There is currently no known pharmacological treatment to hereditary motor and sensory neuropathies. However, the majority of people with these diseases are able to walk and be self-sufficient. Some methods of relief for the disease include physical therapy, stretching, braces, and sometimes orthopedic surgery. Since foot disorders are common with neuropathy disorders precautions must be taken to strengthen these muscles and use preventative care and physical therapy to prevent injury and deformities.

Hereditary motor and sensory neuropathies are relatively common and are often inherited with other neuromuscular conditions, and these co morbidities cause an accelerated progression of the disease.

Most forms HMSN affects males earlier and more severely than females, but others show no predilection to either sex. HMSN affects all ethnic groups. With the most common forms having no racial prediliections, but other recessively inherited forms tend to impact specific ethnic groups. Onset of HMSN in most common in early childhood, with clinical effects occurring before the age of 10, but some symptoms are lifelong and progress slowly. Therefore, these symptoms do not appear until later in life.

Treatment for individuals with PLS is symptomatic. Baclofen and tizanidine may reduce spasticity. Quinine or phenytoin may decrease cramps. Some patients who do not receive adequate relief from oral treatment may consider intrathecal baclofen (i.e., infusion of medication directly into the cerebrospinal fluid via a surgically placed continuous infusion pump). However, patients are carefully selected for this type of procedure to ensure that they will likely benefit from this invasive procedure.

Physical therapy often helps prevent joint immobility. Speech therapy may be useful for those with involvement of the facial muscles. Physiotherapy treatment focuses on reducing muscle tone, maintaining or improving range of motion, increasing strength and coordination, and improving functional mobility. In PLS, stretching is thought to improve flexibility and can also reduce muscle spasticity and cramps.

Patients with PLS may find it beneficial to have an evaluation, as well as follow-up visits at multidisciplinary clinics, similar to those available for people with ALS. These multidisciplinary clinics may provide patients with the necessary treatment that they require by having an occupational therapist, physical therapist, speech language pathologist, dietician and nutritionist, all in one site.

Patients can often live with PLS for many years and very often outlive their neurological disease and succumb to some unrelated condition. There is currently no effective cure, and the progression of symptoms varies. Some people may retain the ability to walk without assistance, but others eventually require wheelchairs, canes, or other assistive devices.

The disease has only been identified as distinct from SMA recently, so research is still experimental, taking place mostly in animal models. Several therapy pathways have been devised which include gene therapy, whereby an "IGHMBP2" transgene is delivered to the cell using a viral vector; small-molecule drugs like growth factors (e.g., IGF-1 and VEGF) or olesoxime; and transplantation of healthy motor neurons grown "in vitro" from the patient's stem cells. Studies in amyotrophic lateral sclerosis are also considered helpful because the condition is relatively similar to SMARD1.

The Roussy–Lévy syndrome is not a fatal disease and life expectancy is normal. However, due to progressive muscle wasting patients may need supportive orthopaedic equipment or wheelchair assistance.

There is no cure for MMA. Treatment consists of muscle strengthening exercises and training in hand coordination. It has been proposed that the changes in this disease are from compression of the spinal cord in flexion due to forward shifting of the posterior dural sac. There have been treatments studies ranging from use of a cervical collar to anterior cervical fusion and posterior decompression.

The importance of correctly recognizing progressive muscular atrophy as opposed to ALS is important for several reasons.

- 1) the prognosis is a little better. A recent study found the 5-year survival rate in PMA to be 33% (vs 20% in ALS) and the 10-year survival rate to be 12% (vs 6% in ALS).

- 2) Patients with PMA do not suffer from the cognitive change identified in certain groups of patients with MND.

- 3) Because PMA patients do not have UMN signs, they usually do not meet the "World Federation of Neurology El Escorial Research Criteria" for “Definite” or “Probable” ALS and so are ineligible to participate in the majority of clinical research trials such as drugs trials or brain scans.

- 4) Because of its rarity (even compared to ALS) and confusion about the condition, some insurance policies or local healthcare policies may not recognize PMA as being the life-changing illness that it is. In cases where being classified as being PMA rather than ALS is likely to restrict access to services, it may be preferable to be diagnosed as "slowly progressive ALS" or "lower motor neuron predominant" ALS.

An initial diagnosis of PMA could turn out to be slowly progressive ALS many years later, sometimes even decades after the initial diagnosis. The occurrence of upper motor neurone symptoms such as brisk reflexes, spasticity, or a Babinski sign would indicate a progression to ALS; the correct diagnosis is also occasionally made on autopsy.

Physiotherapy intervention aims to improve balance and gait of OPCA patients, by stimulating neuroplastic changes in the atrophied neural structure. A challenge-oriented treatment program has previously been shown to be beneficial for individuals with ataxia from OPCA. The treatment program was composed of repetitive training with task challenges (e.g. obstacle course) and/or novel motor skills acquisition over a 12-week period under the supervision of a physiotherapist. Task challenges were progressed only when the patient showed mastery of a task.

Overground harness systems may be used to allow OPCA patients to challenge their balance without chance of falling. Furthermore, home exercise programs and/or aquatic exercises are used to allow more repetitions to facilitate balance learning. Treatment programs should be frequently monitored and adjusted based on a patient's progress. Outcome measures such as the Berg Balance Scale, Dynamic Gait Index and activities-specific balance confidence scales are useful to assess patient’s progress over time.

In terms of treatment for neuromuscular diseases (NMD), "exercise" might be a way of managing them, as NMD individuals would gain muscle strength. In a study aimed at results of exercise, in muscular dystrophy and Charcot-Marie-Tooth disease, the later benefited while the former did not show benefit; therefore, it depends on the disease Other management routes for NMD should be based on medicinal and surgical procedures, again depending on the underlying cause.

Physical therapy is the predominant treatment of symptoms. Orthopedic shoes and foot surgery can be used to manage foot problems.

No specific treatment is known that would prevent, slow, or reverse HSP. Available therapies mainly consist of symptomatic medical management and promoting physical and emotional well-being. Therapeutics offered to HSP patients include:

- Baclofen – a voluntary muscle relaxant to relax muscles and reduce tone. This can be administered orally or intrathecally. (Studies in HSP )

- Tizanidine – to treat nocturnal or intermittent spasms (studies available )

- Diazepam and clonazepam – to decrease intensity of spasms

- Oxybutynin chloride – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Tolterodine tartate – an involuntary muscle relaxant and spasmolytic agent, used to reduce spasticity of the bladder in patients with bladder control problems

- Botulinum toxin – to reduce muscle overactivity (existing studies for HSP patients)

- Antidepressants (such as selective serotonin re-uptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors) – for patients experiencing clinical depression

- Physical therapy – to restore and maintain the ability to move; to reduce muscle tone; to maintain or improve range of motion and mobility; to increase strength and coordination; to prevent complications, such as frozen joints, contractures, or bedsores.

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

Hereditary motor and sensory neuropathy with proximal dominance (HMSN-P) is an autosomal dominant neurodegenerative disorder that is defined by extensive involuntary and spontaneous muscle contractions, asthenia, and atrophy with distal sensory involvement following. The disease starts presenting typically in the 40s and is succeeded by a slow and continuous onslaught. Muscle spasms and muscle contractions large in number are noted, especially in the earliest stages. The presentation of HMSN-P is quite similar to amyotrophic lateral sclerosis and has common neuropathological findings. Sensory loss happens as the disease progresses, but the amount of sensation lost varies from case to case. There have been other symptoms of HMSN-P reported such as urinary disturbances and a dry cough.

Two large families in Japan have been identified with the disease locus to chromosome 3q. From descendants of Japan, HMSN-P was brought to Brazil, from there it is a pretty isolated disease. Through clinical studies, researchers identified that TFG mutations on chromosome 3q13.2 causes HMSN-P. "The presence of TFG/ubiquitin- and/or TDP-43-immunopositive cytoplasmic inclusions in motor neurons and cytosolic aggregation composed of TDP-43 in cultured cells expressing mutant TFG indicate a novel pathway of motor neuron death"

There is no pharmacological treatment for Roussy–Lévy syndrome.

Treatment options focus on palliative care and corrective therapy. Patients tend to benefit greatly from physical therapy (especially water therapy as it does not place excessive pressure on the muscles), while moderate activity is often recommended to maintain movement, flexibility, muscle strength and endurance.

Patients with foot deformities may benefit from corrective surgery, which, however, is usually a last resort. Most such surgeries include straightening and pinning the toes, lowering the arch, and sometimes, fusing the ankle joint to provide stability. Recovering from these surgeries is oftentimes long and difficult. Proper foot care including custom-made shoes and leg braces may minimize discomfort and increase function.

While no medicines are reported to treat the disorder, patients are advised to avoid certain medications as they may aggravate the symptoms.

There is no known cure to DSMA1, and care is primarily supportive. Patients require respiratory support which may include non-invasive ventilation or tracheal intubation. The child may also undergo additional immunisations and offered antibiotics to prevent respiratory infections. Maintaining a healthy weight is also important. Patients are at risk of undernutrition and weight loss because of the increased energy spent for breathing. Physical and occupational therapy for the child can be very effective in maintaining muscle strength.

There is no published practice standard for the care in DSMA1, even though the Spinal Muscular Atrophy Standard of Care Committee has been trying to come to a consensus on the care standards for DSMA1 patients. The discrepancies in the practitioners’ knowledge, family resources, and differences in patient’s culture and/or residency have played a part in the outcome of the patient.

Hereditary spastic paraplegia (HSP) is a group of inherited diseases whose main feature is a progressive gait disorder. The disease presents with progressive stiffness (spasticity) and contraction in the lower limbs. HSP is also known as hereditary spastic paraparesis, familial spastic paraplegia, French settlement disease, or Strumpell-Lorrain disease. The symptoms are a result of dysfunction of long axons in the spinal cord. The affected cells are the primary motor neurons, therefore the disease is an upper motor neuron disease. HSP is not a form of cerebral palsy even though it physically may appear and behave much the same as spastic diplegia. The origin of HSP is different from cerebral palsy. Despite this, some of the same anti-spasticity medications used in spastic cerebral palsy are sometimes used to treat HSP symptoms.

HSP is caused by defects in transport of proteins, structural proteins, cell maintaining proteins, lipids, and other substances through the cell. Long nerve processes (axons) are affected because long distances make nerve cells particularly sensitive to defects in these mentioned mechanisms.

The disease was first mentioned in 1876 by Adolph Seeligmüller, a German neurologist, who described a family of four affected children with spasticity. Further cases were described in 1883 by Adolph Strümpell, a German neurologist. Those cases were described more extensively in 1888 by Maurice Lorrain, a French physician. Due to their contribution in describing the disease, it is still named Strümpell-Lorrain disease in French speaking countries. The term "hereditary spastic paraplegia" was coined by Anita Harding in 1983.

Treatment is palliative, not curative (as of 2009).

Treatment options for lower limb weakness such as foot drop can be through the use of Ankle Foot Orthoses (AFOs) which can be designed or selected by an Orthotist based upon clinical need of the individual. Sometimes tuning of rigid AFOs can enhance knee stability.

A motor neuron disease (MND) is any of several neurological disorders that selectively affect motor neurons, the cells that control voluntary muscles of the body. They include amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), progressive bulbar palsy (PBP) and pseudobulbar palsy. Spinal muscular atrophies (SMA) are sometimes included in the group by some neurologists but it is different disease with clear genetic cause. They are neurodegenerative in nature and cause increasing disability and eventually, death.

In the United States, the term is often used to denote ALS, the most common disorder in the group. In the United Kingdom, the term is also spelled "motor neurone disease" (MND) and is sometimes used for the entire group; but mostly it refers to ALS.

While MND refers to a specific subset of similar diseases, there are numerous other diseases of motor neurons that are referred to collectively as "motor neuron disorders", for instance disease belonging to spinal muscular atrophies. However, they are not classified as "motor neuron diseases" by the tenth International Statistical Classification of Diseases and Related Health Problems (ICD-10), which is the definition followed in this article.

In 1993, A. E. Hardnig proposed to classify hereditary motor neuropathies into seven groups based on age at onset, mode of inheritance, and presence of additional features. This initial classification has since been widely adopted and expanded and currently looks as follows:

Note: Acronym "HMN" is also used interchangeably with "DHMN".

Since December 2016, autosomal recessive proximal spinal muscular atrophy can be treated with nusinersen. No cure is known to any of the remaining disorders of the spinal muscular atrophies group. The main objective there is to improve quality of life which can be measured using specific questionnaires. Supportive therapies are widely employed for patients who often also require comprehensive medical care involving multiple disciplines, including pulmonology, neurology, orthopedic surgery, critical care, and clinical nutrition. Various forms of physiotherapy and occupational therapy are frequently able to slow down the pace of nerve degeneration and muscle wasting. Patients also benefit greatly from the use of assistive technology.

MMA mostly occurs in males between the ages of 15 and 25. Onset and progression are slow. MMA is seen most frequently in Asia, particularly in Japan and India; it is much less common in North America.

Distal hereditary motor neuropathy type V (dHMN V) is a particular type of neuropathic disorder. In general, distal hereditary motor neuropathies affect the axons of distal motor neurons and are characterized by progressive weakness and atrophy of muscles of the extremities. It is common for them to be called "spinal forms of Charcot-Marie-Tooth disease (CMT)", because the diseases are closely related in symptoms and genetic cause. The diagnostic difference in these diseases is the presence of sensory loss in the extremities. There are seven classifications of dHMNs, each defined by patterns of inheritance, age of onset, severity, and muscle groups involved. Type V (sometimes notated as Type 5) is a disorder characterized by autosomal dominance, weakness of the upper limbs that is progressive and symmetrical, and atrophy of the small muscles of the hands.

Despite being rarer than ALS, PMA was described earlier, when in 1850 French neurologist François Aran () described 11 cases which he termed "atrophie musculaire progressive". Contemporary neurologist Guillaume-Benjamin-Amand Duchenne de Boulogne also claimed to have described the condition 1 year earlier, although the written report was never found. The condition has been called progressive muscular atrophy (PMA), spinal muscular atrophy (SMA), Aran–Duchenne disease, Duchenne–Aran disease, Aran–Duchenne muscular atrophy, and Duchenne–Aran muscular atrophy. The name "spinal muscular atrophy" is ambiguous as it refers to any of various spinal muscular atrophies, including the autosomal recessive spinal muscular atrophy caused by a genetic defect in the "SMN1" gene.