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.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development.

Thereafter, a period of observation of around 9 to 12 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

This is most commonly achieved through the use of fresnel prisms. These slim flexible plastic prisms can be attached to the patient's glasses, or to plano glasses if the patient has no refractive error, and serve to compensate for the inward misalignment of the affected eye. Unfortunately, the prism only correct for a fixed degree of misalignment and, because the affected individual's degree of misalignment will vary depending upon their direction of gaze, they may still experience diplopia when looking to the affected side. The prisms are available in different strengths and the most appropriate one can be selected for each patient. However, in patients with large deviations, the thickness of the prism required may reduce vision so much that binocularity is not achievable. In such cases it may be more appropriate simply to occlude one eye temporarily. Occlusion would never be used in infants though both because of the risk of inducing stimulus deprivation amblyopia and because they do not experience diplopia.

Other management options at this initial stage include the use of botulinum toxin, which is injected into the ipsilateral medial rectus (botulinum toxin therapy of strabismus). The use of BT serves a number of purposes. Firstly, it helps to prevent the contracture of the medial rectus which might result from its acting unopposed for a long period. Secondly, by reducing the size of the deviation temporarily it might allow prismatic correction to be used where this was not previously possible, and, thirdly, by removing the pull of the medial rectus it may serve to reveal whether the palsy is partial or complete by allowing any residual movement capability of the lateral rectus to operate. Thus, the toxin works both therapeutically, by helping to reduce symptoms and enhancing the prospects for fuller ocular movements post-operatively, and diagnostically, by helping to determine the type of operation most appropriate for each patient.

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.

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.

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".

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.

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.

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.

There is no treatment of conjugate gaze palsy itself, so the disease or condition causing the gaze palsy must be treated, likely by surgery. As stated in the causes section, the gaze palsy may be due to a lesion caused by stroke or a condition. Some of the conditions such as Progressive supra nuclear palsy are not curable, and treatment only includes therapy to regain some tasks, not including gaze control. Other conditions such as Niemann-Pick disease type C have limited drug therapeutic options. Stroke victims with conjugate gaze palsies may be treated with intravenous therapy if the patent presents early enough, or with a surgical procedure for other cases.

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.

Congenital fourth cranial nerve palsy can be treated with strabismus surgery, where muscle attachment sites on the globe are modified to realign the eyes. Some eye doctors prefer conservative or no management of congenital fourth nerve palsy.

Other eye doctors recommend surgery early in a patient's life to prevent the compensatory torticollis and facial asymmetry that develop with age.

Prism lenses set to make minor optical changes in the vertical alignment may be prescribed instead of or after surgery to fine-tune the correction. Prism lenses do not address torsional misalignment and this may limit their use in certain cases. An additional consideration of prism lenses is that they must be worn at all times. Prism lenses reduce vertical fusional demands by allowing the eyes to rest in their vertically misaligned state. When they are removed the patient may experience vertical diplopia they find hard to resolve due to the rested state of their eyes.

Cases of congenital fourth nerve palsy vary in magnitude and way they affect the motion of the superior oblique muscle. Therefore different surgeries are available dependent upon the type of misalignment. Sometimes surgery on more than one eye muscle is required. In some simpler, unilateral cases a single surgery may suffice. In these cases the main problem is that the inferior oblique muscle of the same eye acts unopposed by the weakened superior oblique muscle, pulling the eye up. An example of a safe and effective procedure is a disinsertion of the inferior oblique muscle to allow it to reattach itself further down the globe of the eye. This acts to 'weaken' its action and allow the eye to move back into a more neutral alignment.

In all cases of congenital fourth nerve palsy, it is important to see an experienced strabismologist about management/treatment options. A strabismologist is an ophthalmologist (eye doctor) specialising in eye movement disorders.

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.

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.

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 prognosis of a lesion in the visual neural pathways that causes a conjugate gaze palsy varies greatly. Depending on the nature of the lesion, recovery may happen rapidly or recovery may never progress. For example, optic neuritis, which is caused by inflammation, may heal in just weeks, while patients with an ischemic optic neuropathy may never recover.

- "For acquired fourth nerve palsy, see fourth nerve palsy"

Congenital fourth nerve palsy is a condition present at birth characterized by a vertical misalignment of the eyes due to a weakness or paralysis of the superior oblique muscle.

Other names for fourth nerve palsy include superior oblique palsy and trochlear nerve palsy.

When looking to the right/left the nerve/muscle isn't strong enough or is too long and the eye drifts up.

In any manifestation of spastic CP, clonus of the affected limb(s) may intermittently result, as well as muscle spasms, each of which results from the pain and/or stress of the tightness experienced, indicating especially hard-working and/or exhausted musculature. The spasticity itself can and usually does also lead to very early onset of muscle-stress symptoms like arthritis and tendinitis, especially in ambulatory individuals in their mid-20s and early-30s. As compared to other types of CP, however, and especially as compared to hypotonic CP or more general paralytic mobility disabilities, spastic CP is typically more easily manageable by the person affected, and medical treatment can be pursued on a multitude of orthopaedic and neurological fronts throughout life.

Physical therapy and occupational therapy regimens of assisted stretching, strengthening, functional tasks, and/or targeted physical activity and exercise are usually the chief ways to keep spastic CP well-managed, although if the spasticity is too much for the person to handle, other remedies may be considered, such as various antispasmodic medications, botox, baclofen, or even a neurosurgery known as a selective dorsal rhizotomy (which eliminates the spasticity by eliminating the nerves causing it).

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.

As age increases, spasticity makes for more noticeable effects in bones and joints and muscle function. This is often mistakenly said to mean that "spasticity increases as people with spastic CP age", which is a misrepresentation of the knock-on effects of spasticity with age. The clinical reality is that spasticity intensities remain constant but an increasing age in to middle-adulthood and the early elder years self-evidently changes the body structure, body response times and body adaptiveness capabilities markedly, leading to very different interplays between the body's spasticity and the body itself as the body 'degrades' across the twilight years.

That being said, cerebral palsy, including spastic cerebral palsy, is notable for a glaring overall research deficiency—the fact that it is one of the very few "major" groups of conditions on the planet in human beings for which medical science has not yet (as of 2011) collected wide-ranging empirical data on the development and experiences of young adults, the middle aged and older adults. An especially puzzling aspect of this lies in the fact that cerebral palsy as defined by modern science was first "discovered" and specifically addressed well over 100 years ago and that it would therefore be reasonable to expect by now that at least some empirical data on the adult populations with these conditions would have long since been collected, especially over the second half of the 20th century when existing treatment technologies rapidly improved and new ones came into being. The vast majority of empirical data on the various forms of cerebral palsy is concerned near-exclusively with children (birth to about 10 years of age) and sometimes pre-teens and early teens (11–13). Some doctors attempt to provide their own personal justifications for keeping their CP specialities purely paediatric, but there is no objectively apparent set of reasons backed by any scientific consensus as to why medical science has made a point of researching adult cases of multiple sclerosis, muscular dystrophy and the various forms of cancer in young and older adults, but has failed to do so with CP.

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.

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.