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.

Corticosteroids such as prednisone improve recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery.

Physiotherapy

To increase strength of muscle

To improve muscle functions

Electrical modalities =Electric stimulation.etc.

Occupational Therapy

Positioning, ROM, Sensory, Splinting

Physiotherapy can be beneficial to some individuals with Bell’s palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve. It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles. To reduce pain, heat can be applied to the affected side of the face. There is no high quality evidence to support the role of electrical stimulation for Bell's palsy.

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.

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.

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.

There are a number of potential treatments for spasmodic dysphonia, including botox, surgery and voice therapy. A number of medications have also been tried including anticholinergics (such as benztropine) which have been found to be effective in 40-50% of people, but which are associated with a number of side effects.

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.

Voice therapy appears to be ineffective in cases of true spasmodic dysphonia, however as it is difficult to distinguish between spasmodic dysphonia and functional dysphonias and misdiagnosis is relatively common, a trial of voice therapy is often recommended before more invasive procedures are tried. Some also state that it is useful for mild symptoms and as an add-on to botox therapy and others report success in more severe cases. Laryngeal manual therapy, which is massaging of the neck and cervical structures, also shows positive results for intervention of functional dysphonia.

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.

Mild cases are managed by limiting activity, keeping a healthy body weight, and avoiding exposure to high ambient temperatures. Mild sedatives can be used to decrease anxiety and panting and therefore improve respiration. Corticosteroids may also be administered in acute cases to decrease inflammation and edema of the larynx.

Severe acute symptoms, such as difficulty breathing, hyperthermia, or aspiration pneumonia, must be stabilized with sedatives and oxygen therapy and may require steroid or antibiotic medications. Sometimes a tracheotomy is required to allow delivery of oxygen. Once the patient is stabilized, surgical treatment may be beneficial especially when paralysis occurs in both aretynoid cartilages (bilateral paralysis). The surgery (aretynoid lateralization, or a "laryngeal tieback") consists of suturing one of the aretynoid cartilages in a maximally abducted (open) position. This reduces the signs associated with inadequate ventilation (such as exercise intolerance or overheating) but may exacerbate the risk of aspiration and consequent pneumonia. Tying back only one of the aretynoid cartilages instead of both helps reduce the risk of aspiration. Afterwards the dog will still sound hoarse, and will need to be managed in the same way as those with mild cases of LP.

Recent studies have found that many dogs with laryngeal paralysis have decreased motility of their esophagus. Animals with a history of regurgitation or vomiting should be fully evaluated for esophageal or other gastrointestinal disorders. Dogs with megaesophagus or other conditions causing frequent vomiting or regurgitation are at high risk for aspiration pneumonia after laryngeal tie-back. Permanent tracheostomy is an alternative surgical option for these dogs to palliate their clincical signs.

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.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.

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.

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.

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.

Time is the only treatment necessary in more than 90% of infant cases. In other cases, surgery may be necessary. Most commonly, this involves cutting the aryepiglottic folds to let the supraglottic airway spring open. Trimming of the arytenoid cartilages or the mucosa/ tissue over the arytenoid cartilages can also be performed as part of the supraglottoplasty. Supraglottoplasty can be performed bilaterally (on both the left and right sides at the same time), or be staged where only one side is operated on at a time.

Treatment of gastroesophageal reflux disease can also help in the treatment of laryngomalacia, since gastric contents can cause the back part of the larynx to swell and collapse even further into the airway.

In some cases, a temporary tracheostomy may be necessary.

Laryngomalacia becomes symptomatic after the first few months of life (2–3 months), and the stridor may get louder over the first year, as the child moves air more vigorously. Most of the cases resolve spontaneously and less than 15% of the cases will need surgical intervention. Parents need to be supported and educated about the condition.

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).

Indirect therapies take into account external factors that may influence vocal production. This incorporates maintenance of vocal hygiene practices, as well as the prevention of harmful vocal behaviours. Vocal hygiene includes adequate hydration of the vocal folds, monitoring the amount of voice use and rest, avoidance of vocal abuse (e.g., shouting, clearing of the throat), and taking into consideration lifestyle choices that may affect vocal health (e.g., smoking, sleeping habits). Vocal warm-ups and cool-downs may be employed to improve muscle tension and decrease risk of injury before strenuous vocal activities. It should be taken into account that vocal hygiene practices alone are minimally effective in treating dysphonia, and thus should be paired with other therapies.

Medical and surgical treatments have been recommended to treat organic dysphonias. An effective treatment for spasmodic dysphonia (hoarseness resulting from periodic breaks in phonation due to hyperadduction of the vocal folds) is botulinum toxin injection. The toxin acts by blocking acetylcholine release at the thyro-arytenoid muscle. Although the use of botlinum toxin injections is considered relatively safe, patients' responses to treatment differ in the initial stages; some have reported experiencing swallowing problems and breathy voice quality as a side-effect to the injections. Breathiness may last for a longer period of time for males than females.

Surgeries involve myoectomies of the laryngeal muscles to reduce voice breaks, and laryngoplasties, in which laryngeal cartilage is altered to reduce tension.

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.

Currently, there are no treatments prescribed for PVL. All treatments administered are in response to secondary pathologies that develop as a consequence of the PVL. Because white matter injury in the periventricular region can result in a variety of deficits, neurologists must closely monitor infants diagnosed with PVL in order to determine the severity and extent of their conditions.

Patients are typically treated with an individualized treatment. It is crucial for doctors to observe and maintain organ function: visceral organ failure can potentially occur in untreated patients. Additionally, motor deficits and increased muscle tone are often treated with individualized physical and occupational therapy treatments.

CBPS is commonly treated with anticonvulsant therapy to reduce seizures. Therapies include anticonvulsant drugs, adrenocorticotropic hormone therapy, and surgical therapy, including focal corticectomy and callosotomy. Special education, speech therapy, and physical therapy are also used to help children with intellectual disability due to CBPS.