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.

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.

Because the causes of CP are varied, a broad range of preventative interventions have been investigated.

Electronic fetal monitoring has not helped to prevent CP, and in 2014 the American College of Obstetricians and Gynecologists, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists, and the Society of Obstetricians and Gynaecologists of Canada have acknowledged that there are no long-term benefits of electronic fetal monitoring. Prior to this, electronic fetal monitoring was widely used to prop up obstetric litigation.

In those at risk of an early delivery, magnesium sulphate appears to decrease the risk of cerebral palsy. It is unclear if it helps those who are born at term. In those at high risk of preterm labor a review found that moderate to severe CP was reduced by the administration of magnesium sulphate, and that adverse effects on the babies from the magnesium sulphate were not significant. Mothers who received magnesium sulphate could experience side effects such as respiratory depression and nausea. Caffeine is used to treat apnea of prematurity and reduces the risk of cerebral palsy in premature babies, but there are also concerns of long term negative effects. A moderate level of evidence has been shown for giving women antibiotics during preterm labour when their waters had not broken was associated with an increased risk of cerebral palsy in the child. Additionally, allowing a preterm birth to proceed rather than trying to delay the birth also had a moderate level of evidence for increased risk of cerebral palsy in the child.

Cooling high-risk full-term babies shortly after birth may reduce disability, but this may only be useful for some forms of the brain damage that causes CP.

Current forms of prevention are focused during pregnancy, while others are focused immediately after birth. Some methods that have been used include prolonging the pregnancy using interventions such as 17-alpha progesterone, limiting the number of gestations during pregnancy (for pregnancies induced by assistive reproductive technology), antenatal steroid for mothers likely to deliver prematurely, high caffeine for premature births with extremely low birth weights.

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.

Although no cure exists, there are many different treatments which are currently being used to help control symptoms. These include short term treatment with some drugs (such as Botox) which relax the muscles, use of temperature changes to control muscle tremors, and a balanced approach of coordinated care and support involving physical therapists, orthopedic surgeons, and psychiatrists.

Because there is no cure for ataxic cerebral palsy, current methods of treatment are diverse, often consisting of multiple focuses designed to limit the severity of symptoms. Many children suffering from ataxic cerebral palsy are treated by teams consisting of individuals from numerous disciplines, including physical therapists, occupational therapist, orthopedic surgeons, and psychiatrists. Treatment by such teams involves multiple approaches. Providing a primary care medical home to support children suffering from common symptoms of nutritional deficiencies, pain, dental care, bowel and bladder continence, and orthopedic complications is an essential aspect of treatment. In addition, utilizing diagnostic techniques to identify the nature and severity of brain abnormalities has become increasingly beneficial for treatment in recent years.

Different medications have been used to temporarily treat ataxic cerebral palsy. Medications like primidone and benzodiazepine, while not recommended for long term use, can alleviate some of the tremor symptoms. Botox which relaxes tightened muscles has been effective in treating voice, hand and head tremors. A few recently published papers outlined a potential method for treating intention tremor which consisted of cooling the forearm by wrapping it in a cryomanchet using a circulating fluid. After the treatment most patients experienced reduced tremor for up to half an hour. This practical, however short-term treatment can facilitate performing normal daily activities like applying make up, eating, or signing documents. This potential treatment method is also significant in that it reduces one’s reliance on caregivers.

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.

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

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 different modes of treatment for people with paralysis in their upper limbs. For example, behavioral and environmental treatments may include physiotherapy, occupational therapy, motor learning, strength training, and neurodevelopment treatment. Another treatment may be through the use of splints and casts. Electrophysical agents may be used such as neuromuscular electrical stimulation (NMES). Sometimes pharmacological treatments are necessary such as Botulinum toxin type A. On more severe cases surgery of the upper limbs may be required.

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.

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.

Over time, the approach to CP management has shifted away from narrow attempts to fix individual physical problems such as spasticity in a particular limb to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

Because cerebral palsy has "varying severity and complexity" across the lifespan, it can be considered a collection of conditions for management purposes. A multidisciplinary approach for cerebral palsy management is recommended, focusing on "maximising individual function, choice and independence" in line with the International Classification of Functioning, Disability and Health's goals. The team may include a paediatrician, a health visitor, a social worker, a physiotherapist, an orthotist, a speech and language therapist, an occupational therapist, a teacher specialising in helping children with visual impairment, an educational psychologist, an orthopaedic surgeon, a neurologist and a neurosurgeon.

Various forms of therapy are available to people living with cerebral palsy as well as caregivers and parents. Treatment may include one or more of the following: physical therapy; occupational therapy; speech therapy; water therapy; drugs to control seizures, alleviate pain, or relax muscle spasms (e.g. benzodiazepines); surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; rolling walkers; and communication aids such as computers with attached voice synthesisers. A Cochrane review published in 2004 found a trend toward benefit of speech and language therapy for children with cerebral palsy, but noted the need for high quality research. A 2013 systematic review found that many of the therapies used to treat CP have no good evidence base; the treatments with the best evidence are medications (anticonvulsants, botulinum toxin, bisphosphonates, diazepam), therapy (bimanual training, casting, constraint-induced movement therapy, context-focused therapy, fitness training, goal-directed training, hip surveillance, home programmes, occupational therapy after botulinum toxin, pressure care) and surgery (selective dorsal rhizotomy).

Mild cases of hemifacial spasm may be managed with sedation or carbamazepine (an anticonvulsant drug). Microsurgical decompression and botulinum toxin injections are the current main treatments used for hemifacial spasm.

Berger, in 1876, first reported a case of 12-year-old child with progressive bulbar paralysis

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.

Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries.

Practical surgical procedures used for treating synkinesis are neurolysis and selective myectomy. Neurolysis has been shown to be effective in relieving synkinesis but only temporarily and unfortunately symptoms return much worse than originally. Selective myectomy, in which a synkinetic muscle is selectively resected, is a much more effective technique that can provide permanent relief and results in a low recurrence rate; unfortunately, it also has many post-operative complications that can accompany including edema, hematoma, and ecchymosis. Therefore, surgical procedures are very minimally used by doctors and are used only as last-resort options for patients who do not respond well to non-invasive treatments.

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.

There are several ways of getting diplegia in the arms. It is very common for people with Cerebral Palsy to have diplegia of the arms. Although most people with Cerebral Palsy have diplegia in their legs, some people have diplegia in their arms. Other ways of getting paralysis of both arms is through a traumatic event or injury.

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.

Where full recovery has not occurred after the 9 to 12 month 'watch and wait' period, management will take either a 'conservative' or a surgical course.

Although HSP is a progressive condition, the prognosis for individuals with HSP varies greatly. It primarily affects the legs although there can be some upperbody involvement in some individuals. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

Medications that impede the release of excitatory neurotransmitters have been used to control or prevent spasms. Treatment with intrathecal baclofen, a gamma-aminobutyric acid (GABA) agonist, decreases muscle tone and has been shown to decrease the frequency of muscle spasms in ADCP patients. Tetrabenazine, a drug commonly used in the treatment of Huntington's disease, has been shown to be effective treating chorea.