Chorea is characterized by brief, semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next.

These 'dance-like' movements of chorea often occur with athetosis, which adds twisting and writhing movements. Walking may become difficult, and include odd postures and leg movements.

Unlike ataxia, which affects the quality of voluntary movements, or Parkinsonism, which is a hindrance of voluntary movements, the movements of chorea and ballism occur on their own, without conscious effort. Thus, chorea is said to be a hyperkinetic movement disorder.

When chorea is serious, slight movements will become thrashing motions; this form of severe chorea is referred to as ballism or ballismus.

Holmes tremor is typically characterized by a low frequency tremor (below 4.5 Hz) that has a repeated series of rest and intention tremors. These tremors move slowly and are generally specific to an upper area of the body. They can consist of postural tremors in nearby muscles as well. These tremors involve uncontrollable shaking despite efforts to be still. Holmes tremor is considered a rest-intention posture tremor. These irregular movements occur while muscles are at rest, but worsen during voluntary muscle contractions. Symptoms usually appear delayed one to twenty-four months after the lesion is created.

Chorea (or choreia, occasionally) is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias. The term "chorea" is derived from the Greek word "χορεία" (=dance; see choreia), as the quick movements of the feet or hands are comparable to dancing.

The term hemichorea refers to chorea of one side of the body, such as chorea of one arm but not both (analogous to hemiballismus).

Wilson's disease (WD) is a rare inherited disorder in which patients have a problem metabolizing copper. In patients with WD, copper accumulates in the liver and other parts of the body, particularly the brain, eyes and kidneys. Upon accumulation in the brain, patients may experience speech problems, incoordination, swallowing problems, and prominent hyperkinetic symptoms including tremor, dystonia, and gait difficulties. Psychiatric disturbances such as irritability, impulsiveness, aggressiveness, and mood disturbances are also common.

A multitude of movement disorders have been observed after either ischemic or hemorrhagic stroke. Some examples include athetosis, chorea with or without hemiballismus, tremor, dystonia, and segmental or focal myoclonus, although the prevalence of these manifestations after stroke is quite low. The amount of time that passes between stroke event and presentation of hyperkinesia depends on the type of hyperkinetic movement since their pathologies slightly differ. Chorea tends to affect older stroke victims while dystonia tends to affect younger ones. Men and women have an equal chance of developing the hyperkinetic movements after stroke. Strokes causing small, deep lesions in the basal ganglia, brain stem and thalamus are those most likely to be associated with post-stroke hyperkinesia.

Ataxia is a motor disorder that affects the spinal cord, brain and brainstem. Symptoms of ataxia include tremors, lack of coordination, loss of balance, instability, inaccuracy, clumsiness, gait problems, speech problems, and involuntary eye movements. Medication is the main treatment of ataxia. Some of these medicines include selegiline, amantadine, entacapone, dopamine agonists, and anticholinergics (“Movement Disorders”).

Motor disorders are malfunctions of the nervous system that cause involuntary or uncontrollable movements or actions of the body (Stone). These disorders can cause lack of intended movement or an excess of involuntary movement (Mandal). Symptoms of motor disorders include tremors, jerks, twitches, spasms, contractions, or gait problems.

The most common first sign of MSA is the appearance of an "akinetic-rigid syndrome" (i.e. slowness of initiation of movement resembling Parkinson's disease) found in 62% at first presentation. Other common signs at onset include problems with balance (cerebellar ataxia) found in 22% at first presentation, followed by genito-urinary problems (9%). For men, the first sign can be erectile dysfunction (inability to achieve or sustain an erection). Women have also reported reduced genital sensitivity. Both men and women often experience problems with their bladders including urgency, frequency, incomplete bladder emptying, or an inability to pass urine (retention). About 1 in 5 MSA patients will fall in their first year of disease.

MSA is characterized by a combination of the following, which can be present in any combination:

- autonomic dysfunction

- parkinsonism (muscle rigidity +/ tremor and slow movement)

- ataxia (Poor coordination / unsteady walking)

A variant with combined features of MSA and Lewy body dementia may also exist. There have also been occasional instances of frontotemporal lobar degeneration associated with MSA.

Symptoms vary according to the kind of dystonia involved. In most cases, dystonia tends to lead to abnormal posturing, in particular on movement. Many sufferers have continuous pain, cramping, and relentless muscle spasms due to involuntary muscle movements. Other motor symptoms are possible including lip smacking.

Early symptoms may include loss of precision muscle coordination (sometimes first manifested in declining penmanship, frequent small injuries to the hands, and dropped items), 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 temporomandibular joint disorder. The voice may crack frequently or become harsh, triggering frequent throat clearing. Swallowing can become difficult and accompanied by painful cramping.

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 some cases with patients who already have dystonia, a subsequent tramatic injury or the effects of general anethesia during an unrelated surgery can cause the symptoms to progress rapidly.

An accurate diagnosis may be difficult because of the way the disorder manifests itself. Sufferers may be diagnosed as having similar and perhaps related disorders including Parkinson's disease, essential tremor, carpal tunnel syndrome, TMD, Tourette's syndrome, conversion disorder or other neuromuscular movement disorders. It has been found that the prevalence of dystonia is high in individuals with Huntington's disease, where the most common clinical presentations are internal shoulder rotation, sustained fist clenching, knee flexion, and foot inversion. Risk factors for increased dystonia in patients with Huntington's disease include long disease duration and use of antidopaminergic medication.

Intention tremors are common among individuals with multiple sclerosis (MS). One common symptom of multiple sclerosis is ataxia, a lack of coordinated muscle movement caused by cerebellar lesions characteristic of multiple sclerosis. The disease often destroys physical and cognitive function of individuals.

Intention tremors can be a first sign of multiple sclerosis, since loss or deterioration of motor function and sensitivity are often one of the first symptoms of cerebellar lesions.

Intention tremors have a variety of other recorded causes as well. These include a variety of neurological disorders, such as stroke, alcoholism, alcohol withdrawal, peripheral neuropathy, Wilson's disease, Creutzfeldt–Jakob disease, Guillain–Barré syndrome and fragile X syndrome, as well as brain tumors, low blood sugar, hyperthyroidism, hypoparathyroidism, insulinoma, normal aging, and traumatic brain injury. Holmes tremor, a rubral or midbrain tremor, is another form of tremor that includes intention tremors, among other symptoms. This disease affects the proximal muscles of the head, shoulders, and neck. Tremors of this disease occur at frequencies of 2–4 Hz or more.

Intention tremor is also known to be associated with infections, West Nile virus, rubella, H. influenza, rabies, and varicella. A variety of poisons have been shown to cause intention tremor, including mercury, methyl bromide, and phosphine. In addition, vitamin deficiencies have been linked to intention tremor, especially deficiency in vitamin E. Pharmacological agents such as anti-arrhythmic drugs, anti-epileptic agents, benzodiazepine, cyclosporine, lithium, neuroleptics, and stimulants have been known to cause intention tremor. Some ordinary activities including ingesting too much caffeine, cigarettes, and alcohol, along with stress, anxiety, fear, anger and fatigue

have also been shown to cause intention tremor by negatively affecting the cerebellum, brainstem, or thalamus, as discussed in mechanisms.

Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). The symptoms include tremors and writhing movements of the body and limbs, and abnormal movements in the face, mouth, and tongue including involuntary lip smacking, repetitive pouting of the lips, and tongue protrusions.

Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1.

Myoclonus dystonia includes the rapid contractions of myoclonus alongside the abnormal postures classified under dystonia, as well as neurological and psychiatric issues. This disease typically begins during childhood with symptoms of myoclonus and slight dystonia, most commonly cervical dystonia or writer’s cramp. Dystonia symptoms tend to not get exaggerated over the course of the disease and is rarely the only associated symptom, while the myoclonus symptoms can become more severe. Psychiatric issues are clinically diagnosed with the aforementioned symptoms and include depression, anxiety, personality disorders and addiction. Obsessive-compulsive disorder is associated with myoclonus dystonia as both have been found to have a commonality on chromosome 7 in various studies.

Neurological symptoms are relatively common in those with myoclonus dystonia. Any neurological abnormalities won’t normally be present in those affected at a young age. Neurological testing has been performed to determine the origins of these symptoms and multiple parts of the brain have been pinpointed including the brainstem, neocortex, pallidum, and thalamus. These cause various effects in those diagnosed with myoclonus dystonia including changes in posture and tremors, and very rarely dementia and ataxia.

"Ballism" was defined by Meyers in 1968 as "Repetitive, but constantly varying, large amplitude involuntary movements of the proximal parts of the limbs. This activity is almost ceaseless and movements are often complex and combined". Hemiballismus is usually characterized by involuntary flinging motions of the extremities. The movements are often violent and have wide amplitudes of motion. They are continuous and random and can involve proximal or distal muscles on one side of the body. Some cases even include the facial muscles. It is common for arms and legs to move together. The more a patient is active, the more the movements increase. With relaxation comes a decrease in movements. Physicians can measure the severity of the disorder by having the patient perform a series of basic, predetermined tasks and counting the hemiballistic movements during a set time session. The physicians then rate the patient on a severity scale. This scale gives scientists and clinicians a way to compare patients and determine the range of the disorder.

The name "hemiballismus" literally means "half ballistic", referring to the violent, flailing movements observed on one side of the body.

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- "hyperkinetic" and "hypokinetic".

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

Dystonia is a response to simultaneous contraction of agonist and antagonist muscles seen as twisting and contorting that affect posture and stance. Other symptoms can include tremors and muscle spasms due to various interactions of muscle, contractions and movement. Dystonia can be either primary or secondary with the latter being more common. Primary dystonia or “pure” dystonia is only physiological in origin. Secondary dystonia has multiple origins that are physiological, pathological or neurological.

Tourette syndrome is a disorder that is characterized by behavioral and motor tics, OCD, and Attention-deficit hyperactivity disorder (ADHD). For this reason, it is commonly believed that pathologies involving limbic, associative, and motor circuits of the basal ganglia are likely. Since the realization that syndromes such as Tourette Syndrome and OCD are caused by dysfunction of the non-motor loops of basal ganglia circuits, new treatments for these disorders, based on treatments originally designed to treat movement disorders are being developed.

Sydenham's chorea is a disorder characterized by rapid, uncoordinated jerking movements primarily affecting the face, hands and feet. It is a result of an autoimmune response that occurs following infection by group A β-hemolytic streptococci that destroys cells in the corpus striatum of the basal ganglia.

Risk factors for Holmes tremor include excess exposure to heavy metals, such as mercury and lead, as well as an increased intake of various drugs and toxins. Researchers found that raising the dose of antidepressants or neuroleptics elevate the risk for developing Holmes tremor. Increasing intake of coffee, tea, or other stimulants can also cause for greater risk of development. Tremors depend on dosage and amount of exposure to these factors and will typically decrease dramatically if the intake is reduced. Hyperthyroidism and hyperglycemia also increase the likelihood of developing Holmes tremor.

Segmental dystonias affect two adjoining parts of the body:

- Hemidystonia affects an arm and foot on one side of the body.

- Multifocal dystonia affects many different parts of the body.

- Generalized dystonia affects most of the body, frequently involving the legs and back.

Though it is often most associated with Parkinson's disease, hypokinesia can be present in a wide variety of other conditions.

The disease typically starts in one limb, typically one leg. Progressive dystonia results in clubfoot and tiptoe walking. The symptoms can spread to all four limbs around age 18, after which progression slows and eventually symptoms reach a plateau. There can be regression in developmental milestones (both motor and mental skills) and failure to thrive in the absence of treatment.

In addition, SS is typically characterized by signs of parkinsonism that may be relatively subtle. Such signs may include slowness of movement (bradykinesia), tremors, stiffness and resistance to movement (rigidity), balance difficulties, and postural instability. Approximately 25 percent also have abnormally exaggerated reflex responses (hyperreflexia), particularly in the legs. These symptoms can result in a presentation that is similar in appearance to that of Parkinson's Disease.

Many patients experience improvement with sleep, are relatively free of symptoms in the morning, and develop increasingly severe symptoms as the day progresses (i.e., diurnal fluctuation). Accordingly, this disorder has sometimes been referred to as "progressive hereditary dystonia with diurnal fluctuations." Yet some SS patients do not experience such diurnal fluctuations, causing many researchers to prefer other disease terms.

- Other symptoms - footwear

- excessive wear at toes, but little wear on heels, thus replacement of shoes every college term/semester.

- Other symptoms - handwriting

- near normal handwriting at infants/kindergarten (ages 3–5 school) years.

- poor handwriting at pre-teens (ages 8–11 school) years.

- very poor (worse) handwriting during teen (qv GCSE/A level-public exams) years.

- bad handwriting (worsening) during post-teen (qv university exams) years.

- very bad handwriting (still worsening) during adult (qv post-graduate exams) years.

- worsening pattern of sloppy handwriting best observed by school teachers via termly reports.

- child sufferer displays unhappy childhood facial expressions (depression.?)

Intention tremor, also known as cerebellar tremor, is a dyskinetic disorder characterized by a broad, coarse, and low frequency (below 5 Hz) tremor. The amplitude of an intention tremor increases as an extremity approaches the endpoint of deliberate and visually guided movement (hence the name intention tremor). An intention tremor is usually perpendicular to the direction of movement. When experiencing an intention tremor, one often overshoots or undershoots their target, a condition known as dysmetria. Intention tremor is the result of dysfunction of the cerebellum, particularly on the same side as the tremor in the lateral zone, which controls visually guided movements. Depending on the location of cerebellar damage, these tremors can be either unilateral or bilateral.

A variety of causes have been discovered to date, including damage or degradation of the cerebellum due to neurodegenerative diseases, trauma, tumor, stroke, or toxicity. There is currently no established pharmacological treatment; however, some success has been seen using treatments designed for essential tremors.

The 'core' neuroacanthocytosis syndromes are chorea acanthocytosis and McLeod syndrome. Acanthocytes are nearly always present in these conditions and they share common clinical features. Some of these features are also seen in the other neurological syndromes associated with neuroacanthocytosis.

A common feature of the core syndromes is chorea: involuntary dance-like movements. In neuroacanthocytosis, this is particularly prominent in the face and mouth which can cause difficulties with speech and eating. These movements are usually abrupt and irregular and present during both rest and sleep.

Individuals with neuroacanthocytosis also often suffer from parkinsonism, the uncontrolled slowness of movements, and dystonia, abnormal body postures. Many affected individuals also have cognitive (intellectual) impairment and psychiatric symptoms such as anxiety, paranoia, depression, obsessive behavior, and pronounced emotional instability. Seizures may also be a symptom of neuroacanthocytosis.

Onset differs between individual neuroacanthocytosis syndromes but is usually between ages 20 and 40. Affected individuals usually live for 10–20 years after onset.

Acute dystonia is a sustained muscle contraction that sometimes appears soon after administration of antipsychotic medications. Any muscle in the body may be affected, including the jaw, tongue, throat, arms, or legs. When the throat muscles are involved, this type of dystonia is called an acute laryngospasm and is a medical emergency because it can impair breathing. Older antipsychotics such as Haloperidol or Fluphenazine are more likely to cause acute dystonia than newer agents. Giving high doses of antipsychotics by injection also increases the risk of developing acute dystonia.

Methamphetamine, other amphetamines and dopaminergic stimulants including cocaine and pemoline can produce choreoathetoid dyskinesias; the prevalence, time-frame and prognosis are not well established. Amphetamines also cause a dramatic increase in choreoathetoid symptoms in patients with underlying chorea such as Sydenham’s, Huntington’s, and Lupus. Long-term use of amphetamines may increase the risk of Parkinson's disease (PD): in one retrospective study with over 40,000 participants it was concluded that amphetamine abusers generally had a 200% higher chance of developing PD versus those with no history of abuse; the risk was much higher in women, almost 400%. There remains some controversy as of 2017.

Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa () for prolonged periods of time. LID commonly first appears in the foot, on the most affected side of the body. There are three main types that can be classified on the basis of their course and clinical presentation following an oral dose of :

- Off-period dystonia – correlated to the akinesia that occurs before the full effect of sets in, when the plasma levels of are low. In general, it occurs as painful spasms in the foot. Patients respond to therapy.

- Diphasic dyskinesia – occurs when plasma L-DOPA levels are rising or falling. This form occurs primarily in the lower limbs (though they can happen elsewhere) and is usually dystonic (characterized by apparent rigidity within muscles or groups thereof) or (characterized by involuntary movement of muscles) and will not respond to dosage reductions.

- Peak-dose dyskinesia – the most common form of levodopa-induced dyskinesia; it correlates with the plateau plasma level. This type usually involves the upper limbs more (but could also affect the head, trunk and respiratory muscles), is choreic (of chorea), and less disabling. Patients will respond to reduction but may be accompanied by deterioration of parkinsonism. Peak-dose L-DOPA-induced dyskinesia has been suggested to be associated with cortical dysregulation of dopamine signaling.