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.

Geniospasm is movement disorder of the mentalis muscle.

It is a benign genetic disorder linked to chromosome 9q13-q21 where there are episodic involuntary up and down movements of the chin and lower lip. The movements consist of rapid fluttering or trembling at about 8 Hz superimposed onto a once per three seconds movement of higher amplitude and occur symmetrically in the V shaped muscle. The tongue and buccal floor muscles may also be affected but to a much lesser degree.

The movements are always present but extreme episodes may be precipitated by stress, concentration or emotion and commence in early childhood.

The condition is extremely rare and in a study in 1999 only 23 families in the world were known to be affected, although it may be under-reported. Inheritance is aggressively autosomal dominant. In at least two studies the condition appeared spontaneously in the families.

The condition responds very well to regular botulinus toxin injections into the mentalis muscle which paralyse the muscle but cause no impairment of facial expression or speech.

Although essential tremor is often mild, people with severe tremor have difficulty performing many of their routine activities of daily living. ET is generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.

In some cases Meige's syndrome can be reversed when it is caused by medication. It has been theorized that it is related to cranio-mandibular orthopedic misalignment, a condition that has been shown to cause a number of other movement disorders (Parkinon's, tourettes, and torticollis). This theory is supported by the fact that the trigeminal nerve is sensory for blink reflex, and becomes hypertonic with craniomandibular dysfunction. Palliative treatments are available, such as botulinum toxin injections.

The main symptoms involve involuntary blinking and chin thrusting. Some patients may experience excessive tongue protrusion, squinting, light sensitivity, muddled speech, or uncontrollable contraction of the platysma muscle. Some Meige's patients also have "laryngeal dystonia" (spasms of the larynx). Blepharospasm may lead to embarrassment in social situations, and oromandibular dystonia can affect speech, making it difficult to carry on the simplest conversations. This can cause difficulty in both personal and professional contexts, and in some cases may cause patients to withdraw from social situations.

The condition tends to affect women more frequently than men.

There is a group called myoclonic dystonia where some cases are hereditary and have been associated with a missense mutation in the dopamine-D2 receptor. Some of these cases have responded well to alcohol.

Other genes that have been associated with dystonia include CIZ1, GNAL, ATP1A3, and PRRT2. Another report has linked THAP1 and SLC20A2 to dystonia.

By 1990, 65 patients had been reported in the literature, with no sex or ethnic preference notable. Some individuals present with minimal malformation; rarely patients have died during infancy as a result of severe central nervous system involvement or respiratory complications. Several syndromes are related to the Freeman–Sheldon syndrome spectrum, but more information is required before undertaking such nosological delineation.

There are little data on prognosis. Rarely, some patients have died in infancy from respiratory failure; otherwise, life expectancy is considered to be normal.

Paroxysmal tonic upgaze (PTU) of childhood is a rare and distinctive neuro-ophthalmological syndrome characterized by episodes of sustained upward deviation of the eyes. Symptoms normally appear in babies under one year of age and are characterized by an upward stare or gaze, with the eyes rolled back, while the chin is typically held low.

Babies suffering from PTU may exhibit normal or slightly jerky side-to-side eye movement, nausea, irritability, frequent sleep, developmental and language delays, vertigo and loss of muscle tone.

The condition is generally regarded as having a benign outcome, in the sense that it improves, rather than worsens over time. The average age of recovery is at about 2.5 years.

PTU was first described in 1988. As of 2002, approximately fifty cases had been diagnosed. Because the condition is so rare, the majority of physicians have never seen it, and thus may not recognize it. Videotaping a child both in and out of the upgaze state can be vital for reaching a diagnosis.

ET is one of the most common neurological diseases, with a prevalence of approximately 4% in persons age 40 and older and considerably higher among persons in their 60s, 70s, 80s, with an estimated 20% of individuals in their 90s and over. Aside from enhanced physiological tremor, it is the most common type of tremor and one of the most commonly observed movement disorders.

The syndrome primarily affects young males. Preliminary studies suggest that prevalence may be 1.8 per 10,000 live male births. 50% of those affected do not live beyond 25 years of age, with deaths attributed to the impaired immune function.

In 1983, Bringewald postulated that superior oblique myokymia resulted from vascular compression of the trochlear nerve (fourth cranial nerve), which controls the action of the superior oblique muscle in the eye. By 1998, there had been only one reported case of compression of the trochlear nerve by vessels.

More recently, magnetic resonance imaging experiments have shown that neurovascular compression at the root exit zone of the trochlear nerve can result in superior oblique myokymia.

Abasia (from Greek: "a-", without and "basis", step) is the inability to walk owing to impairment in motor coordination.

The term covers a spectrum of medical disorders such as:

- choreic abasia: caused by chorea of the legs

- paralytic abasia: caused by paralysis of the leg muscles

- spastic abasia: caused by spastic stiffening of the leg muscles

- trembling abasia: caused by trembling of the legs

Abasia is frequently accompanied by astasis, an inability to stand, see Astasia-abasia.

Treatment can include pharmaceutical or surgical means. The drug carbamazepine (Tegretol) has been used successfully. Other drugs used with variable success include gabapentin and, recently, memantine. Successful surgery options include superior oblique tenectomy accompanied by inferior oblique myectomy. However, "Overall, the bulk of the ophthalmic literature would agree with the viewpoint that invasive craniotomy surgical procedures should be justified only by the presence of intractable and absolutely unbearable symptoms."

Samii et al. and Scharwey and Samii described a patient who had superior oblique myokymia for 17 years. The interposition of a Teflon pad between the trochlear nerve and a compressing artery and vein at the nerve's exit from the midbrain led to a remission lasting for a follow-up of 22 months.

Writer's cramp, also called mogigraphia and scrivener's palsy, is a disorder caused by cramps or spasms of certain muscles of the hand and/or forearm, and presents itself while performing fine motor tasks, such as writing or playing an instrument. Writer's cramp is a task-specific focal dystonia of the hand. 'Focal' refers to the symptoms being limited to one location (the hand in this case), and 'task-specific' means that symptoms first occur only when the individual engages in a particular activity. Writer's cramp first affects an individual by interfering with their ability to write, especially for prolonged periods of time.

Although the cause of writer's cramp is not well known, it was historically believed to be the result of excessive fine motor activity, possibly complicated by a tense or otherwise inappropriate writing technique. More recently, Karin Rosenkranz et al. have suggested that this is not necessarily the case. Musician's cramp (a similar focal dystonia which affects some 1% of instrumentalists) has historically been grouped together with writer's cramp because of this and their common task-specificity. Rosenkranz et al. have more recently identified significant differences between the two populations, however. No matter exactly how it arises, researchers generally agree that these types of focal dystonia are the result of a basal ganglia and/or sensorimotor cortex malfunction in the brain.

Early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, dropped items and a noticeable increase in dropped or chipped dishes), cramping pain with sustained use and trembling. Significant muscle pain and cramping may result from very minor exertions like holding a book and turning pages. It may become difficult to find a comfortable position for arms and legs with even the minor exertions associated with holding arms crossed causing significant pain similar to restless leg syndrome. Affected persons may notice trembling in the diaphragm while breathing, or the need to place hands in pockets, under legs while sitting or under pillows while sleeping to keep them still and to reduce pain. Trembling in the jaw may be felt and heard while lying down, and the constant movement to avoid pain may result in the grinding and wearing down of teeth, or symptoms similar to TMD. The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping. Patients may also present with varying degree of disability and symptoms, such as experiencing more difficulty writing down-stroke as compared to writing upstroke.

Electrical sensors (EMG) inserted into affected muscle groups, while painful, can provide a definitive diagnosis by showing pulsating nerve signals being transmitted to the muscles even when they are at rest. The brain appears to signal portions of fibers within the affected muscle groups at a firing speed of about 10 Hz causing them to pulsate, tremble and contort. When called upon to perform an intentional activity, the muscles fatigue very quickly and some portions of the muscle groups do not respond (causing weakness) while other portions over-respond or become rigid (causing micro-tears under load). The symptoms worsen significantly with use, especially in the case of focal dystonia, and a "mirror effect" is often observed in other body parts: use of the right hand may cause pain and cramping in that hand as well as in the other hand and legs that were not being used. Stress, anxiety, lack of sleep, sustained use and cold temperatures can worsen symptoms.

Direct symptoms may be accompanied by secondary effects of the continuous muscle and brain activity, including disturbed sleep patterns, exhaustion, mood swings, mental stress, difficulty concentrating, blurred vision, digestive problems and short temper. People with dystonia may also become depressed and find great difficulty adapting their activities and livelihood to a progressing disability. Side effects from treatment and medications can also present challenges in normal activities.

In some cases, symptoms may progress and then plateau for years, or stop progressing entirely. The progression may be delayed by treatment or adaptive lifestyle changes, while forced continued use may make symptoms progress more rapidly. In others, the symptoms may progress to total disability, making some of the more risky forms of treatment worth considering in the future.

Mäkelä-Bengs et al. (1997,1998) performed a genome-wide screening and linkage analysis and assigned the LCCS locus to a defined region of 9q34.

Benign familial infantile epilepsy (BFIE), also known as benign familial infantile seizures (BFIS) or benign familial infantile convulsions (BFIC) is an epilepsy syndrome. Affected children, who have no other health or developmental problems, develop seizures during infancy. These seizures have focal origin within the brain but may then spread to become generalised seizures. The seizures may occur several times a day, often grouped in clusters over one to three days followed by a gap of one to three months. Treatment with anticonvulsant drugs is not necessary but they are often prescribed and are effective at controlling the seizures. This form of epilepsy resolves after one or two years, and appears to be completely benign. The EEG of these children, between seizures, is normal. The brain appears normal on MRI scan.

A family history of epilepsy in infancy distinguishes this syndrome from the non-familial classification (see benign infantile epilepsy), though the latter may be simply sporadic cases of the same genetic mutations. The condition is inherited with an autosomal dominant transmission. There are several genes responsible for this syndrome, on chromosomes 2, 16 and 19. It is generally described as idiopathic, meaning that no other neurological condition is associated with it or causes it. However, there are some forms that are linked to neurological conditions. One variant known as infantile convulsions and choreoathetosis (ICCA) forms an association between BFIE and paroxysmal kinesigenic choreoathetosis and has been linked to the PRRT2 gene on chromosome 16. An association with some forms of familial hemiplegic migraine (FHM) has also been found. Benign familial infantile epilepsy is not genetically related to benign familial neonatal epilepsy (BFNE), which occurs in neonates. However, a variation with seizure onset between two days and seven months called "benign familial neonatal–infantile seizures" (BFNIS) has been described, which is due to a mutation in the SCN2A gene.

M2DS is one of the several types of X-linked intellectual disability. The cause of M2DS is a duplication of the MECP2 or Methyl CpG binding protein 2 gene located on the X chromosome (Xq28). The MeCP2 protein plays a pivotal role in regulating brain function. Increased levels of MECP2 protein results in abnormal neural function and impaired immune system. Mutations in the MECP2 gene are also commonly associated with Rett syndrome in females. Advances in genetic testing and more widespread use of Array Comparative Genomic Hybridization has led to increased diagnosis of MECP2 duplication syndrome. It is thought to represent ~1% of X-linked male mental disability cases.

There is no treatment for FTHS, though identification of TKS4 mutation as a causative factor may eventually provide new opportunities for neonatal screening in high-risk families.

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

The most comprehensive assessment so far has estimated RBD prevalence to be about 0.5% in individuals aged 15 to 100. It is far more common in males: most studies report that only about a tenth of sufferers are female. This may partially be due to a referral bias, as violent activity carried out by men is more likely to result in harm and injury and is more likely to be reported than injury to male bed partners by women, or it may reflect a true difference in prevalence as a result of genetic or androgenic factors. The mean age of onset is estimated to be about 60 years.

Various conditions are very similar to RBD in that sufferers exhibit excessive sleep movement and potentially violent behavior. Such disorders include sleepwalking and sleep terrors, which are associated with other stages of sleep, nocturnal seizures and obstructive sleep apnea which can induce arousals from REM sleep associated with complex behaviors. Because of the similarities between the conditions, polysomnography plays an important role in confirming RBD diagnosis.

It is now apparent that RBD appears in association with a variety of different conditions. Narcolepsy has been reported as a related disorder. Both RBD and narcolepsy involve dissociation of sleep states probably arising from a disruption of sleep control mechanisms. RBD has also been reported following cerebrovascular accident and neurinoma (tumor), indicating that damage to the brain stem area may precipitate RBD. RBD is usually chronic. However, it may be acute and sudden in onset if associated with drug treatment or withdrawal (particularly with alcohol withdrawal). 60% of RBD is idiopathic. This includes RBD that is found in association with conditions such as Parkinson's disease and dementia with Lewy bodies, where it is often seen to precede the onset of neurodegenerative disease. Monoamine oxidase inhibitors, tricyclic antidepressants, Selective serotonin reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD.

Lethal congenital contracture syndrome 1 (LCCS1), also called Multiple contracture syndrome, Finnish type, is an autosomal recessive genetic disorder characterized by total immobility of a fetus, detectable at around the 13th week of pregnancy. LCCS1 invariably leads to prenatal death before the 32nd gestational week. LCCS1 is one of 40 Finnish heritage diseases. It was first described in 1985 and since then, approximately 70 cases have been diagnosed.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.