Successful treatment of the associated underlying disorder, such as GORD or hiatus hernia, may provide relief.

Sandifer syndrome is not typically life-threatening and the prognosis is typically good.

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia. DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.

CMM has clear severe impacts on a patient’s ability to carry out daily manual tasks. It is recommended that children be placed under more forgiving school environments, allowing more time for written evaluations and limiting handwritten assignments, to ease the burden of the movement disability. Furthermore, because of patients’ inability to perform pure unilateral movements and their difficulty with tasks requiring skilled bimanual coordination, young and new members to the workforce are encouraged to consider professions that do not require complex bimanual movements, repetitive or sustained hand movements, or extensive handwriting, to reduce overuse, pain, and discomfort in upper limbs.

Because of its pronounced and obviously noticeable signs and symptoms, CMM patients can suffer social stigma, however physicians need to make it clear to parents, family, and friends that the disorder bears no relation to intellectual abilities. However, the rarity of this neurologic disease, found in one in a million people, makes its societal and cultural significance quite limited.

Infantile convulsions and choreoathetosis (ICCA) syndrome is a neurological genetic disorder with an autosomal dominant mode of inheritance. It is characterized by the association of benign familial infantile epilepsy (BIFE) at age 3–12 months and later in life with paroxysmal kinesigenic choreoathetosis. The ICCA syndrome was first reported in 1997 in four French families from north-western France and provided the first genetic evidence for common mechanisms shared by benign infantile seizures and paroxysmal dyskinesia. The epileptic origin of PKC has long been a matter of debates and PD have been classified as reflex epilepsies.Indeed, attacks of PKC and epileptic seizures have several characteristics in common, they both are paroxysmal in presentation with a tendency to spontaneous remission, and a subset of PKC responds well to anticonvulsants. This genetic disease has been mapped to chromosome 16p-q12. More than 30 families with the clinical characteristics of ICCA syndrome have been described worldwide so far.

In affected individuals presenting with the ICCA syndrome, the human genome was screened with microsatellite markers regularly spaced, and strong evidence of linkage with the disease was obtained in the pericentromeric region of chromosome 16, with a maximum lod score, for D16S3133 of 6.76 at a recombination fraction of 0. The disease gene has been mapped at chromosome 16p12-q12.This linkage has been confirmed by different authors. The chromosome 16 ICCA locus shows complicated genomic architecture and the ICCA gene remains unknown.

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.

Almost all patients respond positively to antiepileptic (anticonvulsant) drugs. One of the drugs most often mentioned in the literature is carbamazepine, and is the most widely used drug for treating PKD. Other anticonvulsants like valproic acid, phenytoin and clonazepam are common alternatives. Other categories of drugs have also been used, such as dopamine affecting drugs like Levodopa or Tetrabenazine. Individuals with the disorder can also modify their behavior to lessen their attacks without the influence of drug therapy. For example, decreasing stress to avoid precipitants can help patients decrease the number of attacks. In addition, avoiding any sudden movements can also prevent an attack. In order to prevent an attack, some individuals use their auras as a warning, while others purposefully perform slow gestures or movements prior to a triggering movement. Many, if not most, individuals end up growing out of the attacks with age, even without medicinal therapy, but some patients will go back to having attacks after a period of remission. In regards to secondary PKD, treatment of the primary condition can lessen the PKD attacks in those individuals.

Currently there is no cure for dysmetria itself as it is actually a symptom of an underlying disorder. However, isoniazid and clonazepam have been used to treat dysmetria. Frenkel exercises treat dysmetria. There have also been numerous reported cases of chiropractic neurology as an effective holistic treatment for dysmetria. Cannabis has been used in trials in the U.K. and displayed some success, though it is not legal to use in some U.S. states.

Researchers now are testing different possibilities for treating dysmetria and ataxia. One opportunity for treatment is called rehearsal by eye movement. It is believed that visually guided movements require both lower- and higher-order visual functioning by first identifying a target location and then moving to acquire what is sought after. In one study, researchers used visually guided stepping which is parallel to visually guided arm movements to test this treatment. The patients suffered from saccadic dysmetria which in turn caused them to overshoot their movements 3. The patients first walked normally and were then told to twice review the area that was to be walked through 3. After rehearsal with eye movements, the patients improved their motor performance. Researchers believe that prior rehearsal with the eyes might be enough for a patient who suffers from motor dysmetria as a result of saccadic dysmetria to complete a motor task with enhanced spatial awareness.

Research has also been done for those patients who suffer from MS. Deep brain stimulation (DBS) remains a viable possibility for some MS patients though the long-term effects of this treatment are currently under review. The subjects who have undergone this treatment had no major relapse for six months and disabling motor function problems. Most subjects benefited from the implantation of the electrodes and some reported that their movement disorder was gone after surgery. However, these results are limiting at this time because of the small range of subjects who were used for the experiment and it is unknown whether this is a viable option for all MS patients who suffer from motor control problems.

One form of treatment that has produced a more integrated body awareness is mirror therapy, in which the individual who denies that the affected limb belongs to their body looks into a mirror at the limb. Patients looking into the mirror state that the limb does belong to them; however body ownership of the limb does not remain after the mirror is taken away.

As of 2013 low quality evidence supports the use of bisphosphonates. A 2009 review found "very limited data reviewed showed that bisphosphonates have the potential to reduce pain associated with bone loss in patients with CRPS I, however, at present there is not sufficient evidence to recommend their use in practice".

Surgical, chemical, or radiofrequency sympathectomy — interruption of the affected portion of the sympathetic nervous system — can be used as a last resort in patients with impending tissue loss, edema, recurrent infection, or ischemic necrosis. However, there is little evidence that these permanent interventions alter the pain symptoms of the affected patients, and in addition to the normal risks of surgery, such as bleeding and infection, sympathectomy has several specific risks, such as adverse changes in how nerves function.

Different medications are tried in an effort to find a combination that is effective for a specific person. Not all people will respond well to the same medications. Medications that have had positive results in some include: diphenhydramine, benzatropine and atropine. anti-Parkinsons agents (such as ropinirole and bromocriptine), and muscle relaxants (such as diazepam).

- Anticholinergics

Medications such as anticholinergics (benztropine), which act as inhibitors of the neurotransmitter acetylcholine, may provide some relief. In the case of an acute dystonic reaction, diphenhydramine is sometimes used (though this drug is well known as an antihistamine, in this context it is being used primarily for its anticholinergic role).. See also Procyclidine.

- Baclofen

A baclofen pump has been used to treat patients of all ages exhibiting muscle spasticity along with dystonia. The pump delivers baclofen via a catheter to the thecal space surrounding the spinal cord. The pump itself is placed in the abdomen. It can be refilled periodically by access through the skin. Baclofen can also be taken in tablet form

- Botulin toxin injection

Botulinum toxin injections into affected muscles have proved quite successful in providing some relief for around 3–6 months, depending on the kind of dystonia. Botox or Dysport injections have the advantage of ready availability (the same form is used for cosmetic surgery) and the effects are not permanent. There is a risk of temporary paralysis of the muscles being injected or the leaking of the toxin into adjacent muscle groups, causing weakness or paralysis in them. The injections have to be repeated, as the effects wear off and around 15% of recipients will develop immunity to the toxin. There is a Type A and a Type B toxin approved for treatment of dystonia; often, those that develop resistance to Type A may be able to use Type B.

- Muscle relaxants

Clonazepam, an anti-seizure medicine, is also sometimes prescribed. However, for most, their effects are limited and side-effects like mental confusion, sedation, mood swings, and short-term memory loss occur.

- Parkinsonian drugs

Dopamine agonists: One type of dystonia, dopamine-responsive dystonia, can be completely treated with regular doses of L-DOPA in a form such as Sinemet (carbidopa/levodopa). Although this does not remove the condition, it does alleviate the symptoms most of the time. (In contrast, dopamine antagonists can sometimes cause dystonia.)

Ketogenic Diet

A Ketogenic diet consisting of 70% fats (focusing on medium chain triglycerides and unsaturated fats), 20% protein and 10% carbohydrates (any sugar) has shown strong promise as a treatment for Dystonia.

The specific molecular mechanism that underpins this movement disorder is not well known. However, most researchers suggest that it follows an autosomal dominant genetic inheritance pattern in which mutations in certain genes give rise to structural abnormalities in nervous system networks responsible for voluntary skeletal muscle movement, which, in turn, result in the functional movement abnormalities seen in patients. Despite being autosomal dominant, it is important to note that the disease has variable expressivity. That is, patients who have inherited a mutated dominant allele, along with their genetically affected parent, can be symptomatic or asymptomatic for CMM disorder. The genes that currently have evidence to be associated with CMM disorder include "DCC" (deleted in colorectal carcinoma), "DNAL4" (dynein axonemal light chain 4), and "RAD51 (recombination protein A)".

"DCC" encodes a receptor for "NTN1" (netrin-1), a protein thought to be responsible for axon guidance and neuronal cell migration during development. A mutation of this gene (including nonsense, splice site mutation, insertions, frameshift) has been identified as a possible cause for CMM disorder. Experiments in mice also support the claim that CMM disorder is associated with genetic mutations in "DCC". "Kanga" mice, lacking the P3 intracellular domain of the "DCC" receptor, show a hopping gait, moving their hind legs in a strictly paired fashion, as do kangaroos.

"DNAL4" encodes a component of dynein motor complex in commissural neurons of the corpus callosum. In contrast to "DCC", "DNAL4" is thought to have a recessive inheritance pattern for the CMM disorder. In CMM disorder patients, researchers found splice site mutations on "DNAL4", which caused skipping of exon 3, and thereby omission of 28 amino acids from "DNAL4" protein. This mutant "DNAL4" protein, in turn, could lead to faulty cross-hemisphere wiring, resulting in CMM.

"RAD51" maintains genome integrity by repairing DNA double-strand breaks through homologous recombination. "RAD51" heterozygous mutations, specifically premature termination codons, have been found in many CMM disorder patients through genome-wide linkage analysis and exome sequencing. In a mouse model, researchers also found "RAD51" products in corticospinal tract axons at the pyramidal decussation. They therefore suggest that "RAD51" might be a gene that, when haploinsufficient, causes CMM disorder in humans.

Despite identification of three prospective genes, no genotype-phenotype correlations have yet been found. That is, the severity of clinical signs and symptoms does not correlate with the type of genetic variant. Mutations in the above genes account for a total of about 35 percent of cases. Mutations in other genes that have not been identified likely account for the other cases of this disorder.

Rhythmic Movement Disorder (or RMD) is a neurological disorder characterized by involuntary (however may sometimes be voluntary), repetitive movements of large muscle groups immediately before and during sleep often involving the head and neck. It was independently described first in 1905 by Zappert as jactatio capitis nocturna and by Cruchet as rhythmie du sommeil. The majority of RMD episodes occur during NREM sleep, although REM movements have been reported. RMD is often associated with other psychiatric conditions or mental retardation. The disorder often leads to bodily injury from unwanted movements. Because of these incessant muscle contractions, patients’ sleep patterns are often disrupted. It differs from Restless Legs Syndrome in that RMD involves involuntary muscle contractions before and during sleep while Restless Legs Syndrome is the urge to move before sleep. RMD occurs in both males and females, often during early childhood with symptoms diminishing with age. Many sufferers also have other sleep related disorders, like sleep apnea. The disorder can be differentially diagnosed into small subcategories, including sleep related bruxism, thumb sucking, hypnagonic foot tremor, and rhythmic sucking, to name a few. In order to be considered pathological, the ICSD-II requires that in the sleep-related rhythmic movements should “markedly interfere with normal sleep, cause significant impairment in daytime function, or result in self-inflicted bodily injury that requires medical treatment (or would result in injury if preventive measures were not used)”

Somatoparaphrenia is a type of monothematic delusion where one denies ownership of a limb or an entire side of one's body. Even if provided with undeniable proof that the limb belongs to and is attached to their own body, the patient produces elaborate confabulations about whose limb it really is, or how the limb ended up on their body. In some cases, delusions become so elaborate that a limb may be treated and cared for as if it were a separate being.

Somatoparaphrenia differs from a similar disorder, asomatognosia, which is characterized as loss of recognition of half of the body or a limb, possibly due to paralysis or unilateral neglect. For example, asomatognosic patients may mistake their arm for the doctor's. However, they can be shown their limb and this error is temporarily corrected.

Somatoparaphrenia has been reported to occur predominately in the left arm of one's body, and it is often accompanied by left-sided paralysis and anosognosia (denial or lack of awareness) of the paralysis. The link between somatoparaphrenia and paralysis has been documented in many clinical cases and while the question arises as to whether paralysis is necessary for somatoparaphrenia to occur, anosognosia is not, as documented by cases with somatoparaphrenia and paralysis with no anosognosia.

Medication is often not necessary in children as symptoms usually alleviate spontaneously as the child ages. However, because the disorder may affect wakeful behavior, many adults who continue to suffer from RMD may seek treatment. Benzodiazepines or tricyclic antidepressants have been considered as therapeutic options in managing the disorder. Infantile and adolescent RMD respond well to low doses of clonazepam. Prescription medications such as ropinirole or pramipexole given to restless legs syndrome patients do not show any clinical improvement in many patients with RMD.

There is no cure for Machado-Joseph Disease. However, treatments are available for some symptoms. For example, spasticity can be reduced with antispasmodic drugs, such as baclofen. The Parkinsonian symptoms can be treated with levodopa therapy. Prism glasses can reduce diplopic symptoms. Physiotherapy/Physical Therapy and/or occupational therapy can help patients by prescribing mobility aids to increase the patients' independence, providing gait training, and prescribing exercises to maintain the mobility of various joints and general health to decrease the likelihood of falls or injuries as a result of falls. Walkers and wheelchairs can greatly help the patient with everyday tasks. Some patients will experience difficulties with speech and swallowing, therefore a Speech-Language Pathologist can assist the patients to improve their communicating abilities and their issues with swallowing.

One approach that has received public interest is the use of a mirror box. The mirror box provides a reflection of the intact hand or limb that allows the patient to "move" the phantom limb, and to unclench it from potentially painful positions.

As of 2011, however, the quality of evidence is low. There is a wide range in the effectiveness of this approach. The potential for a person to benefit from mirror therapy is not predictable and appears to be related to the subjective ability of the patient to internalize the reflection of a complete limb as their own limb. About 40% of people do not benefit from mirror therapy.

Paroxysmal kinesigenic dyskinesia has been shown to be inherited in an autosomal dominant fashion. In 2011, the PRRT2 gene on chromosome 16 was identified as the cause of the disease. The researchers looked at the genetics of eight families with strong histories of PKD. They employed whole genome sequencing, along with Sanger sequencing to identify the gene that was mutated in these families. The mutations in this gene included a nonsense mutation identified in the genome of one family and an insertion mutation identified in the genome of another family. The researchers then confirmed this gene as the cause of PKD when it was not mutated in the genome of 1000 control patients. Researchers found PRRT2 mutations in 10 of 29 sporadic cases affected with PKD, thus suggests PRRT2 is the gene mutated in a subset of PKD and PKD is genetically heterogeneous. The mechanism of how PRRT2 causes PKD still requires further investigation. However, researchers suggest it may have to do with PRRT2's expression in the basal ganglia, and the expression of an associated protein, SNAP25, in the basal ganglia as well.

Mirror-touch synesthesia is a rare condition which causes individuals to experience the same sensation (such as touch) that another person feels. For example, if someone with this condition were to observe someone touching their cheek, they would feel the same sensation on their own cheek. Synesthesia, in general, is described as a condition in which a stimulus causes an individual to experience an additional sensation. Synesthesia is usually a developmental condition; however, recent research has shown that mirror touch synesthesia can be acquired after sensory loss following amputation.

Patients with severe forms of MJD have a life expectancy of approximately 35 years. Those with mild forms have a normal life expectancy. The cause of death of those who die early is often aspiration pneumonia.

There are several different ways to treat frontal lobe epileptic seizures, however, the most common form of treatment is through the use of anticonvulsant medications that help to prevent seizures from occurring. In some cases, however, when medications are ineffective, a neurologist may choose to operate on the patient in order to remove the focal area of the brain in which the seizures are occurring. Other treatments that can be administered to aid in reducing the occurrence of seizures include the implementation of a specific, regimented diet and/or the implantation of a vagus nerve stimulator.