Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include:

- Grimacing

- Tongue movements

- Lip smacking

- Lip puckering

- Pursing of the lips

- Excessive eye blinking

Rapid, involuntary movements of the limbs, torso, and fingers may also occur. In some cases, an individual's legs can be so affected that walking becomes difficult or impossible. These symptoms are the opposite of patients who are diagnosed with Parkinson's disease. Parkinson's patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving.

Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low.

Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder, and as a result patients are prescribed neuroleptic drugs, which increase the probability that the patient will develop a severe and disabling case, and shortening the typical survival period.

Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. Tardive dystonia is similar to standard dystonia but permanent. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body. In some extreme cases, afflicted individuals experience so much internal torture that they lose their ability to sit still. Tardive tourettism is a tic disorder featuring the same symptoms as Tourette syndrome. The two disorders are extremely close in nature and often can only be differentiated by the details of their respective onsets. Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

"AIMS Examination": This test is used when psychotropic medications have been prescribed because patients sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). The test is not meant to tell whether there is an absence or presence of tardive dyskinesia. It just scales to level of symptoms indicated by the actions observed. The levels range from none to severe. The AIMS examination was constructed in the 1970s to measure involuntary facial, trunk, and limb movements. It is best to do this test before and after the administration of the psychotropic drugs. Taking the AIMS consistently can help to track severity of TD over time.

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.

Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements. This may include grimacing, sticking out the tongue or smacking of the lips. Additionally there may be rapid jerking movements or slow writhing movements. In about 20% of people, decreased functioning results.

Tardive dyskinesia occurs in some people as a result of long-term use of neuroleptic medications (antipsychotics, metoclopramide). These medications are usually used for mental illness, but may also be given for gastrointestinal or neurological problems. The condition typically only develops after months to years of use. The diagnosis is based on the symptoms after ruling out other potential causes.

Efforts to prevent the condition include not using or using the lowest possible dose of neuroleptics. Treatment include stopping the neuroleptic medication if possible or switching to clozapine. Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms. With treatment some see a resolution of symptoms while others do not.

Rates in those on atypical antipsychotics are about 20% while those on typical antipsychotics have rates of about 30%. Risk is greater in older people. The term "tardive dyskinesia" first came into use in 1964.

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.

This is characterized by attacks of involuntary movements (dystonia, chorea, or ballism), which are typically triggered by sudden voluntary movements, but can also be triggered by involuntary movements as well (for example, hyperventilating). These voluntary movements usually involve whole body activity such as standing, walking, and running. The age of onset is typically in childhood or early adolescence with most cases reporting improvement or complete remission with aging. Attacks last from seconds to minutes and are known to be at higher risk of occurring during stress, fear, cold, heat, or menstruation.

The paroxysmal dyskinesias are mainly classified by their triggers and on the basis of the duration and frequency of the attacks. The three main types are paroxysmal kinesigenic dyskinesia (PKD), paroxysmal non-kinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced (exertion-induced) dyskinesia (PED).

Adiadochokinesia is a dyskinesia consisting of inability to perform the rapid alternating movements of diadochokinesia. Called also "adiadochocinesia", "adiadochokinesis", and "adiadokokinesia".

Compare with dysdiadochokinesia, which is an impairment of the ability to perform rapidly alternating movements.

Paroxysmal kinesigenic choreathetosis (PKC) also called paroxysmal kinesigenic dyskinesia (PKD) is a hyperkinetic movement disorder characterized by attacks of involuntary movements, which are triggered by sudden voluntary movements. The number of attacks can increase during puberty and decrease in a person's 20s to 30s. Involuntary movements can take many forms such as ballism, chorea or dystonia and usually only affect one side of the body or one limb in particular. This rare disorder only affects about 1 in 150,000 people with PKD accounting for 86.8% of all the types of paroxysmal dyskinesias and occurs more often in males than females. There are two types of PKD, primary and secondary. Primary PKD can be further broken down into familial and sporadic. Familial PKD, which means the individual has a family history of the disorder, is more common, but sporadic cases are also seen. Secondary PKD can be caused by many other medical conditions such as multiple sclerosis (MS), stroke, pseudohypoparathyroidism, hypocalcemia, hypoglycemia, hyperglycemia, central nervous system trauma, or peripheral nervous system trauma. PKD has also been linked with infantile convulsions and choreoathetosis (ICCA) syndrome, in which patients have afebrile seizures during infancy (benign familial infantile epilepsy) and then develop paroxysmal choreoathetosis later in life. This phenomenon is actually quite common, with about 42% of individuals with PKD reporting a history of afebrile seizures as a child.

Oromandibular Symptoms

- difficulty opening the mouth (trismus)

- clenching or grinding of the teeth (bruxism)

- spasms of jaw opening

- sideways deviation or protrusion of the jaw

- lip tightening and pursing

- drawing back (retraction) of the corners of the mouth

- deviation or protrusion of the tongue.

- jaw pain

- difficulties eating and drinking

- difficulties speaking (dysarthria)

Blepharospasm symptoms

- the first symptom to appear is an increased rate of blinking

- uncontrollable squinting/closing of eyes

- light sensitivity (photophobia)

- squinting/eyes closing during speech

- uncontrollable eyes closing shut (rare instances completely causing blindness)

In addition, in some patients, the dystonic spasms may sometimes be provoked by certain activities, such as talking, chewing, or biting. Particular activities or sensory tricks may sometimes temporarily alleviate OMD symptoms, including chewing gum, talking, placing a toothpick in the mouth, lightly touching the lips or chin, or applying pressure beneath the chin.

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.

The Greek word "blepharon" means "eyelid". Spasm means "uncontrolled muscle contraction". The term blepharospasm ['blef-a-ro-spaz-m] can be applied to any abnormal blinking or eyelid tic or twitch resulting from any cause, ranging from dry eyes to Tourette's syndrome to tardive dyskinesia. The blepharospasm referred to here is officially called benign essential blepharospasm (BEB) to distinguish it from the less serious secondary blinking disorders. "Benign" indicates the condition is not life-threatening, and "essential" is a medical term meaning "of unknown cause". It is both a cranial and a focal dystonia. Cranial refers to the head and focal indicates confinement to one part. The word dystonia describes abnormal involuntary sustained muscle contractions and spasms. Patients with blepharospasm have normal eyes. The visual disturbance is due solely to the forced closure of the eyelids.

Oromandibular dystonia (OMD) is a form of focal dystonia that affects varying areas of the head and neck including the lower face, jaw, tongue and larynx. The spasms may cause the mouth to pull open, shut tight, or move repetitively. Speech and swallowing may be distorted. It is often associated with dystonia of the cervical muscles (Spasmodic Torticollis), eyelids (Blepharospasm), or larynx (Spasmodic Dysphonia).

In patients with OMD, involuntary contractions may involve the muscles used for chewing (masticatory muscles). These may include the thick muscle in the cheek that closes the jaw (masseter muscle) and the broad muscle that draws back the lower jaw and closes the mouth (temporalis muscle). Some patients may also experience involuntary contractions of the wide muscle at the side of the neck (platysmal muscle). This muscle draws down the corner of the mouth and lower lip or other muscle groups.

Choreoathetosis is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing).

It is caused by many different diseases and agents. It is a symptom of several diseases, including Lesch-Nyhan Syndrome, phenylketonuria, and Huntington disease.

Choreoathetosis is also a common presentation of dyskinesia as a side effect of levodopa-carbidopa in the treatment of Parkinson disease.

Initial symptoms include restlessness, agitation, malaise, or a fixed stare. Then comes the more characteristically described extreme and sustained upward deviation of the eyes. In addition, the eyes may converge, deviate upward and laterally, or deviate downward. The most frequently reported associated findings are backwards and lateral flexion of the neck, widely opened mouth, tongue protrusion, and ocular pain. However it may also be associated with intensely painful jaw spasm which may result in the breaking of a tooth. A wave of exhaustion may follow an episode. The abrupt termination of the psychiatric symptoms at the conclusion of the crisis is most striking.

Other features that are noted during attacks include mutism, palilalia, eye blinking, lacrimation, pupil dilation, drooling, respiratory dyskinesia, increased blood pressure and heart rate, facial flushing, headache, vertigo, anxiety, agitation, compulsive thinking, paranoia, depression, recurrent fixed ideas, depersonalization, violence, and obscene language.

It is often not realized that in addition to the acute presentation, oculogyric crisis can develop as a recurrent syndrome, triggered by stress, and exposure to the above drugs.

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.

Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting.

Other causes can include postencephalitic Parkinson's, Tourette's syndrome, multiple sclerosis, neurosyphilis, head trauma, bilateral thalamic infarction, lesions of the fourth ventricle, cystic glioma of the third ventricle, herpes encephalitis, kernicterus and juvenile Parkinson's.

The bilateral form of FCMS ("also known as facio-labio-pharyngo-glosso-laryngo-brachial paralysis)" is consistent with the classic presentation of bilateral corticobulbar involvement. It is characterized by well-preserved automatic and reflex movements. It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula forming the gyri of the frontal, temporal, and parietal lobes.

The unilateral operculum syndrome is a very rare form of FCMS caused by the formation of unilateral lesions. In this form of FCMS, the unaffected hemisphere of the brain compensates for the unilateral lesion. Usually, this occurs when the unaffected region is the individual's dominant hemisphere.

Sydenham's chorea is characterized by the abrupt onset (sometimes within a few hours) of neurologic symptoms, classically chorea, usually affecting all four limbs. Other neurologic symptoms include behavior change, dysarthria, gait disturbance, loss of fine and gross motor control with resultant deterioration of handwriting, headache, slowed cognition, facial grimacing, fidgetiness and hypotonia. Also, there may be tongue fasciculations ("bag of worms") and a "milk sign", which is a relapsing grip demonstrated by alternate increases and decreases in tension, as if hand milking.

Non-neurologic manifestations of acute rheumatic fever are carditis, arthritis, erythema marginatum, and subcutaneous nodules.

The PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) syndrome is similar, but is not characterized by Sydenham's motor dysfunction. PANDAS presents with tics and/or a psychological component (e.g., OCD) and occurs much earlier, days to weeks after GABHS infection rather than 6–9 months later. It may be confused with other conditions such as lupus and Tourette syndrome.

Movements cease during sleep, and the disease usually resolves after several months. Unlike in Huntington's disease, which is generally of adult onset and associated with an unremitting autosomal dominant movement disorder and dementia, neuroimaging in Sydenham's chorea is normal and other family members are unaffected. Other disorders that may be accompanied by chorea include abetalipoproteinemia, ataxia-telangiectasia, biotin-thiamine-responsive basal ganglia disease, Fahr disease, familial dyskinesia-facial myokymia (Bird-Raskind syndrome) due to an ADCY5 gene mutation, glutaric aciduria, Lesch-Nyhan syndrome, mitochondrial disorders, Wilson disease, hyperthyroidism, lupus erythematosus, pregnancy (chorea gravidarum), and side effects of certain anticonvulsants or psychotropic agents.

Although it may be asymptomatic, symptoms usually are more likely to be present and more severe with larger tongue enlargements. Signs and symptoms include:

- Dyspnea - difficult, noisy breathing, obstructive sleep apnea or airway obstruction

- Dysphagia - difficulty swallowing and eating

- Dysphonia - disrupted speech, possibly manifest as lisping

- Sialorrhea - drooling

- Angular cheilitis - sores at the corners of the mouth

- Crenated tongue - indentations on the lateral borders of the tongue caused by pressure from teeth ("pie crust tongue")

- Open bite malocclusion - a type of malocclusion of the teeth

- Mandibular prognathism - enlarged mandible

- Mouth breathing

- Orthodontic abnormalities - including diastema and tooth spacing

A tongue that constantly protrudes from the mouth is vulnerable to drying out, ulceration, infection or even necrosis.

The ICD-10 lists macroglossia under "other congenital malformations of the digestive system". Definitions of macroglossia have been proposed, including "a tongue that protrudes beyond the teeth during [the] resting posture" and "if there is an impression of a tooth on the lingual border when the patients slightly open their mouths". Others have suggested there is no objective definition of what constitutes macroglossia. Some propose a distinction between "true macroglossia", when histologic abnormalities correlate with the clinical findings of tongue enlargement, and "relative macroglossia", where histology does not provide a pathologic explanation for the enlargement. Common examples of true macroglossia are vascular malformations, muscular enlargement and tumors; whilst Down syndrome is an example of relative macroglossia. "Pseudomacryglossia" refers to a tongue that is of normal size but gives a false impression of being too large in relation to adjacent anatomical structures. The Myer classification subdivides macroglossia into generalized or localized.

The health care provider will perform a physical exam. Detailed questions will be asked about the symptoms.

If a streptococcus infection is suspected, tests will be done to confirm the infection. These include:

- Throat swab

- Anti-DNAse B blood test

- Antistreptolysin O (ASO) blood test

Further testing may include:

- Blood tests such as ESR, CBC

- MRI or CT scan of the brain

Most of the signs and symptoms of the Joubert syndrome appear very early in infancy with most children showing delays in gross motor milestones. Although other signs and symptoms vary widely from individual to individual, they generally fall under the hallmark of cerebellum involvement or in this case, lack thereof. Consequently, the most common features include ataxia (lack of muscle control), hyperpnea (abnormal breathing patterns), sleep apnea, abnormal eye and tongue movements, and hypotonia in early childhood. Other malformations such as polydactyly (extra fingers and toes), cleft lip or palate, tongue abnormalities, and seizures may also occur. Developmental delays, including cognitive, are always present to some degree.

Those suffering from this syndrome often exhibit specific facial features such as a broad forehead, arched eyebrows, ptosis (droopy eyelids), hypertelorism (widely spaced eyes), low-set ears and a triangle shaped mouth. Additionally, this disease can include a broad range of other abnormalities to other organ systems such as retinal dystrophy, kidney diseases, liver diseases, skeletal deformities and endocrine (hormonal) problems.

Joubert syndrome is a rare autosomal recessive genetic disorder that affects the cerebellum, an area of the brain that controls balance and coordination.

Joubert syndrome is one of the many genetic syndromes associated with syndromic retinitis pigmentosa. The syndrome was first identified in 1969 by pediatric neurologist Marie Joubert in Montreal, Quebec, Canada, while working at the Montreal Neurological Institute and McGill University.

Ankyloglossia can affect eating, speech, and oral hygiene as well as have mechanical/social effects. Ankyloglossia can also prevent the tongue from contacting the anterior palate. This can then promote an infantile swallow and hamper the progression to an adult-like swallow which can result in an open bite deformity. It can also result in mandibular prognathism; this happens when the tongue contacts the anterior portion of the mandible with exaggerated anterior thrusts.

Ankyloglossia, also known as tongue-tie, is a congenital oral anomaly that may decrease mobility of the tongue tip and is caused by an unusually short, thick lingual frenulum, a membrane connecting the underside of the tongue to the floor of the mouth. Ankyloglossia varies in degree of severity from mild cases characterized by mucous membrane bands to complete ankyloglossia whereby the tongue is tethered to the floor of the mouth.