One review found that antivirals (such as aciclovir) are ineffective in improving recovery from Bell's palsy beyond steroids alone in mild to moderate disease. Another review found a benefit but stated the evidence was not very good to support this conclusion.

In severe disease it is also unclear. One 2015 review found no effect regardless of severity. Another review found a small benefit when added to steroids in those with severe disease.

They are commonly prescribed due to a theoretical link between Bell's palsy and the herpes simplex and varicella zoster virus. There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out.

Steroids have been shown to be effective at improving recovery in Bell's palsy while antivirals have not. In those who are unable to close their eyes, eye protective measures are required.

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.

In many cases recovery happens spontaneously and no treatment is needed. This spontaneous recovery can occur because distance between the injury location and the deltoid muscle is small. Spontaneous recovery may take as long as 12 months.

In order to combat pain and inflammation of nerves, medication may be prescribed.

Surgery is an option, but it has mixed results within the literature and is usually avoided because only about half of people who undergo surgery see any positive results from it. Some suggest that surgical exploration should be considered if no recovery occurs after 3 to 6 months. Some surgical options include nerve grafting, neurolysis, or nerve reconstruction. Surgery results are typically better for younger patients (under 25) and for nerve grafts less than six centimeters.

For some, recovery does not occur and surgery is not possible. In these cases, most patients’ surrounding muscles can compensate, allowing them to gain a satisfactory range of motion back. Physical therapy or Occupational therapy will help retrain and gain muscle tone back.

Bell's palsy is the most common cause of acute facial nerve paralysis. There is no known cause of Bell's palsy, although it has been associated with herpes simplex infection. Bell's palsy may develop over several days, and may last several months, in the majority of cases recovering spontaneously. It is typically diagnosed clinically, in patients with no risk factors for other causes, without vesicles in the ear, and with no other neurological signs. Recovery may be delayed in the elderly, or those with a complete paralysis. Bell's palsy is often treated with corticosteroids.

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.

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.

In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals.

If the injury is axonal (the underlying nerve fiber itself is damaged) then full recovery may take months or years ( or could be permanent). EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

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.

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

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.

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.

Botox (botulinum toxin) is a new and versatile tool for the treatment of synkinesis. Initially used for reducing hyperkinesis after facial palsy, Botox was later attempted on patients with post-facial palsy synkinesis to reduce unwanted movements. The effects of Botox have shown to be remarkable, with synkinetic symptoms disappearing within 2 or 3 days. The most common treatment targets are the orbicularis oculi, depressor anguli oris (DAO), mentalis, platysma and the contralateral depressor labii inferioris muscles. Due to the short span of Botox effects though, patients must come back to the doctor for re-injection approximately every 3 months. More notable is that in a majority of patients, various synkinetic movements completely disappeared after 2-3 sessions of trimonthly Botox injections.

A more specific synkinesis, crocodile tears syndrome (hyperlacrimation upon eating), has been shown to respond exceedingly well to Botox injection. Botox is injected directly into the lacrimal gland and has shown to reduce hyperlacrimation within 24–48 hours. The procedure was shown to be simple and safe with very little chance of side-effects (although on rare occasions ptosis can occur due to botulinum toxin diffusion). Furthermore, reduction in hyper-lacrimation was shown to last longer than the expected 3 months (about 12 months).

Since Botox can mimic facial paralysis, an optimized dose has been determined that reduces involuntary synkinesis of the muscle while not affecting muscle tone.

PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders.

Currently, tendon transfers are being studied as a means of improving radial, medial, and ulnar nerve palsy.

Some babies recover on their own; however, some may require specialist intervention.

Neonatal/pediatric neurosurgery is often required for avulsion fracture repair. Lesions may heal over time and function return. Physiotherapeutic care is often required to regain muscle usage.

Although range of motion is recovered in many children under one year in age, individuals who have not yet healed after this point will rarely gain full function in their arm and may develop arthritis.

The three most common treatments for Erb's Palsy are: Nerve transfers (usually from the opposite arm or limb), Sub Scapularis releases and Latissimus Dorsi Tendon Transfers.

Nerve transfers are usually performed on babies under the age of 9 months since the fast development of younger babies increases the effectiveness of the procedure. They are not usually carried out on patients older than this because when the procedure is done on older infants, more harm than good is done and can result in nerve damage in the area where the nerves were taken from. Scarring can vary from faint scars along the lines of the neck to full "T" shapes across the whole shoulder depending on the training of the surgeon and the nature of the transplant.

Subscapularis releases, however, are not time limited. Since it is merely cutting a "Z" shape into the subscapularis muscle to provide stretch within the arm, it can be carried out at almost any age and can be carried out repeatedly on the same arm; however, this will compromise the integrity of the muscle.

Latissimus Dorsi Tendon Transfers involve cutting the Latissimus Dorsi in half horizontally in order to 'pull' part of the muscle around and attach it to the outside of the biceps. This procedure provides external rotation with varying degrees of success. A side effect may be increased sensitivity of the part of the biceps where the muscle will now lie, since the Latissimus Dorsi has roughly twice the number of nerve endings per square inch of other muscles.

The treatment and management of radial neuropathy can be achieved via the following methods:

- Physical therapy or occupational therapy

- Surgery(depending on the specific area and extent of damage)

- Splinting

Mime therapy was introduced in the Netherlands in 1980. It was initially designed to treat facial palsy by improving symmetry of the face both at rest and during movement. It was then later observed that people who had post-facial palsy synkinesis also benefited from this therapy. It wasn’t until 2003 that Beurskens and Heymans were able to experimentally conclude that mime therapy was indeed a good treatment choice for synkinesis. Furthermore, later studies by Beurskens et al. have shown that benefits obtained from mime therapy are stable one year after therapy.

Current mime therapy consists of a combination of procedures designed to promote symmetry of the face at rest and during movement to control synkinesis. The components include: massage, stretching exercises, exercises to coordinate both halves of the face, etc. The overall aim of mime therapy is to develop a conscious connection between the use of facial muscles and emotional expression. While facial retraining therapy is more focused on treating slight synkinetic movements, mime therapy aims to increase the overall vigor of the muscles through active exercises, while in the process of doing so, teaching the face to decrease unwanted synkinetic movements.

The origins of the vast majority of congenital oculomotor palsies are unknown, or idiopathic to use the medical term. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma.

Oculomotor nerve palsy or third nerve palsy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Thus, damage to this nerve will result in the affected individual being unable to move his or her eye normally. In addition, the nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and the muscles responsible for pupil constriction (sphincter pupillae) . The limitations of eye movements resulting from the condition are generally so severe that the affected individual is unable to maintain normal alignment of their eyes when looking straight ahead, leading to strabismus and, as a consequence, double vision (diplopia).

It is also known as "oculomotor neuropathy".

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.

Many children affected by alternating hemiplegia also suffer from epilepsy. Seizures may occur during an attack but more often occur between attacks. Anti-epilepsy drugs are given to prevent or lessen the seizures, but the drugs often don’t work and have severe side effects that require the patient to discontinue use. Flunarizine, which blocks calcium channels, is an antiepilepsy drugs used in 50% of patients, and has been shown to shorten the duration of attacks as well as reducing the severity of the attacks. While Flunarizine does not stop the attacks, it is most common drug prescribed to treat those suffering from alternating hemiplegia.

There are a number of colloquial terms used to describe radial nerve injuries, which are usually dependent on the causation factor:

- Saturday night palsy from falling asleep with one's arm hanging over the arm rest of a chair, compressing the radial nerve at the spiral groove.

- Honeymoon palsy from another individual sleeping on and compressing one's arm overnight. This can also refer to anterior interosseous nerve palsy from compression on the forearm resulting in an inability to flex the index and thumb tips. In this interpretation, it is a branch of the median nerve and not the radial nerve which is affected.

- Handcuff neuropathy from tight-fitting handcuffs compressing the superficial branch of the distal radial nerve; this is also referred to as cheiralgia paresthetica.

- Crutch palsy from poorly fitted axillary crutches.

- Squash palsy, from traction forces in a manner usually associated with the sport squash, can happen to squash players during prolonged periods between matches.

Progressive Bulbar Palsy is slow in onset, with symptoms starting in most patients around 50–70 years of age. PBP has a life expectancy typically between 6 months and 3 years from onset of first symptoms. It is subtype of the Motor Neurone Diseases (MND) accounting for around 1 in 4 cases. Amyotrophic lateral sclerosis (ALS) is another sub-type. Pure PBP without any EMG or clinical evidence of abnormalities in the legs or arms is possible, albeit extremely rare. Moreover, about twenty-five percent of patients with PBP eventually develop the widespread symptoms common to ALS.