The disease is more commonly found amongst Ashkenazi Jews. The occurrence of torsion dystonia in the Ashkenazi Jewish population as stated by the Department of Epidemiology and Public Health of Yale University School of Medicine in New Haven, CT; "Reports dating to the beginning of this century describe Ashkenazi Jewish (AJ) families with multiple cases of ITD either in siblings (Schwalbe 1908; Bernstein 1912; Abrahamson 1920) or in parents and offspring (Wechsler and Brock 1922; Mankowsky and Czerny 1929; Regensberg 1930). The first comprehensive evaluation of the mode of inheritance of ITD in Jewish and non-Jewish families was described by Zeman and Dyken (1967), who concluded that the disorder was inherited as an autosomal dominant with incomplete penetrance in both populations. Although they concluded that the gene frequency was higher in the AJ population than in non-Jews, no difference in mode of inheritance or disease mechanism was construed."

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.

A 1969 study of torsion dystonia patients found an average IQ 10 points higher than controls matched for age, sex and ethnic background.

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.

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.

Essential tremor (ET, also referred to as benign tremor, familial tremor, or idiopathic tremor) is the most common movement disorder; its cause is unknown. It typically involves a tremor of the arms, hands or fingers but sometimes involving the head, vocal cords or other body parts during voluntary movements such as eating and writing. It is distinct from Parkinson's disease—and often misdiagnosed as such—although some individuals have both conditions. Essential tremor is commonly described as an action tremor (i.e., it intensifies when one tries to use the affected muscles) or postural tremor (i.e., present with sustained muscle tone) rather than a resting tremor, such as is seen in Parkinson’s, which is usually not included among its symptoms.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

Myoclonic dystonia or Myoclonus dystonia syndrome is a rare movement disorder that induces spontaneous muscle contraction causing abnormal posture. The prevalence of myoclonus dystonia has not been reported, however, this disorder falls under the umbrella of movement disorders which affect thousands worldwide. Myoclonus dystonia results from mutations in the SGCE gene coding for an integral membrane protein found in both neurons and muscle fibers. Those suffering from this disease exhibit symptoms of rapid, jerky movements of the upper limbs (myoclonus), as well as distortion of the body's orientation due to simultaneous activation of agonist and antagonist muscles (dystonia).

Myoclonus dystonia is caused by loss-of-function-mutations in the epsilon sarcoglycan gene (SGCE). The disease is dominantly inherited, however SGCE is an imprinted gene, so only the paternal allele is expressed. Therefore, children suffering from this disease inherit the mutation from the father. If the mutated allele is inherited from the mother, the child is not likely to exhibit symptoms.

While no cure has been found for myoclonus dystonia, treatment options are available to those suffering from the disease. Ethanol often ameliorates the symptoms well, and so the syndrome is also called "Alcohol-responsive dystonia". Alcohol may be substituted by benzodiazepines, such as clonazepam, which work through the same mechanism. Deep brain stimulation (DBS) is another viable option that can alleviate symptoms without the unwanted side effects of medications, and has been successful in treating other movement disorders.

To date, there is no single, universal treatment that has been found to cure myoclonus dystonia. However, there are several treatment methods that have been found to be effective for helping to reduce the symptoms associated with the syndrome.

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.

The term ataxia refers to a group of progressive neurological diseases that alter coordination and balance. Ataxias are often characterized by poor coordination of hand and eye movements, speech problems, and a wide-set, unsteady gait. Possible causes of ataxias may include stroke, tumor, infection, trauma, or degenerative changes in the cerebellum. These types of hyperkinetic movements can be further classified into two groups. The first group, hereditary ataxias, affect the cerebellum and spinal cord and are passed from one generation to the next through a defective gene. A common hereditary ataxia is Friedreich's ataxia. in contrast, sporadic ataxias occur spontaneously in individuals with no known family history of such movement disorders.

Agraphia is an acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell. The loss of writing ability may present with other language or neurological disorders; disorders appearing commonly with agraphia are alexia, aphasia, dysarthria, agnosia, and apraxia. The study of individuals with agraphia may provide more information about the pathways involved in writing, both language related and motoric. Agraphia cannot be directly treated, but individuals can learn techniques to help regain and rehabilitate some of their previous writing abilities. These techniques differ depending on the type of agraphia.

Agraphia can be broadly divided into central and peripheral categories. Central agraphias typically involve language areas of the brain, causing difficulty spelling or with spontaneous communication, and are often accompanied by other language disorders. Peripheral agraphias usually target motor and visuospatial skills in addition to language and tend to involve motoric areas of the brain, causing difficulty in the movements associated with writing. Central agraphia may also be called aphasic agraphia as it involves areas of the brain whose major functions are connected to language and writing; peripheral agraphia may also be called nonaphasic agraphia as it involves areas of the brain whose functions are not directly connected to language and writing (typically motor areas).

The history of agraphia dates to the mid-fourteenth century, but it was not until the second half of the nineteenth century that it sparked significant clinical interest. Research in the twentieth century focused primary on aphasiology in patients with lesions from strokes.

Agraphia has a multitude of causes ranging from strokes, lesions, traumatic brain injury, and dementia. Twelve regions of the brain are associated with handwriting. The four distinct functional areas are the left superior frontal area composed of the middle frontal gyrus and the superior frontal sulcus, the left superior parietal area composed of the inferior parietal lobule, the superior parietal lobule and the intraparietal sulcus and lastly the primary motor cortex and the somatosensory cortex. The eight other areas are considered associative areas and are the right anterior cerebellum, the left posterior nucleus of the thalamus, the left inferior frontal gyrus, the right posterior cerebellum, the right superior frontal cortex, the right inferior parietal lobule, the left fusiform gyrus and the left putamen. The specific type of agraphia resulting from brain damage will depend on which area of the brain was damaged.

Phonological agraphia is linked to damage in areas of the brain involved in phonological processing skills (sounding out words), specifically the language areas around the sylvian fissure, such as Broca's area, Wernicke's area, and the supramarginal gyrus.

Lexical agraphia is associated with damage to the left angular gyrus and/or posterior temporal cortex. The damage is typically posterior and inferior to the perisylvian language areas.

Deep agraphia involves damage to the same areas of the brain as lexical agraphia plus some damage to the perisylvian language areas as well. More extensive left hemisphere damage can lead to global agraphia.

Gerstmann's syndrome is caused by a lesion of the dominant (usually the left) parietal lobe, usually an angular gyrus lesion.

Apraxic agraphia with ideomotor apraxia is typically caused by damage to the superior parietal lobe (where graphomotor plans are stored) or the premotor cortex (where the plans are converted into motor commands). Additionally, some individuals with cerebellar lesions (more typically associated with non-apraxic motor dysfunction) develop apraxic agraphia. Apraxic agraphia without ideomotor apraxia may be caused by damage to either of the parietal lobes, the dominant frontal lobe, or to the dominant thalamus.

Visuospatial agraphia typically has a right hemisphere pathology. Damage to the right frontal area of the brain may cause more motor defects, whereas damage to the posterior part of the right hemisphere leads predominantly to spatial defects in writing.