Hereditary Adult-Onset Painful Axonal Polyneuropathy

Hereditary adult-onset painful axonal polyneuropathy is a rare inherited nerve disease. It mainly affects the long nerves in the legs and sometimes the arms. These nerves slowly become damaged along their “axon,” which is the long wire part of the nerve cell. Because of this damage, people develop burning pain, tingling, and numbness that usually start in the feet in adult life and later move upward and into the hands. GARD Information Center+1

Hereditary adult-onset painful axonal polyneuropathy is a very rare genetic nerve disease. Doctors also call it Charcot-Marie-Tooth disease type 2V (CMT2V). In this condition, the long “wires” of the nerves (axons) in the legs and hands slowly become damaged. This damage causes burning pain, tingling, numbness, and weakness that usually start in the feet in adult life and then move upward and later affect the hands. The condition is usually inherited in an autosomal-dominant way, often linked to changes in the NAGLU gene.NCBI+2

This condition is now known to be the same as Charcot-Marie-Tooth disease axonal type 2V (CMT2V) in many medical databases. It is usually passed down in an autosomal dominant way. That means a person can get the disease if they receive one changed (mutated) copy of a gene from either mother or father. The gene usually involved is called NAGLU, which makes an enzyme that works inside small sacs in the cell called lysosomes. Orpha+2NCBI+2

In this disease, the main feature is pain. People often first notice repeated leg pain. Later, they feel constant painful tingling or burning in the feet, and then in the hands. They can also have reduced feeling for vibration, absent ankle reflexes, and a bit of unsteady walking (sensory ataxia). PubMed+2OUP Academic+2

Other names

Doctors and research sites use several other names for the same or very closely related condition. These names come from different databases, but they describe essentially the same inherited painful axonal neuropathy: NCBI+2MalaCards+2

• Charcot-Marie-Tooth disease, axonal, type 2V

• CMT2V

• Autosomal dominant Charcot-Marie-Tooth disease type 2V

• Charcot-Marie-Tooth neuropathy type 2V

• Autosomal dominant CMT type 2 due to NAGLU mutation

• NAGLU Charcot-Marie-Tooth disease

• Hereditary adult-onset painful axonal polyneuropathy (the name you used)

All these names point to a hereditary axonal motor-sensory neuropathy with adult-onset pain, usually linked to a change in the NAGLU gene.

“Axonal” refers to damage to the long fiber (axon) of the nerve cell, rather than mainly to the myelin coating around the nerve. In this disease, the axon in many nerves slowly degenerates. The longest nerves are affected first, which is why symptoms start in the feet. PM&R KnowledgeNow+1

“Polyneuropathy” means many nerves are affected at the same time, usually in a fairly even and “length-dependent” pattern. So both legs are affected in a similar way, then later both hands. The nerves that carry pain and temperature signals are often affected early, so painful burning and pins-and-needles feelings are common. NCBI+1

Because the problem is hereditary and long-standing, the changes develop slowly over years. Many people still walk and move fairly well, but the chronic pain can strongly affect sleep, mood, and quality of life. ScienceDirect+1

Types or clinical patterns

There is no strict official list of “types” inside hereditary adult-onset painful axonal polyneuropathy. However, doctors often notice different clinical patterns in people with the same genetic problem: PubMed+2OUP Academic+2

1. Typical painful sensory-predominant pattern
   In many people the main problem is repeated leg pain that becomes constant burning or tingling in the feet and then hands. Weakness is mild or absent, and pain is the main complaint.

2. Sensory-ataxic pattern
   Some people have more loss of position and vibration sense. They may feel unsteady in the dark, or their walking may look “clumsy.” This is called sensory ataxia, and it happens because the brain gets poor feedback from the feet.

3. Motor-sensory pattern
   A smaller number of people may have mild weakness in the feet or ankles, such as foot drop or trouble climbing stairs, in addition to pain and sensory loss. This pattern is similar to other axonal forms of Charcot-Marie-Tooth disease. PM&R KnowledgeNow

4. Pain-dominant small-fiber-like pattern
   Some patients mainly have burning pain and abnormal feelings without big changes in strength or large-fiber tests early on. This looks similar to small-fiber neuropathy, where tiny pain fibers are especially damaged. NCBI+1

These are not separate genetic types. They are different ways the same basic nerve damage can appear in real life.

Causes

For this specific disorder, the central cause is a pathogenic mutation in the NAGLU gene. However, when doctors see an adult with painful axonal polyneuropathy, they must also think about many other possible causes before confirming this rare hereditary form. So below are:

• the main direct causes or mechanisms of hereditary adult-onset painful axonal polyneuropathy, and

• other diseases that can cause a similar painful axonal polyneuropathy, which must be ruled out.

1. NAGLU gene mutation
   The key cause of this hereditary neuropathy is a harmful change in the NAGLU gene. This gene makes an enzyme in lysosomes. A specific dominant mutation can disturb nerve cell function and lead to axonal degeneration and pain without the full picture of mucopolysaccharidosis. Orpha+1

2. Autosomal dominant family inheritance
   Most affected people have an affected parent or other family members with similar symptoms. Half of the children of an affected parent can inherit the changed gene. This family pattern is a strong clue that the cause is hereditary, not acquired. PubMed+1

3. New (de novo) NAGLU mutation
   Sometimes the NAGLU mutation appears for the first time in a child, without a history in previous generations. This new mutation can still be passed on to the next generation. MDPI+1

4. Axonal degeneration of long sensory and motor nerves
   The mutation causes progressive damage to the axons of long nerves, especially those going to the feet. Over time the axons thin, lose function, and may die back, causing pain and sensory loss. This axonal degeneration is a core mechanism in CMT2 disorders. ScienceDirect+1

5. Lysosomal dysfunction and subtle storage in neurons
   NAGLU is a lysosomal enzyme that helps break down heparan sulfate. When it does not work normally, partly processed molecules may build up in cells. Even if this build-up is mild compared with classic mucopolysaccharidosis IIIB, it may still harm long nerves over time. Orpha+1

6. Age-related vulnerability of long nerves (adult onset)
   Symptoms usually start in adulthood, meaning that nerves can cope for many years but slowly lose their reserve. With age, the combination of the mutation and normal wear and tear on long nerves can finally cross a threshold and cause symptoms. PubMed+1

7. Genetic modifier genes
   Other genes may change how severe or how early symptoms appear. Studies of painful small-fiber and axonal neuropathies show that multiple genes can interact to shape pain and nerve damage. MDPI+1

8. Metabolic stress (for example, high blood sugar) as a worsening factor
   If a person with the NAGLU mutation also has high blood sugar or diabetes, their nerves are under extra metabolic stress. This can worsen symptoms or make them start earlier, even though diabetes alone is not the main cause in this hereditary condition. ScienceDirect+1

9. Mechanical stress on long nerves
   Long periods of standing, walking, or heavy work are normal life activities, but in someone with fragile axons they may contribute to symptom flares, cramps, or pain. This is not a primary cause but an aggravating factor. ScienceDirect+1

10. Diabetic polyneuropathy (important acquired cause to exclude)
    Diabetes is the most common cause of painful distal axonal polyneuropathy worldwide. Doctors must test for diabetes to be sure that pain and axonal changes are not fully explained by high blood sugar alone. ScienceDirect+1

11. Vitamin B12 or other vitamin deficiencies
    Low vitamin B12, folate, or vitamin B6 can damage nerves and cause numbness and tingling. These are treatable causes, so they must be checked and corrected before accepting a rare hereditary diagnosis. ScienceDirect+1

12. Excess alcohol use
    Long-term heavy alcohol intake can cause a painful axonal polyneuropathy, often mixed with poor nutrition. This is another common acquired cause that doctors must consider and treat. ScienceDirect

13. Chemotherapy-induced neuropathy
    Some chemotherapy drugs, such as platinum compounds or taxanes, can damage sensory axons and cause pain. A history of cancer treatment makes this an important alternative explanation. ScienceDirect+1

14. Autoimmune small-fiber neuropathy
    Immune-mediated conditions, such as autoimmune small-fiber neuropathy, can cause burning pain in the feet and hands. In these cases, immune tests and sometimes skin biopsy show a different pattern from hereditary CMT2V. NCBI+1

15. Chronic kidney disease (uremic neuropathy)
    Long-standing kidney failure can damage nerves and cause a length-dependent axonal neuropathy. Blood tests for kidney function help separate this from rare hereditary causes. ScienceDirect

16. Thyroid disease (hypothyroidism)
    Low thyroid hormone can contribute to neuropathy and pain. Diagnosis and treatment of thyroid disease are important in anyone with unexplained neuropathy. ScienceDirect+1

17. Infections such as HIV
    Some chronic viral infections, including HIV, can cause painful distal neuropathy, either from the virus itself or from certain antiviral drugs. Doctors may test for these when neuropathy is unexplained. ScienceDirect

18. Paraneoplastic neuropathy (cancer-related immune reaction)
    Rarely, cancers elsewhere in the body can trigger an immune reaction that attacks nerves, causing a painful axonal polyneuropathy. In such cases, blood tests and imaging look for hidden malignancy. ScienceDirect+1

19. Other hereditary axonal neuropathies (non-NAGLU)
    Many other genes can cause axonal Charcot-Marie-Tooth disease or hereditary sensory and autonomic neuropathy. If gene testing is limited, these other genetic causes must be considered and sometimes found on broader panels. PM&R KnowledgeNow+2Breda Genetics srl+2

20. Idiopathic chronic axonal polyneuropathy
    In some adults, all tests are normal and no clear cause is found. This is called idiopathic chronic axonal polyneuropathy. When a clear NAGLU mutation and family pattern are present, the diagnosis changes from idiopathic to this specific hereditary type. Ovid

Symptoms

1. Recurrent leg pain
   Many people first notice attacks of leg pain, often deep and aching. These episodes may come and go at first. Over time, the pain can become more frequent and then constant. PubMed+1

2. Burning pain in the feet
   A very common symptom is a burning or hot feeling in the soles of the feet. It may feel like the feet are on fire or standing on hot sand. This is due to irritation of pain fibers in the damaged nerves. NCBI+1

3. Pins-and-needles and tingling
   People often describe tingling, prickling, or “pins and needles” in the toes and feet. This may spread up the legs and later appear in the hands. These abnormal feelings are called paresthesias. PubMed+1

4. Numbness or reduced feeling
   As nerves get more damaged, some areas may feel numb. The person may not notice small injuries, heat, or cold as well. This loss of protective sensation can increase the risk of skin injuries. Cleveland Clinic+1

5. Painful sensitivity to light touch (allodynia)
   Sometimes even a light touch from socks or bed sheets can feel painful. This is called allodynia. It happens because damaged nerves send wrong pain signals to the brain. NCBI+1

6. Leg cramps and muscle discomfort
   Cramping in the calves or feet, especially at night, is common. Even if muscle strength is largely normal, irritated nerves can cause sudden tight, painful contractions in the muscles. PubMed+1

7. Reduced vibration sense
   On examination with a tuning fork, doctors often find reduced ability to feel vibration at the big toe or ankles. The person may also notice having trouble feeling the ground well when walking. GARD Information Center+1

8. Loss of ankle reflexes
   Deep tendon reflexes, especially the ankle jerk, are often decreased or absent. The person may not notice this, but the doctor checks it with a reflex hammer as part of the nerve exam. GARD Information Center+1

9. Mild sensory ataxia (unsteady walking)
   Some people feel unsteady, especially in the dark or when their eyes are closed. This happens because their brain gets poor information about where the feet are in space. They may sway or lose balance when standing with feet together and eyes closed (Romberg sign). PubMed+1

10. Sleep disturbance due to pain
    Burning and electric-shock-like pains often get worse at night. This can make it hard to fall asleep or stay asleep. Poor sleep then worsens fatigue and reduces quality of life. Cleveland Clinic+2ScienceDirect+2

11. Symptoms spreading from feet to hands (“stocking-glove” pattern)
    Over time, symptoms often move up the legs to the knees, and later appear in the hands. This “stocking-glove” pattern is typical of length-dependent polyneuropathy, where the longest nerves are affected first. Cleveland Clinic+1

12. Coldness or temperature change in the feet
    Some people feel unusual coldness or heat in the feet, even when the skin is warm to the touch. This comes from faulty temperature signals in damaged nerves. NCBI+1

13. Mild weakness or fatigue in legs
    While this condition is mainly sensory and painful, some individuals may notice mild weakness in foot muscles, especially after many years. Climbing stairs or walking long distances may become tiring. GARD Information Center+2Global Genes+2

14. Fatigue and reduced activity due to chronic pain
    Persistent pain can make people less active. They may avoid walking or exercise out of fear of worsening pain. This inactivity can lead to general tiredness and loss of physical fitness. ScienceDirect+1

15. Emotional distress, anxiety, or low mood
    Living with chronic pain and uncertainty about the future can cause anxiety and low mood. Good care includes not only treating the nerves but also supporting mental health. ScienceDirect+1

Diagnostic tests

Doctors diagnose hereditary adult-onset painful axonal polyneuropathy by combining:

• the history of adult-onset painful sensory symptoms,

• the physical and neurological exam,

• electrodiagnostic tests that show axonal neuropathy,

• lab tests to rule out common acquired causes, and

• genetic testing that finds a pathogenic NAGLU mutation or related CMT2V gene change in the person and family. PubMed+2OUP Academic+2

Physical examination tests (at the bedside)

1. Full neurological examination
   The doctor looks at muscle bulk, strength, and tone in arms and legs, checks reflexes with a hammer, and tests coordination. In this condition, strength may be mostly preserved early, but ankle reflexes are often reduced or absent, and mild unsteadiness may be present. GARD Information Center+2Global Genes+2

2. Sensory examination for touch, pain, temperature, and vibration
   The doctor uses cotton, a pin, warm and cool objects, and a vibrating tuning fork to measure sensation in the toes, feet, legs, fingers, and hands. A length-dependent loss of pain, temperature, and vibration in the feet that slowly spreads upwards suggests an axonal polyneuropathy. Cleveland Clinic+2Johns Hopkins Medicine+2

3. Gait and balance testing (including Romberg test)
   The doctor watches how the person walks, turns, and stands. For the Romberg test, the person stands with feet together and eyes closed. Increased swaying or falls suggest sensory ataxia from loss of position sense in the feet, which supports the diagnosis of sensory-predominant axonal neuropathy. PubMed+1

4. Screening for autonomic signs
   Blood pressure and heart rate may be checked lying and then standing, and the skin may be examined for color, sweating, or dryness. While autonomic problems are not the main feature of this condition, looking for them helps distinguish it from some hereditary sensory and autonomic neuropathies (HSAN). Breda Genetics srl+1

Manual / bedside sensory tests

5. Monofilament (pressure) test
   A thin plastic filament is gently pressed against the skin of the toes and feet. The person says when they feel it. Reduced ability to feel the filament shows loss of protective sensation, which is common in distal polyneuropathies and helps judge risk for foot injuries. Cleveland Clinic+1

6. Vibration test with tuning fork
   A 128-Hz tuning fork is struck and placed on bony points such as the big toe and ankle. The person reports how long they feel the vibration. In this condition, vibration sense is often reduced at the feet early, which is a classic sign of large-fiber sensory involvement. GARD Information Center+2Global Genes+2

7. Pinprick (sharp–dull) test
   A disposable pin or neurotip is used to gently touch the skin, and the person is asked if it feels sharp or dull. Reduced or altered pain sensation in a stocking-glove distribution supports a diagnosis of sensory axonal polyneuropathy. Cleveland Clinic+2Johns Hopkins Medicine+2

8. Temperature discrimination test
   The doctor uses metal and plastic ends of an object, or special devices, to test whether the person can tell cold from warm. Difficulty telling temperature in the feet suggests involvement of small fibers and pain-temperature pathways, commonly affected in painful neuropathies. NCBI+2Practical Neurology+2

Laboratory and pathological tests

9. Basic blood tests (screening panel)
   Doctors often order tests such as blood sugar, HbA1c, kidney function, liver tests, thyroid function, vitamin B12, folate, and complete blood count. These tests help rule out common acquired causes like diabetes, kidney disease, vitamin deficiency, and thyroid disease, which might otherwise explain the neuropathy. ScienceDirect+1

10. Genetic test for NAGLU mutation
    Once a hereditary axonal neuropathy is suspected, targeted genetic testing for NAGLU or a curated CMT2V panel can be done. Finding a clearly pathogenic NAGLU mutation that matches the clinical features and family history confirms the diagnosis of hereditary adult-onset painful axonal polyneuropathy. Orpha+2Monarch Initiative+2

11. Expanded hereditary neuropathy gene panel
    If targeted NAGLU testing is negative, an expanded gene panel for inherited neuropathies (including many CMT and HSAN genes) may be used. This test checks many neuropathy genes at once and can identify other axonal CMT2 or HSAN forms that may look similar. ScienceDirect+2PM&R KnowledgeNow+2

12. Nerve biopsy (for example, sural nerve biopsy)
    In selected cases, a small piece of a sensory nerve in the leg (sural nerve) is removed and examined under the microscope. It can show axonal loss, changes in myelin, and sometimes small storage material in lysosomes. Biopsy is now used less often because gene testing is more available, but it can still be helpful in unclear cases. ScienceDirect+1

13. Skin biopsy for small-fiber nerve density
    A tiny piece of skin is taken, usually from the lower leg, and stained to count small nerve fibers in the skin. Reduced nerve fiber density confirms small-fiber neuropathy, which may coexist with large-fiber axonal damage and explain severe burning pain. NCBI+2Practical Neurology+2

14. Cerebrospinal fluid (CSF) analysis in selected cases
    Sometimes a lumbar puncture is done to analyze CSF. This test is mainly used to rule out inflammatory or immune-mediated neuropathies, which can show high protein or immune cells. In hereditary axonal neuropathies like CMT2V, CSF is usually normal. ScienceDirect+1

Electrodiagnostic and functional tests

15. Nerve conduction studies (NCS)
    Surface electrodes are placed on the skin and small electrical pulses are given to measure how fast and how strongly nerves conduct signals. In hereditary adult-onset painful axonal polyneuropathy, NCS typically show reduced amplitudes (because axons are lost) with relatively preserved conduction velocities (because myelin is less affected). This pattern is typical of axonal CMT type 2. ScienceDirect+2PM&R KnowledgeNow+2

16. Electromyography (EMG)
    A thin needle electrode is inserted into muscles to record their electrical activity. EMG can show signs of chronic denervation and reinnervation in distal muscles, supporting the diagnosis of long-standing axonal motor involvement. It also helps exclude other diseases like motor neuron disease or muscle disorders. PM&R KnowledgeNow+1

17. Quantitative sensory testing (QST)
    QST uses computer-controlled devices to measure thresholds for feeling warmth, cold, vibration, or pain. It gives a more detailed picture of sensory function than simple bedside tests. In painful axonal neuropathies, QST often shows abnormal thresholds in the feet and sometimes hands. Practical Neurology+1

Imaging tests

18. MRI of the spine
    MRI of the cervical and lumbar spine helps rule out spinal cord or nerve root compression, such as from disk herniation or spinal stenosis, which can mimic or worsen neuropathic symptoms in the legs. A normal MRI supports the idea that the problem is peripheral neuropathy, not a central nervous system issue. Practical Neurology+1

19. MRI of the brain (if other neurological signs are present)
    If someone has unusual features such as spasticity, weakness, or vision problems, a brain MRI may be done to exclude multiple sclerosis, stroke, or other central causes. In pure hereditary adult-onset painful axonal polyneuropathy, the brain MRI is usually normal, which helps further narrow the diagnosis to peripheral nerves. ScienceDirect+1

20. Ultrasound or MR neurography of peripheral nerves
    High-resolution ultrasound or MR neurography can sometimes show thinning or other structural changes of peripheral nerves. While not routinely needed for this diagnosis, these imaging methods can help distinguish hereditary neuropathies from focal compressive neuropathies and guide nerve biopsy if required. Practical Neurology+1

Non-pharmacological treatments

1. Education about the disease and self-management
   Education helps you understand why you have pain, numbness, and weakness and what you can realistically expect. The purpose is to reduce fear and confusion and to help you take an active role in care. The neurologist explains that this is a genetic, slowly progressive nerve disease, not “in your head.” Simple explanations about nerve damage, pain pathways, pacing of activities, and realistic goals can reduce anxiety and sometimes even lower the feeling of pain intensity.BrainFacts+1

2. Regular follow-up with a neurologist
   Regular visits allow the doctor to track changes in strength, sensation, walking, and pain. The purpose is early detection of progression or complications such as foot deformities, severe balance problems, or depression. The mechanism is simple: by checking reflexes, sensation, nerve tests, and daily function on a schedule, the team can adjust therapies, add aids, or change medicines before problems become severe, helping preserve independence for longer.BrainFacts

3. Physical therapy and personalized exercise program
   Physical therapists design safe exercises to maintain muscle strength, joint movement, and balance. The purpose is to slow stiffness, prevent muscle wasting from disuse, and reduce falls. The mechanism is graded “use it but do not overuse it”: low-impact strength work, stretching, and balance training stimulate muscles and joints without overloading fragile nerves. Regular movement also improves blood flow to nerves and may reduce pain in some people.PM&R KnowledgeNow+1

4. Occupational therapy for daily activities and hand function
   Occupational therapists teach easier ways to dress, cook, write, and use tools when hands and feet are painful or weak. The purpose is to keep independence and reduce frustration. The mechanism is adaptation: they suggest special grips, larger handles, voice-controlled devices, and energy-saving techniques so you can still complete tasks while putting less stress on painful nerves and weak muscles.BrainFacts

5. Aerobic exercise (like walking, stationary cycling, or swimming)
   Gentle aerobic exercise improves heart and lung health, mood, and blood flow. The purpose is to fight fatigue, improve sleep, and support nerve health. The mechanism is that regular moderate activity increases circulation, reduces inflammatory factors, and releases endorphins, which are natural pain-relieving chemicals. It is important to avoid over-exertion; exercising “a bit less than your limit” is usually safer in hereditary neuropathies.Cleveland Clinic+1

6. Strength training with low weights and careful supervision
   Simple strength work (for example, bands or light weights) focuses on muscles around ankles, knees, hips, and hands. The purpose is to maintain muscle power as long as possible and support joints. The mechanism is that muscles get stronger when they are used in a controlled way, which helps compensate partly for nerve damage and improves stability during walking and standing. Over-straining must be avoided because severely weak muscles can be injured easily.PM&R KnowledgeNow

7. Stretching and range-of-motion exercises
   Daily stretching helps keep joints flexible and reduces contractures. The purpose is to prevent the ankles, toes, and fingers from becoming stuck in a fixed position, which can worsen walking and balance. The mechanism is slow, gentle movement of joints and soft tissues through their full range, which keeps tendons and ligaments from tightening and reduces pain from stiffness.

8. Balance and gait training
   Many patients with this disease have loss of position sense and unsteady walking. Balance training uses simple tasks like standing on a stable surface with support, heel-to-toe walking, and practicing safe turns. The purpose is to reduce falls. The mechanism is to train the brain to use vision and the remaining sensation more efficiently and to build core and leg stability.PM&R KnowledgeNow

9. Orthotic devices and proper footwear
   Custom shoe inserts, ankle-foot orthoses (AFOs), and supportive shoes help correct or support foot deformities and weakness. The purpose is to improve walking, reduce pain, and prevent skin breakdown. The mechanism is mechanical: braces hold the foot in a more normal position, prevent ankle rolling, distribute pressure more evenly, and reduce the effort needed to walk, so every step is safer and less painful.BrainFacts+1

10. Pain psychology, cognitive-behavioral therapy (CBT), and coping skills
    Chronic pain affects mood, sleep, and relationships. Psychological therapies teach coping skills, relaxation, and ways to reduce catastrophic thinking (“this pain will destroy my life”). The purpose is to improve quality of life even if nerve damage remains. The mechanism is that changing thoughts and behaviors can reduce pain perception and help the brain filter pain signals more effectively, lowering distress and disability.Cleveland Clinic

11. Mindfulness, relaxation training, and breathing exercises
    Mindfulness practices teach you to notice pain without panicking, and relaxation exercises calm the nervous system. The purpose is to lower stress-related pain spikes and improve sleep. The mechanism is activation of the body’s relaxation response: slower heart rate, lower muscle tension, and decreased stress hormone levels, which may reduce the intensity of chronic neuropathic pain.

12. Sleep hygiene and night-time positioning
    Pain often worsens at night. Sleep hygiene means regular sleep times, avoiding heavy meals and screens before bed, and keeping the bedroom dark and quiet. Good positioning with pillows under the calves or between the knees can reduce nerve pressure. The purpose is to improve sleep quality, which in turn can reduce pain sensitivity during the day.

13. Careful foot and skin care
    Because sensation is reduced, small injuries may go unnoticed and can become ulcers or infections. Daily inspection of feet and legs, moisturizing dry skin, and prompt care of blisters or cuts are essential. The purpose is to prevent wounds and serious infections. The mechanism is early detection and prevention: you find and treat small problems before they become big ones.Cleveland Clinic

14. Fall-prevention and home safety measures
    Removing loose rugs, adding grab bars in the bathroom, using night lights, and keeping floors clear all reduce fall risk. The purpose is to prevent fractures and head injuries in people with poor sensation and balance. The mechanism is reducing environmental hazards so even if your balance is weak, you are less likely to trip or slip.

15. Transcutaneous electrical nerve stimulation (TENS)
    TENS is a small device that sends gentle electrical signals through pads placed on the skin near painful areas. The purpose is short-term pain relief. The mechanism is “gate control”: the mild electrical signal competes with pain signals in the spinal cord and brain, which can make the pain feel weaker or less bothersome for some people.

16. Heat and cold therapy (used carefully)
    Warm packs or warm baths can relax muscles and reduce stiffness, while cold packs may reduce burning pain. The purpose is temporary relief. The mechanism is that temperature changes affect blood flow and nerve signal transmission. Because sensation is reduced, heat and cold must be used very carefully to avoid burns or frostbite.

17. Smoking cessation and limiting alcohol
    Smoking and heavy alcohol use both harm peripheral nerves and blood vessels. The purpose of stopping smoking and limiting alcohol is to avoid extra nerve damage on top of the genetic disease. The mechanism is that you remove toxic exposures that worsen neuropathy, helping remaining nerves work as well as possible.Mayo Clinic+1

18. Nutritional counseling and healthy weight management
    A diet rich in vegetables, fruits, whole grains, lean protein, and healthy fats supports general health and may help nerve function, especially if vitamin deficiencies are present. The purpose is to avoid obesity, high blood sugar, and vitamin shortages that can worsen neuropathy. The mechanism is providing the body with needed vitamins, minerals, and antioxidants while avoiding metabolic stressors such as high sugar and saturated fats.Cleveland Clinic

19. Support groups and peer networks
    Meeting others with hereditary neuropathies in person or online reduces isolation. The purpose is emotional support, practical tips, and motivation to follow treatment plans. The mechanism is social connection and sharing experiences, which can lower depression and help people feel more in control of their condition.BrainFacts

20. Assistive devices and mobility aids
    Canes, walking sticks, walkers, or wheelchairs, when needed, improve safety and allow longer distances with less pain and fatigue. The purpose is to maintain mobility and participation in life, not to “give up.” The mechanism is redistributing load and providing extra stability so damaged nerves and weak muscles do not have to handle all of the work alone.PM&R KnowledgeNow

Drug treatments

Safety reminder: These medicines are examples commonly used for neuropathic pain, based largely on studies in diabetic neuropathy and other nerve pain, not specifically on CMT2V. They must only be used under medical supervision, with doses adjusted by a doctor.

1. Pregabalin (Lyrica)
   Pregabalin is an anti-seizure medicine approved for neuropathic pain such as diabetic peripheral neuropathy and postherpetic neuralgia.FDA Access Data+1 It belongs to the gabapentinoid class and binds to calcium channels in nerve cells to reduce release of pain-transmitting chemicals. Typical adult neuropathic pain doses are 150–300 mg per day divided into two or three doses, but the neurologist adjusts this based on kidney function and side effects. Common side effects include dizziness, drowsiness, weight gain, and ankle swelling.FDA Access Data+1

2. Gabapentin (Neurontin, Gralise, Horizant)
   Gabapentin is another gabapentinoid used widely for neuropathic pain. It reduces abnormal nerve firing by acting on calcium channels. For neuropathic pain, doctors often start with a low evening dose and slowly increase, sometimes up to 1800–3600 mg per day in divided doses in adults, depending on kidney function and tolerance.FDA Access Data+2FDA Access Data+2 Side effects include dizziness, fatigue, and swelling; sudden stopping can cause withdrawal symptoms.

3. Duloxetine (Cymbalta)
   Duloxetine is a serotonin-norepinephrine reuptake inhibitor (SNRI) antidepressant approved for diabetic neuropathic pain and fibromyalgia.FDA Access Data+2FDA Access Data+2 It increases serotonin and norepinephrine levels in the spinal cord, which strengthens the body’s own pain control pathways. The usual adult dose for neuropathic pain is 60 mg once daily. Side effects may include nausea, dry mouth, sleep changes, and increased blood pressure; it must not be stopped suddenly without medical advice.

4. Venlafaxine (extended-release)
   Venlafaxine is another SNRI sometimes used off-label for neuropathic pain when duloxetine is not suitable. It works by enhancing serotonin and norepinephrine in similar ways. Doctors usually start with low doses and titrate slowly. Side effects can include increased blood pressure, sweating, nausea, and sleep disturbance. Because it affects mood, careful monitoring is needed.

5. Amitriptyline
   Amitriptyline is a tricyclic antidepressant used for many types of chronic pain, especially burning nerve pain. It blocks reuptake of serotonin and norepinephrine and also calms overactive pain pathways. For neuropathic pain, doctors often use low doses at night, such as 10–25 mg, and increase gradually if tolerated. Side effects include dry mouth, constipation, drowsiness, and sometimes heart rhythm changes, so it is used with caution, especially in older adults.Cleveland Clinic

6. Nortriptyline
   Nortriptyline is another tricyclic antidepressant that often has fewer sedating and blood pressure effects than amitriptyline. It is used in similar low nightly doses for neuropathic pain. The mechanism is similar—enhancing descending pain inhibition and blocking certain ion channels. Side effects include dry mouth, constipation, and possible heart rhythm issues, so ECG monitoring may be needed in some patients.

7. Topical lidocaine 5% patch
   Lidocaine patches provide local numbing to painful skin areas and are widely used in postherpetic neuralgia and other focal neuropathic pains. They block sodium channels in nerve endings, which stops pain signals from starting. The usual adult regimen is to apply patches to painful areas for up to 12 hours per day, with skin breaks in between. Side effects are mainly local skin irritation; systemic effects are rare when used correctly.Cleveland Clinic

8. Capsaicin 8% patch (Qutenza)
   Qutenza is a high-dose capsaicin patch, FDA-approved for neuropathic pain from postherpetic neuralgia and diabetic peripheral neuropathy.FDA Access Data+2FDA Access Data+2 Capsaicin strongly activates TRPV1 pain receptors in the skin, which then become less sensitive and send fewer pain signals for weeks to months. It is applied by trained staff in a clinic for 30–60 minutes, with protective measures. Side effects include burning pain and redness at the application site during and shortly after treatment.

9. Tramadol
   Tramadol is a weak opioid that also increases serotonin and norepinephrine. It may be used for short-term control of moderate neuropathic pain when first-line drugs are not enough. The mechanism is mixed opioid receptor activation plus monoamine reuptake inhibition. Side effects include nausea, dizziness, constipation, and risk of dependence. It must be used cautiously and usually for limited periods under close medical supervision.

10. Tapentadol
    Tapentadol combines stronger norepinephrine reuptake inhibition with mu-opioid agonist action and is used in some chronic neuropathic pain cases. Its purpose is pain relief when other treatments fail. Side effects include nausea, dizziness, constipation, and risk of dependence and overdose. Because of these risks, many guidelines reserve it for selected patients and recommend careful monitoring.

11. Non-steroidal anti-inflammatory drugs (NSAIDs)
    NSAIDs like ibuprofen or naproxen mainly reduce inflammatory pain, not neuropathic pain, but they may help with secondary muscle and joint aches due to abnormal gait or posture. Their mechanism is blocking COX enzymes that produce prostaglandins, which are inflammatory chemicals. Side effects include stomach irritation, ulcers, kidney issues, and increased cardiovascular risk when used long term.

12. Acetaminophen (paracetamol)
    Acetaminophen may reduce mild background pain or headaches related to chronic disease, but it has limited effect on strong neuropathic pain. Its mechanism is still not fully clear but involves central pain pathways. It is usually safe at recommended doses, but high doses or combined use with alcohol can damage the liver.

13. Baclofen
    Baclofen is a muscle relaxant that activates GABA-B receptors and reduces muscle spasm. In hereditary neuropathies, it may help if painful cramps or spasticity are present. It is usually started at low oral doses and increased slowly. Side effects include drowsiness, weakness, and dizziness; sudden withdrawal can cause serious symptoms, so dose changes must be gradual under medical guidance.

14. Tizanidine
    Tizanidine is another muscle relaxant that acts on alpha-2 adrenergic receptors in the central nervous system. It reduces muscle tone and can ease painful cramps. It is usually taken several times a day. Side effects include drowsiness, dry mouth, and low blood pressure, so doctors monitor blood pressure and liver tests when using it.

15. Clonazepam
    Clonazepam is a benzodiazepine sometimes used for restless legs, myoclonus, or severe night-time cramps associated with neuropathies. It enhances GABA activity and calms abnormal movements and anxiety. Because it can cause dependence, sedation, and falls, it is generally used at the lowest effective dose and for limited durations.

16. Opioid analgesics (e.g., morphine, oxycodone) – last resort
    Strong opioids are sometimes used for severe neuropathic pain that does not respond to other options, but most guidelines recommend extreme caution because of dependence, overdose, and tolerance. They bind to opioid receptors and block pain signals in the brain and spinal cord. They require strict medical supervision, risk-benefit review, and often an opioid treatment agreement.Cleveland Clinic

17. Topical compounded creams (e.g., low-dose ketamine or other agents)
    Some pain clinics use compounded creams containing low-dose ketamine, amitriptyline, or other agents for localized neuropathic pain. The medications act locally on skin nerve endings to reduce pain signaling. Evidence is still limited, and quality varies, so these creams should only be used when prescribed by specialists.

18. Selective serotonin reuptake inhibitors (SSRIs) in selected cases
    SSRIs like sertraline are mainly antidepressants, but treating depression and anxiety can indirectly reduce pain and improve coping. Their direct effect on neuropathic pain is modest, but their purpose is mood stabilization, which can lower perceived pain intensity. Side effects include digestive upset, sleep changes, and, rarely, increased suicidal thoughts in young people, so careful monitoring is important.

19. Alpha-lipoic acid (when prescribed as a “medical food” or drug abroad)
    In some countries, alpha-lipoic acid is used as a prescription antioxidant for diabetic neuropathy. It may reduce oxidative stress in nerves and improve symptoms modestly. Side effects can include nausea and skin rash. Evidence in hereditary neuropathies is limited, so doctors consider it case by case.Cleveland Clinic

20. Drugs for other conditions that may worsen neuropathy (e.g., blood pressure, diabetes control)
    Strict control of blood sugar, blood pressure, and lipid levels with standard medicines can protect nerves from additional damage if those conditions are present. The mechanism is preventing “double hits” to the nerves: genetic damage plus metabolic damage. These medicines are not directly for CMT2V but are critical if a patient also has common diseases like diabetes or hypertension.Mayo Clinic+1

Dietary molecular supplements

Evidence for supplements in hereditary adult-onset painful axonal polyneuropathy is limited. Most data come from diabetic neuropathy or other hereditary neuropathies. Always discuss supplements with your doctor, especially if you take medicines.

1. Alpha-lipoic acid – An antioxidant that may reduce oxidative stress around nerves and improve pain and burning in diabetic neuropathy. Typical studied doses are 600 mg per day, but dosing should be guided by a doctor. It works by neutralizing free radicals and improving blood flow in small vessels. Side effects may include nausea, skin rash, or low blood sugar in people with diabetes.

2. Acetyl-L-carnitine – A form of carnitine that supports mitochondrial energy production in nerve cells. Doses in studies often range from 1000–3000 mg per day, divided. It may help repair nerve fibers and reduce pain in some neuropathies. Possible side effects are mild digestive upset.

3. Vitamin B12 (methylcobalamin) – B12 is critical for myelin and axon health. If a deficiency is present, replacement (oral or injection) can improve neuropathic symptoms. Doses vary from standard multivitamin amounts to higher therapeutic doses chosen by the doctor. It works by supporting myelin repair and DNA synthesis in nerve cells.

4. Vitamin B1 (thiamine or benfotiamine) – Thiamine helps nerves use glucose and supports normal nerve function. Benfotiamine is a fat-soluble form used in some neuropathy studies. Doses vary; a doctor should decide. It may reduce harmful sugar-related products (advanced glycation end products) in nerves. Too much can cause side effects, so medical supervision is needed.

5. Vitamin B6 (pyridoxine – careful with dose) – Small amounts are vital for nerve metabolism, but high doses for long periods can actually cause neuropathy. If a mild deficiency exists, a doctor may recommend a controlled dose. The function is supporting neurotransmitter production and nerve health, but strict dose limits are essential.

6. Vitamin D – Vitamin D supports bone, muscle, and immune health and may influence nerve function and pain sensitivity. If levels are low, doctors often prescribe replacement doses (for example, weekly high-dose or daily moderate-dose regimens). Correcting deficiency can improve muscle function and may help pain indirectly.

7. Omega-3 fatty acids (fish oil) – Omega-3 fats from fish or algae have anti-inflammatory effects. Doses often range from 1000–3000 mg of EPA+DHA per day, depending on heart risk and other conditions. They may reduce systemic inflammation and support nerve cell membranes, possibly easing pain over time. Side effects can include fishy aftertaste and, at high doses, increased bleeding risk.

8. Magnesium – Magnesium is important for muscle relaxation and nerve function. If a deficiency is present, replacement can reduce cramps and improve sleep. Doses and forms (oxide, citrate, glycinate) vary; too much can cause diarrhea. It may act by regulating calcium channels and stabilizing nerve membranes.

9. Coenzyme Q10 (CoQ10) – CoQ10 participates in mitochondrial energy production. Some small studies in neuromuscular diseases suggest potential benefit. Doses often range from 100–300 mg per day. It may improve energy and reduce oxidative stress in nerves and muscles, though evidence is not strong.

10. L-serine (experimental for some hereditary neuropathies) – High-dose L-serine has shown benefit in hereditary sensory and autonomic neuropathy type 1 by lowering toxic by-products and improving nerve function.Neuropathy Commons Doses in trials were high and used under strict medical supervision. For CMT2V, evidence is lacking, so L-serine should only be used within clinical trials or under expert guidance.

Immunity-booster, regenerative, and stem-cell–related drugs

There are no standard “immunity booster” or “stem cell” drugs proven to cure hereditary adult-onset painful axonal polyneuropathy. Some approaches are being researched:

1. Intravenous immunoglobulin (IVIG) – IVIG is a blood product used in autoimmune neuropathies, not usually in purely hereditary forms. It works by modulating the immune system. In CMT2V, it is generally not helpful unless a second autoimmune nerve problem is present. It is given in hospital and carries risks such as headache, thrombosis, and kidney problems.

2. Hematopoietic stem cell transplantation (HSCT) – experimental
   HSCT replaces bone marrow stem cells and is used in some inherited metabolic diseases and autoimmune disorders. In hereditary neuropathies, research is limited and risk is high. The mechanism is replacing faulty immune or metabolic cells, but for NAGLU-related CMT2V, benefit is unproven.

3. Gene therapy (research stage)
   Gene therapy aims to correct the underlying gene error (for example, NAGLU mutations) by delivering a healthy gene to cells. Research in other inherited nerve diseases suggests this might be possible in the future, but human therapy for this exact condition is not yet available. It is considered experimental and only within clinical trials.Practical Neurology+1

4. Neurotrophic factor therapies (e.g., recombinant growth factors)
   Neurotrophins like nerve growth factor (NGF) and neurotrophin-3 support nerve survival and growth. Experimental treatments try to deliver these factors or stimulate their pathways to protect or regrow axons. Some trials in inherited neuropathies have been disappointing or had side effects, so these therapies remain experimental.

5. Mesenchymal stem cell infusions (experimental)
   Mesenchymal stem cells from bone marrow or fat tissue are being studied in several neurological diseases. They may release growth factors and anti-inflammatory molecules that help nerves. For hereditary axonal neuropathies, data are very limited and mostly in small experimental studies. Risks include infection, immune reactions, and unproven benefit, so treatment should only occur in recognized clinical trials.

6. Small-molecule “chaperones” and enzyme-replacement strategies (future options)
   Because NAGLU is a lysosomal enzyme, some researchers are exploring enzyme replacement or small molecules that help the enzyme fold correctly. These strategies are still under study in related metabolic diseases. For CMT2V, their use is theoretical for now but may offer future regenerative approaches.NCBI+1

Surgeries

1. Orthopedic surgery for foot deformities (e.g., high arches, hammer toes)
   Long-standing muscle imbalance can cause high-arched feet and clawed toes, which worsen pain and walking. Orthopedic surgeons may realign bones, release tight tendons, or fuse joints. The purpose is to make the foot more stable, improve weight distribution, reduce calluses and ulcers, and lessen pain.BrainFacts+1

2. Tendon transfer surgery
   When certain muscles are weak and others are relatively strong, surgeons can move (transfer) tendons to improve ankle or toe position. The purpose is to restore better ankle control, reduce tripping, and delay the need for braces. The mechanism is mechanical: a functioning muscle is redirected to do the work of a paralyzed one.

3. Nerve decompression surgery (for superimposed entrapment)
   People with hereditary neuropathy can still develop nerve entrapments like carpal tunnel syndrome. Decompression surgery releases tight tunnels around nerves. The purpose is to relieve extra pressure on already fragile nerves, which may reduce numbness and pain in the affected area.Cleveland Clinic

4. Spinal cord stimulation (neuromodulation)
   Spinal cord stimulators are devices placed near the spinal cord that send mild electrical pulses. For severe neuropathic pain that does not respond to other treatments, this can reduce pain sensations reaching the brain. The purpose is long-term reduction of chronic neuropathic pain and medication needs. This is considered when standard treatments fail and is performed by specialized pain or neurosurgery teams.

5. Surgery for severe contractures or deformities in knees or hips
   In advanced cases with major muscle imbalance, joints may become fixed in abnormal positions. Orthopedic procedures like tendon lengthening or joint fusion may be needed. The purpose is to improve positioning for standing or sitting, reduce pain from abnormal joint stress, and make brace fitting easier.

Preventions

Because this disease is genetic, we cannot fully prevent it, but we can reduce complications and extra nerve damage:

1. Avoid neurotoxic medicines when possible (for example, certain chemotherapy drugs) – always tell your doctor you have a hereditary neuropathy.

2. Do not smoke and avoid heavy alcohol use, which can worsen nerve damage.Mayo Clinic+1

3. Keep blood sugar, blood pressure, and cholesterol in healthy ranges to prevent additional metabolic neuropathy.Right Decisions

4. Protect feet from injury by wearing well-fitting shoes and avoiding walking barefoot.Cleveland Clinic

5. Maintain a healthy body weight to reduce stress on weak muscles and joints.

6. Exercise regularly at a moderate level, using a plan from a physical therapist.

7. Use braces or mobility aids early when recommended, instead of waiting for falls.PM&R KnowledgeNow

8. Manage mood and sleep problems early with psychological and, if needed, medical help.

9. Get vaccinated as advised (e.g., flu, pneumonia, COVID-19) to avoid serious infections that might worsen weakness.

10. Consider genetic counseling for family planning, so relatives understand inheritance patterns and testing options.Monarch Initiative

When to see doctors

You should see a doctor, ideally a neurologist, if:

• You develop new burning pain, tingling, or numbness in the feet or hands that lasts more than a few weeks.

• Pain suddenly worsens, changes character, or starts to disturb sleep most nights.

• You notice new weakness, foot drop, frequent tripping, or difficulty with buttons or writing.

• You have ulcers, wounds, or color changes in your feet or legs, especially if you do not feel them.

• You fall more often, feel very unsteady, or have near-falls at home.

• You develop bladder or bowel problems, severe back pain with leg weakness, or new problems with vision or speech – these may be emergencies.

• Medicines cause strong side effects like severe dizziness, confusion, shortness of breath, swelling, rash, or thoughts of self-harm – seek urgent help.

• You are planning pregnancy or major surgery and already have this neuropathy, so your doctors can plan safe care.

What to eat and what to avoid

1. Eat plenty of colorful vegetables and fruits every day to provide vitamins, minerals, and antioxidants that support general nerve and vascular health.

2. Choose whole grains (brown rice, oats, whole-wheat bread) instead of refined grains to keep blood sugar more stable.

3. Include lean protein sources (fish, skinless poultry, eggs, beans, lentils, tofu) to support muscle repair and immune function.

4. Use healthy fats like olive oil, nuts, seeds, and fatty fish (rich in omega-3) to reduce inflammation.Cleveland Clinic

5. Ensure adequate vitamin B12, B1, and D intake through diet or supplements only as advised by your doctor after testing.

6. Limit sugary drinks, sweets, and refined carbohydrates to avoid blood sugar spikes that can damage nerves.

7. Avoid heavy alcohol use, which is toxic to nerves; if you drink, keep it within guidelines set by your doctor.Mayo Clinic

8. Reduce very salty processed foods to protect blood pressure and heart health.

9. Avoid fad diets that severely cut out entire food groups, because they can lead to vitamin and mineral deficiencies that worsen neuropathy.

10. Drink enough water, especially if you take medicines that can cause dizziness or constipation.

FAQs

1. Is hereditary adult-onset painful axonal polyneuropathy the same as Charcot-Marie-Tooth disease?
   This condition is considered a form of Charcot-Marie-Tooth disease, specifically type 2V, which mainly affects the axons of motor and sensory nerves and often involves NAGLU gene changes.NCBI+1

2. At what age do symptoms usually start?
   Symptoms usually appear in adulthood, often in mid-life, with recurrent leg pain or burning feet. Over time, tingling, numbness, weakness, and balance problems can develop in the legs and, later, the hands.Global Genes+1

3. Is this disease fatal?
   The disease can cause disability but is not usually directly life-shortening. Most people live a normal lifespan but may need braces, walking aids, or other supports. Serious complications like falls, fractures, or infections should be prevented as much as possible.BrainFacts

4. Can this neuropathy be cured?
   At present there is no cure that fully reverses the genetic nerve damage. Treatments focus on reducing pain, preserving function, and preventing complications. Research into gene therapy and other advanced treatments is ongoing.Practical Neurology+1

5. Will I definitely end up in a wheelchair?
   Not everyone needs a wheelchair. Some people have mild symptoms for many years; others have more severe progression. Early use of braces, physical therapy, and fall-prevention measures can keep you walking for longer.PM&R KnowledgeNow

6. Can exercise make my nerves worse?
   Over-strenuous exercise may increase pain or fatigue, but gentle, well-planned exercise usually helps. A physical therapist can design a safe program to keep muscles strong and joints flexible without pushing damaged nerves too hard.PM&R KnowledgeNow

7. Should my family members be tested?
   Because this condition is usually autosomal dominant, each child of an affected person has a 50% chance of inheriting the gene change. Genetic counseling can help relatives decide about genetic testing and understand the pros and cons.Monarch Initiative+1

8. Is pregnancy safe if I have this disease?
   Many people with hereditary neuropathies have safe pregnancies, but extra planning is needed. Weakness and balance issues may worsen temporarily. Medicines for neuropathic pain may need adjustment. Pre-pregnancy counseling with neurology and obstetrics teams is recommended.

9. Can stress worsen my symptoms?
   Stress does not cause the disease, but it can make pain and fatigue feel worse and disturb sleep. Stress-management techniques like mindfulness, CBT, and relaxation can reduce symptom intensity and improve quality of life.Cleveland Clinic

10. Are there special shoes I should wear?
    Supportive shoes with wide toe boxes, good cushioning, and sometimes custom orthotic inserts are helpful. A podiatrist or orthotist can recommend the best footwear to protect your feet and improve walking stability.BrainFacts

11. Why do I have pain if my nerves are “dying”?
    Damaged nerves can fire in an abnormal, overactive way and send false pain signals even when there is no injury. This is called neuropathic pain. Medicines and other treatments aim to quiet these misfiring nerves and change how the brain perceives the signals.Cleveland Clinic

12. Can alternative therapies like acupuncture help?
    Some people report pain relief with acupuncture, massage, or yoga, though scientific evidence is mixed. If used, these should be additions to, not replacements for, medical care, and they should be provided by qualified practitioners who understand your diagnosis.

13. Is it safe to drive if I have this neuropathy?
    It depends on your strength, sensation, and reaction time. If your feet are very numb or weak, driving may be unsafe. Your doctor can advise and may suggest specialist driving assessments or hand-control adaptations.

14. Should I avoid all medicines that list “neuropathy” as a side effect?
    Some medicines are clearly risky for people with existing neuropathy and should be avoided or used only if absolutely necessary (for example, some chemotherapy drugs). Your neurologist and other doctors can review your medicine list and choose safer options whenever possible.Right Decisions

15. What is the most important thing I can do right now?
    The most important steps are: get a clear diagnosis from a neurologist, work with a multidisciplinary team (physical therapy, occupational therapy, pain management), protect your feet and prevent falls, manage general health (no smoking, healthy weight, controlled blood pressure and blood sugar), and seek emotional support. Small, steady changes add up to a big difference over time.

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 22, 2025.

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