?
   Yes. CMT1C is one specific subtype of Charcot-Marie-Tooth disease type 1, caused by mutations in the LITAF/SIMPLE gene. All CMT1 types are hereditary demyelinating neuropathies, but details like severity and age of onset can differ. PMC+2PMC+2

2. Can CMT1C be cured right now?
   No. There is currently no cure that repairs the gene change or fully stops nerve damage in CMT1C. Treatment focuses on rehabilitation, bracing, sometimes surgery, and careful pain and symptom control. Research on gene and nerve-protective therapies is active but still experimental. ScienceDirect+3PMC+3PMC+3

3. Can exercise make my neuropathy worse?
   Properly guided exercise with a knowledgeable physiotherapist is usually helpful, not harmful. Over-training very weak muscles can cause extra fatigue, but tailored aerobic and strengthening programs have been shown to improve function and reduce fatigue in CMT. cbphysiotherapy+3Pod NMD+3Charcot-Marie-Tooth Disease+3

4. Do I have to wear braces all the time?
   Braces are tools, not punishments. Many people with CMT wear AFOs during walking or outdoor activities but may be able to remove them at home or for short distances. Your orthotist and therapist will explain when braces give the most benefit and how to balance support with muscle use. Custom Orthotic+4Charcot-Marie-Tooth Association+4Charcot-Marie-Tooth Disease+4

5. Will I definitely need foot surgery?
   Not everyone with CMT1C will need surgery. Good bracing, footwear and therapy can delay or prevent operations in many people. Surgery is considered when deformity, pain or instability remain severe despite conservative treatment. Wiley Online Library+3PubMed+3NMD Journal+3

6. Are neuropathic pain medicines addictive?
   Drugs like pregabalin, gabapentin, duloxetine and amitriptyline are not classic opioids, but pregabalin and gabapentin can cause dependence and withdrawal if stopped suddenly after long use. Opioids like tramadol have clear addiction and overdose risks and must be used very carefully or avoided. FDA Access Data+5NCBI+5FDA Access Data+5

7. Can supplements replace my medicines or braces?
   No. Supplements like alpha-lipoic acid, acetyl-L-carnitine or CoQ10 may offer modest benefit in some neuropathies, but they cannot replace structured rehab, orthoses or proven pain medicines. Think of them as possible “extras,” always discussed with your doctor. Bioscientifica+6PubMed+6PMC+6

8. Is it safe for a teenager with CMT1C to take these drugs and supplements?
   Safety depends on age, weight, other health problems and interactions with other medicines. Many drugs in this list are not approved in children or teens for neuropathic pain, and doses must be carefully adjusted. This is why you must always rely on your neurologist or pediatric specialist for decisions. FDA Access Data+4FDA Access Data+4FDA Access Data+4

9. Will CMT1C shorten my life?
   For many people, CMT1C mostly affects mobility and sensation rather than vital organs. Most patients have a normal life expectancy but may need more support devices over time. Staying active, preventing falls and protecting feet are key to a good quality of life. PMC+1

10. Can diet alone stop my neuropathy from progressing?
    No diet can change the underlying gene mutation, but healthy eating can support muscles, bones and general health. Good nutrition also helps weight control and lowers the risk of other illnesses that could worsen disability. Charcot-Marie-Tooth Association+1

11. Should my family members be tested for CMT1C?
    Because CMT1C is hereditary, genetic counseling and testing may be offered to family members, especially if they have symptoms or are planning children. A genetics team can explain the pattern of inheritance and what testing can and cannot tell you. PMC+2ScienceDirect+2

12. Is it okay to play sports or do gym class?
    Many people with CMT safely do sports, but the type and intensity should be tailored. Low-impact activities like swimming, cycling, yoga and carefully chosen gym exercises are usually better than high-impact running and jumping. Your physio can suggest safe options and advise your school. Charcot-Marie-Tooth Association+3Pod NMD+3Charcot-Marie-Tooth Disease+3

13. What about pregnancy and CMT1C in the future?
    Many people with CMT have successful pregnancies, but carrying extra weight and delivery can be more tiring on weak legs and feet. Some pain medicines are not safe in pregnancy, so treatment plans may need to change. Genetic counseling before pregnancy can explain chances of passing on the gene. PMC+2FDA Access Data+2

14. Are there real clinical trials for CMT1 subtypes?
    Yes. International networks run trials on exercise programs, orthotic designs, symptom-control drugs and experimental gene or nerve-protective therapies for different CMT types. Trial lists change over time, so your neurologist or major CMT organizations can help you find current studies. PMC+2PMC+2

15. What is the most important thing I can do right now?
    The single most important action is to build a consistent routine: regular physiotherapy and stretching, using your braces or footwear correctly, protecting your feet, sleeping well, and staying emotionally supported. Medicines and possible future therapies work best when they sit on top of this strong daily foundation. European CMT Federation+4Physiopedia+4CMT Australia+4

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: December 25, 2025.

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