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.

Some of the most prevalent symptom types in people exhibiting CBD pertain to identifiable movement disorders and problems with cortical processing. These symptoms are initial indicators of the presence of the disease. Each of the associated movement complications typically appear asymmetrically and the symptoms are not observed uniformly throughout the body. For example, a person exhibiting an alien hand syndrome (explained later) in one hand, will not correspondingly display the same symptom in the contralateral limb. Predominant movement disorders and cortical dysfunctions associated with CBD include:

- Parkinsonism

- Alien hand syndrome

- Apraxia (ideomotor apraxia and limb-kinetic apraxia)

- Aphasia

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.

Alien hand syndrome has been shown to be prevalent in roughly 60% of those people diagnosed with CBD. This disorder involves the failure of an individual to control the movements of his or her hand, which results from the sensation that the limb is “foreign.” The movements of the alien limb are a reaction to external stimuli and do not occur sporadically or without stimulation. The presence of an alien limb has a distinct appearance in CBD, in which the diagnosed individual may have a “tactile mitgehen.” This mitgehen (German, meaning “to go with”) is relatively specific to CBD, and involves the active following of an experimenter’s hand by the subject’s hand when both hands are in direct contact. Another, rarer form of alien hand syndrome has been noted in CBD, in which an individual’s hand displays an avoidance response to external stimuli. Additionally, sensory impairment, revealed through limb numbness or the sensation of prickling, may also concurrently arise with alien hand syndrome, as both symptoms are indicative of cortical dysfunction. Like most of the movement disorders, alien hand syndrome also presents asymmetrically in those diagnosed with CBD.

A tic can be defined as a repeated, individually recognizable, intermittent movement or movement fragments that are almost always briefly suppressible and are usually associated with awareness of an urge to perform the movement. These abnormal movements occur with intervening periods of normal movement. These movements are predictable, often triggered by stress, excitement, suggestion, or brief voluntary suppressibility. Many children say that the onset of tics can stem from the strong urge to move. Tics can be either muscular (alter normal motor function) or vocal (alter normal speech) in nature and most commonly involve the face, mouth, eyes, head, neck or shoulder muscles. Tics can also be classified as simple motor tics (a single brief stereotyped movement or movement fragment), complex motor tics (a more complex or sequential movement involving multiple muscle

groups), or phonic tics (including simple, brief phonations or vocalizations).

When both motor and vocal tics are present and persist for more than one year, a diagnosis of Tourette syndrome (TS) is likely. TS is an inherited neurobehavioral disorder characterized by both motor and vocal tics. Many individuals with TS may also develop obsessions, compulsions, inattention and hyperactivity. TS usually begins in childhood. Up to 5% of the population suffers from tics, but at least 20% of boys will have developed tics at some point in their lifetimes.

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.

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.

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

"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.

Tremor is the uncontrollable shaking of an arm or a leg. Twitches or jerks of body parts may occur due to a startling sound or unexpected, sudden pain. Spasms and contractions are temporary abnormal resting positions of hands or feet. Spasms are temporary while contractions could be permanent. Gait problems are problems with the way one walks or runs. This can mean an unsteady pace or dragging of the feet along with other possible irregularities (Stone).

Parkinsonian gait (or festinating gait, from Latin "festinare" [to hurry]) is the type of gait exhibited by patients suffering from Parkinson's disease (PD). This disorder is caused by a deficiency of dopamine in the basal ganglia circuit leading to motor deficits. Gait is one of the most affected motor characteristics of this disorder although symptoms of Parkinson's disease are varied.

Parkinsonian gait is characterized by small shuffling steps and a general slowness of movement (hypokinesia), or even the total loss of movement (akinesia) in the extreme cases. Patients with PD demonstrate reduced stride length and walking speed during free ambulation while double support duration and cadence rate are increased. The patient has difficulty starting, but also has difficulty stopping after starting. This is due to muscle hypertonicity.

Patients with Parkinson's disease exhibit gait characteristics that are markedly different from normal gait. While the list of abnormal gait characteristics given below is the most discussed, it is certainly not exhaustive.

Hypokinesia refers to decreased bodily movement. One of the two categories of movement disorders, hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Patients with hypokinetic disorders like Parkinson's disease experience muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.

The other category of movement disorder resulting from damage to the basal ganglia, hyperkinesia, features an exaggeration of unwanted motion, like twitching or writhing in Huntington's disease or Tourette syndrome.

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.

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.

The symptoms for PKD are varied from case to case, however, typically they consist of involuntary movements. Such contractile movements include dystonia, chorea, athetosis, and ballism. For example, “Her attacks were characterized as sudden unilateral stiffness of upper and lower limbs followed by an involuntary extrarotation of the arm and leg.” Another frequently occurring symptom is the presence of an aura before the attack. These sensations manifest in several forms, usually described as a tingling in the target limb.

A single limb is the most frequently affected area; however it is possible for an attack to affect more than one limb. When more than one limb is affected, the two limbs are usually unilateral (same side), even though cases of bilateral (opposite sides) symptoms have also been observed. Another frequently affected area is the torso, with some PKD patients twisting their body.

Attacks experienced by PKD patients typically last less than a minute, however longer attack can occur. To further distinguish between PKD and epilepsy, patients typically retain consciousness during their attacks, and are able to recall the attacks even after they have ended. Despite retaining consciousness, patients are usually incapable of speech during the attack and may experience great pain in the affected area. The frequency of attacks vary greatly. Some patients have been noted as having hundreds of attacks per day, while others go months without an attack.

The attacks consist of dystonia, chorea, and athetosis just like PKD. They are mostly of the limbs, and are usually unilateral or asymmetric. What sets PNKD apart from PKD is that the attacks can last anywhere from four minutes to four hours, but shorter and longer attacks have been reported as well.

The attacks also affect the limbs, usually unilaterally, but bilateral symptoms have also been experienced. PNKD patients usually report the presence of an aura before an attack as well; however they are usually different from those of PKD patients. Once again the aura varies, but is typically felt in the target limb. Another frequently noted aura is dizziness

PNKD patients experience attacks that last much longer than those of PKD. These attacks vary in length and can last anywhere between four minutes and four hours. Similar to the difference between length of attacks, the intervals between attacks are much longer. The Interval between PNKD patients’ attacks is from one day to several months.

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.

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.

Ballismus or ballism (called hemiballismus or hemiballism in its unilateral form) is a very rare movement disorder. It is a type of chorea caused in most cases by a decrease in activity of the subthalamic nucleus of the basal ganglia, resulting in the appearance of flailing, ballistic, undesired movements of the limbs. It can also appear rarely due to certain metabolic abnormalities. It is a rare movement disorder, being 500 times rarer than Parkinson's disease. Hemiballismus can cause significant disability. Symptoms can decrease during sleep.

Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.

In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.

Athetosis can vary from mild to severe motor dysfunction; it is generally characterized by unbalanced, involuntary movements of muscle and a difficulty maintaining a symmetrical posture. The associated motor dysfunction can be restricted to a part of body or present throughout the body, depending on the individual and the severity of the symptom. One of the pronounced signs can be observed in the extremities in particular, as the writhing, convoluted movement of the digits. Athetosis can appear as early as 18 months from birth with first signs including difficulty feeding, hypotonia, spasm, and involuntary writhing movements of the hands, feet, and face, which progressively worsen through adolescence and at times of emotional distress. Athetosis is caused by lesions in several brain areas such as the hippocampus and the motor thalamus, as well as the corpus striatum; therefore children during the developmental age could possibly suffer from cognitive deficits such as speech impairment, hearing loss, and failed or delayed acquirement of sitting balance.

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.

Paroxysmal kinesigenic dyskinesia is diagnosed using a strict set of guidelines. These criteria were studied and confirmed by Bruno et al. in a study of 121 individuals with PKD. The age at onset is between 1 and 20 years old. The attacks of involuntary movements last less than one minute and have a known trigger, usually a sudden voluntary movement. For example, if a PKD patient stands up or begins walking after being sedentary for a period of time, or a person goes from a walk to a run, it can trigger an attack. Persons with PKD do not lose consciousness during attacks and have a full memory of the entire attack. Lastly, people with the disorder have a good response to medication and are usually prescribed anticonvulsants. The study also found that patients with familial PKD exhibit symptoms that follow the diagnostic criteria closely, while sporadic PKD individuals may deviate slightly. Prior to criteria for diagnosis being set out, many patients with PKD were often diagnosed with some form of epilepsy. Many patients also experience an aura, similar to those experienced with epilepsy, preceding their attacks. Some patients describe it as a tingling sensation in the affected limb or “butterflies in their stomach.” Some individuals also have precipitants, such as stress and anxiety, that make it more likely for attacks to occur.

The above diagnostic criteria also set PKD apart from the other paroxysmal dyskinesias, which include paroxysmal nonkinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced dyskinesia (PED). While PKD attacks last less than one minute, PNKD attacks last a few minutes to a few hours, and as the name suggests, the attacks do not occur because of a sudden voluntary movement like PKD. Additionally, PKD can almost always be managed with drug therapy, while PNKD is not as responsive to anticonvulsants. PED, on the other hand, separates itself from PKD in that it is caused by prolonged exercise. Attacks from PED will cease soon after exercise is stopped.

Symptoms include mental deterioration, language disorder, transient ischemic attack, muscle ataxia, and impaired movements including change of walk, slowness of movements, and change in posture. These symptoms usually coincide with multiple falls, epilepsy, fainting, and uncontrollable bladder.

Because Binswanger’s disease affects flow processing speed and causes impaired concentration, the ability to do everyday tasks such as managing finances, preparing a meal and driving may become very difficult.