There is no current treatment, however management of hereditary neuropathy with liability to pressure palsy can be done via:

- Occupational therapist

- Ankle/foot orthosis

- Wrist splint (medicine)

- Avoid repetitive movements

People who suffer from neurotmesis often face a poor prognosis. They will more than likely never regain full functionality of the affected nerve, but surgical techniques do give people a better chance at regaining some function. Current research is focused on new ways to regenerate nerves and advance surgical techniques.

The first line of treatment is often to treat the patients pain with neuropathic drugs such as tricyclic antidepressants, serotonin reuptake inhibitors, and anticonvulsants. The second lines of drugs to treat pain are non-steroidal anti-inflammatories, tramadol, and opioids. Other techniques used to facilitate healing of the nerve and pain are either static or dynamic splinting that can both help protect the injured part as well as improve function. Sometimes surgery is an option, although the prognosis is still very poor of regaining function of the affected nerve. The goal of surgery is to join healthy nerve to unhealthy nerve. The most common surgical techniques include external neurolysis, end-to-end repair, nerve grafting, and nerve transfer from somewhere else in the body.

There are several options of treatment when iatrogenic (i.e., caused by the surgeon) spinal accessory nerve damage is noted during surgery. For example, during a functional neck dissection that injures the spinal accessory nerve, injury prompts the surgeon to cautiously preserve branches of C2, C3, and C4 spinal nerves that provide supplemental innervation to the trapezius muscle. Alternatively, or in addition to intraoperative procedures, postoperative procedures can also help in recovering the function of a damaged spinal accessory nerve. For example, the Eden-Lange procedure, in which remaining functional shoulder muscles are surgically repositioned, may be useful for treating trapezius muscle palsy.

Signals from the sciatic nerve and it branches can be blocked, in order to interrupted transmission of pain signal from the innervation area, by performing a regional nerve blockade called a sciatic nerve block.

Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.

Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve. Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."

While conservative approaches for rehabilitation are ideal, some patients will not improve and surgery is still an option. Patients with large cervical disk bulges may be recommended for surgery, however most often conservative management will help the herniation regress naturally. Procedures such as foraminotomy, laminotomy, or discectomy may be considered by neurosurgeons and orthopedic surgeons.

Ideally, effective treatment aims to resolve the underlying cause and restores the nerve root to normal function. Common conservative treatment approaches include physical therapy and chiropractic. A systematic review found moderate quality evidence that spinal manipulation is effective for the treatment of acute lumbar radiculopathy and cervical radiculopathy. Only low level evidence was found to support spinal manipulation for the treatment of chronic lumbar radiculopathies, and no evidence was found to exist for treatment of thoracic radiculopathy.

People with diabetes mellitus are at higher risk for any kind of peripheral neuropathy, including ulnar nerve entrapments.

Cubital tunnel syndrome is more common in people who spend long periods of time with their elbows bent, such as when holding a telephone to the head. Flexing the elbow while the arm is pressed against a hard surface, such as leaning against the edge of a table, is a significant risk factor. The use of vibrating tools at work or other causes of repetitive activities increase the risk, including throwing a baseball.

Damage to or deformity of the elbow joint increases the risk of cubital tunnel syndrome. Additionally, people who have other nerve entrapments elsewhere in the arm and shoulder are at higher risk for ulnar nerve entrapment. There is some evidence that soft tissue compression of the nerve pathway in the shoulder by a bra strap over many years can cause symptoms of ulnar neuropathy, especially in very large-breasted women.

Surgical decompression can give excellent results if the clinical picture and the EMG suggest a compression neuropathy.

In brachial plexus neuritis, conservative management may be more appropriate.

Spontaneous recovery has been reported, but is said to be delayed and incomplete.

There is a role for physiotherapy and this should be directed specifically towards the pattern of pain and symptoms. Soft tissue massage, stretches and exercises to directly mobilise the nerve tissue may be used.⁠

A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.

Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option. Local anesthesia often is used to counteract the initial discomfort of the capsaicin. Some current research in animal models has shown that depleting neurotrophin-3 may oppose the demyelination present in some peripheral neuropathies by increasing myelin formation.

High-quality evidence supports the use of cannabis for neuropathic pain.

The facial nerve is the seventh of 12 cranial nerves. This cranial nerve controls the muscles in the face. Facial nerve palsy is more abundant in older adults than in children and is said to affect 15-40 out of 100,000 people per year. This disease comes in many forms which include congenital, infectious, traumatic, neoplastic, or idiopathic. The most common cause of this cranial nerve damage is Bell's palsy (idiopathic facial palsy) which is a paralysis of the facial nerve. Although Bell's palsy is more prominent in adults it seems to be found in those younger than 20 or older than 60 years of age. Bell's Palsy is thought to occur by an infection of the herpes virus which may cause demyelination and has been found in patients with facial nerve palsy. Symptoms include flattening of the forehead, sagging of the eyebrow, and difficulty closing the eye and the mouth on the side of the face that is affected. The inability to close the mouth causes problems in feeding and speech. It also causes lack of taste, acrimation, and sialorrhea.

The use of steroids can help in the treatment of Bell's Palsy. If in the early stages, steroids can increase the likelihood of a full recovery. This treatment is used mainly in adults. The use of steroids in children has not been proven to work because they seem to recover completely with or without them. Children also tend to have better recovery rates than older adults. Recovery rate also depends on the cause of the facial nerve palsy (e.g. infections, perinatal injury, congenital dysplastic). If the palsy is more severe patients should seek steroids or surgical procedures. Facial nerve palsy may be the indication of a severe condition and when diagnosed a full clinical history and examination are recommended.

Although rare, facial nerve palsy has also been found in patients with HIV seroconversion. Symptoms found include headaches (bitemporal or occipital), the inability to close the eyes or mouth, and may cause the reduction of taste. Few cases of bilateral facial nerve palsy have been reported and is said to only effect 1 in every 5 million per year.

Treatment can include pharmaceutical or surgical means. The drug carbamazepine (Tegretol) has been used successfully. Other drugs used with variable success include gabapentin and, recently, memantine. Successful surgery options include superior oblique tenectomy accompanied by inferior oblique myectomy. However, "Overall, the bulk of the ophthalmic literature would agree with the viewpoint that invasive craniotomy surgical procedures should be justified only by the presence of intractable and absolutely unbearable symptoms."

Samii et al. and Scharwey and Samii described a patient who had superior oblique myokymia for 17 years. The interposition of a Teflon pad between the trochlear nerve and a compressing artery and vein at the nerve's exit from the midbrain led to a remission lasting for a follow-up of 22 months.

Treatment is based on the underlying cause, if any. Where the likely underlying condition is known, treatment of this condition is indicated treated to reduce progression of the disease and symptoms. For cases without those conditions, there is only symptomatic treatment.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

Cubital tunnel syndrome may be prevented or reduced by maintaining good posture and proper use of the elbow and arms, such as wearing an arm splint while sleeping to maintain the arm is in a straight position instead of keeping the elbow tightly bent. A recent example of this is popularization of the concept of cell phone elbow.

Non-surgical treatment of radial tunnel syndrome includes rest, NSAID, therapy with modalities, work modification, ergonomic modification, injection if associated with lateral epicondylitis.

Patients whose conditions are more adapted to surgical intervention are those who do not respond to prolonged conservative treatment. The patient must have pain with resisted supination, positive middle finger test, positive electrodiagnostic findings, and pain relief after anesthetic injection into the radial tunnel. Based on 2002 data, surgical decompression leads to 60-70% good or excellent results.

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.

Among the signs/symptoms of hereditary neuropathy with liability to pressure palsy are the following (different symptoms are caused by different nerves, such as the "foot drop" is caused by the "peroneal nerve"):

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Fourth cranial nerve palsy also known as Trochlear nerve palsy, is a condition affecting Cranial Nerve 4 (IV), the Trochlear Nerve, which is one of the Cranial Cranial Nerves that causes weakness or paralysis to the Superior Oblique Muscle that it innervates. This condition often causes vertical or near vertical double vision as the weakened muscle prevents the eyes from moving in the same direction together.

Because the fourth cranial nerve is the thinnest and has the longest intracranial course of the cranial nerves, it is particularly vulnerable to traumatic injury.

To compensate for the double-vision resulting from the weakness of the superior oblique, patients characteristically tilt their head down and to the side opposite the affected muscle.

When present at birth, it is known as congenital fourth nerve palsy.

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.

Botulinum toxin is highly effective in the treatment of hemifacial spasm. It has a success rate equal to that of surgery, but repeated injections may be required every 3 to 6 months. The injections are administered as an outpatient or office procedure. Whilst side effects occur, these are never permanent. Repeated injections over the years remain highly effective. Whilst the toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery. Patients with HFS should be offered a number of treatment options. Very mild cases or those who are reluctant to have surgery or Botulinum toxin injections can be offered medical treatment, sometimes as a temporary measure. In young and fit patients microsurgical decompression and Botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, Botulinum toxin injection is the treatment of first choice. Imaging procedures should be done in all unusual cases of hemifacial spasm and when surgery is contemplated. Patients with hemifacial spasm were shown to have decreased sweating after botulinum toxin injections. This was first observed in 1993 by Khalaf Bushara and David Park. This was the first demonstration of nonmuscular use of BTX-A. Bushara further showed the efficacy of botulinum toxin in treating hyperhidrosis (excessive sweating). BTX-A was later approved for the treatment of excessive underarm sweating. This is technically known as severe primary axillary hyperhidrosis – excessive underarm sweating with an unknown cause which cannot be managed by topical agents (see focal hyperhidrosis).

Microvascular decompression appears to be the most popular surgical treatment at present. Microvascular decompression relieves pressure on the facial nerve, which is the cause of most hemifacial spasm cases. Excellent to good results are reported in 80% or more cases with a 10% recurrence rate. In the present series approximately 10% had previously failed surgery. Serious complications can follow microsurgical decompressive operations, even when performed by experienced surgeons. These include cerebellar haematoma or swelling, brain stem infarction (blood vessel of the brain stem blocked), cerebral infarction (ischemic stroke resulting from a disturbance in the blood vessels supplying blood to the brain), subdural haematoma and intracerebral infarction (blockage of blood flow to the brain). Death or permanent disability (hearing loss) can occur in 2% of patients of hemifacial spasm.

Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH.

It is possible for a disorder of more than one cranial nerve to occur at the same time, if a trauma occurs at a location where many cranial nerves run together, such as the jugular fossa. A brainstem lesion could also cause impaired functioning of multiple cranial nerves, but this condition would likely also be accompanied by distal motor impairment.

A neurological examination can test the functioning of individual cranial nerves, and detect specific impairments.