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 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.

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.

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.

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.

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".

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.

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.

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.

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.

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.

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.

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).

As a matter of everyday maintenance, muscle stretching, range of motion exercises, yoga, contact improvisation, modern dance, resistance training, and other physical activity regimens are often utilized by those with spastic CP to help prevent contractures and reduce the severity of symptoms.

Major clinical treatments for spastic diplegia are:

- Baclofen (and its derivatives), a gamma amino butyric acid (GABA) substitute in oral (pill-based) or intrathecal form. Baclofen is essentially chemically identical to the GABA that the damaged, over-firing nerves cannot absorb, except that it has an extra chemical 'marker' on it that makes the damaged nerves 'think' it is a different compound, and thus those nerves will absorb it. Baclofen is noted for being the sole medication available for GABA-deficiency-based spasticity which acts on the actual cause of the spasticity rather than simply reducing symptomatology as muscle relaxants and painkillers do. The intrathecal solution is a liquid injected into the spinal fluid for trial, and if successful in reducing spasticity, thereafter administered via an intrathecal pump, which has variously been proven potentially very dangerous on one or another level with long-term use (see article), including sudden and potentially lethal baclofen overdose, whereas the oral route, which comes in 10- or 20-milligram tablets and the dosage of which can be gently titrated either upward or downward, as well as safely ceased entirely, has not.

- Antispasmodic muscle relaxant chemicals such as tizanidine and botulinum toxin (Botox), injected directly into the spastic muscles; Botox wears off every three months.

- Phenol and similar chemical 'nerve deadeners', injected selectively into the over-firing nerves in the legs on the muscle end to reduce spasticity in their corresponding muscles by preventing the spasticity signals from reaching the legs; Phenol wears off every six months.

- Orthopedic surgery to release the spastic muscles from their hypertonic state, a usually temporary result because the spasticity source is the nerves, not the muscles; spasticity can fully reassert itself as little as one year post-surgery.

- Selective dorsal rhizotomy, a neurosurgery directly targeting and eliminating ("cutting" or "lesioning") the over-firing nerve rootlets and leaving the properly firing ones intact, thereby permanently eliminating the spasticity but compelling the person to spend months re-strengthening muscles that will have been severely weakened by the loss of the spasticity, due to the fact of those muscles not really having had actual strength to begin with.

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.

There is no known cure for cerebral palsy, however there is a large array of treatments proven effective at improving quality of life and relieving some of the symptoms associated with CP, especially SHCP. Some treatments are aimed at improving mobility, strengthening muscle and improving coordination. Although CP is due to permanent damage and is not progressive in nature, without treatment the symptoms can become worse, intensifying in pain and severity, and create complications that were not initially present. Some treatments are preventative measures to help prevent further complications, such as complete paralysis of the arm due to non-use and subsequent worsening hypertonia and joint contracture. Others forms of treatment are corrective in nature. Many treatments target symptoms that are indirectly related to or caused by the SHCP. Many of these treatments are common for other forms of CP as well. Treatment is individualized based on each case and the specific needs of the patient. Treatments are often combined with other forms of treatment and a long term treatment plan is created and continuously evaluated. Treatment can include the following:

- "Physical therapy" – Physical therapy is the most common form of treatment (source needed). It may include sensory stimulation, stretching, strengthening and positioning. Constraint-induced movement therapy is a newer form of physical therapy for SHCP that involves casting or splinting the unaffected arm to promote use of the affected arm (Taub). The theory behind constraint-induced movement therapy is that new neural pathways are created. Alternative forms of physical therapy include yoga and dance. Physical therapy may also include the use of braces while not actively involved with the therapist.

- "Occupational therapy" – Occupational therapy evaluates and treats patients through selected activities in order to enable people to function as effectively and independently as possible in daily life. Occupational therapy is geared toward the individual to achieve optimal results and performance while learning to cope with their disability.

- "Speech therapy" – Due to difficulties in speech, speech therapy is often necessary. Aside from helping with understanding language and increasing communication skills, speech therapists can also assist children that have difficulty eating and drinking.

- "Behavioral therapy" — Psychotherapy and counseling are heavily used in treatment of individuals with SHPD to help them cope emotionally with their needs and frustrations. Counseling through social work can be very beneficial for social issues and adjustments to society. Psychotherapy becomes a more important aspect of therapy when more serious issues such as depression become problematic. Play therapy is a common treatment for all young children with or without disabilities, but can be very useful helping children with SHCP. This therapy again is individualized geared to improve emotional and social development; reduce aggression; improve cooperation with others; assist a child in processing a traumatic event or prepare for an upcoming event such as surgery.

- "Surgery" – Although surgery may become necessary in some cases, physical therapy and the consistent use of braces can help mitigate the need for surgery. Surgical procedures are painful with long and difficult recoveries and do not cure the condition. Most common, is surgery that effectively lengthens the muscle. This type of surgery is usually performed on the legs, but can be performed on the arms as well. Surgeries also may be necessary to realign joints. Other, less popular surgical techniques try to reduce spasticity by severing selected overactive nerves that control muscles. This procedure, known as selective dorsal root rhizotomy, is still somewhat controversial, and is generally used only on the lower extremities of severe cases. Other experimental surgical techniques are also being investigated. The benefits of surgery can also be negated or reversed if the patient does not participate in physical therapy and braces (or casts) are not worn regularly.

- "Medicinal" – Medication targeting symptoms associated with spasticity is also a relatively new treatment that is utilized, but is still in the early stages of development. Drugs such as baclofen, benzodiazepines (e.g., diazepam), tizanidin, and sometimes dantrolene have shown promise in the effort to diminish spasticity. Botulinum toxin ("Botox") type A may reduce spasticity a few months at a time and has frequently been considered a beneficial treatment for children with SHCP and other forms of CP. Botox has been shown to be especially beneficial to reducing spasticity in the gastrocnemius (calf) muscle. This therapy can improve range of motion, reduce deformity, improve response to occupational and physical therapy, and delay the need for surgery. Botox injections have also shown advantages for upper extremities. There is still some doubt for the effectiveness, and some side effects to the relaxed muscles have been a loss of strength for patients with some muscle control. Casting, in conjunction with Botox injections may be an additional option for better results. Research is constantly investing in new improvements and more experimental therapy and treatment.

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.

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.

- "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.

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.

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 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.