Tardive dyskinesia

Last updated
Tardive dyskinesia
Other namesLinguofacial dyskinesia, tardive dystonia, tardive oral dyskinesia [1]
Dopamine-3d-CPK.png
Tardive dyskinesia is believed to involve the neurotransmitter dopamine.
Pronunciation
Specialty Neurology, psychiatry
Symptoms Involuntary, repetitive body movements [1]
Causes Neuroleptic medications (antipsychotics), metoclopramide [1] [2]
Diagnostic method Based on symptoms after ruling out other potential causes [1]
Differential diagnosis Huntington's disease, cerebral palsy, Tourette syndrome, dystonia [2]
PreventionUsing lowest possible dose of neuroleptic medication [3]
TreatmentStopping neuroleptic medication if possible, switching to clozapine [1]
Medication Valbenazine, tetrabenazine, botulinum toxin [1] [4]
Prognosis Variable [1]
Frequency20% (atypical antipsychotics)
30% (typical antipsychotics) [5]

Tardive dyskinesia (TD) is a disorder that results in involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips. [1] Additionally, there may be chorea or slow writhing movements. [1] In about 20% of people with TD, the disorder interferes with daily functioning. [3] If TD is present in the setting of a long-term drug therapy, reversibility can be determined primarily by severity of symptoms and how long symptoms have been present before the long-term drug has been stopped.

Contents

Tardive dyskinesia occurs in some people as a result of long-term use of dopamine-receptor-blocking medications such as antipsychotics and metoclopramide. [1] [2] These medications are usually used for mental illness but may also be given for gastrointestinal or neurological problems. [1] The condition typically develops only after months to years of use. [1] [3] The diagnosis is based on the symptoms after ruling out other potential causes. [1]

Efforts to prevent the condition include either using the lowest possible dose or discontinuing use of neuroleptics. [3] Treatment includes stopping the neuroleptic medication if possible or switching to clozapine. [1] Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms. [1] [4] With treatment, some see a resolution of symptoms, while others do not. [1]

Rates in those on atypical antipsychotics are about 20%, while those on typical antipsychotics have rates of about 30%. [5] The risk of acquiring the condition is greater in older people, [3] for women, as well as patients with mood disorders and/or medical diagnoses receiving antipsychotic medications. [6] The term "tardive dyskinesia" first came into use in 1964. [3]

Signs and symptoms

Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include: [7]

In some cases, an individual's legs can be so affected that walking becomes difficult or impossible. [9] These symptoms are the opposite of people who are diagnosed with Parkinson's disease. People with Parkinson's have difficulty moving, whereas people with tardive dyskinesia have difficulty not moving. [10]

Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the rate of people affected is relatively low. [11]

Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder, [12] and as a result, people are prescribed neuroleptic drugs, which increase the probability that the person will develop a severe and disabling case, and shortening the typical survival period. [13]

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 tension 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. [10]

"AIMS Examination": This test is used when psychotropic medications have been prescribed because people 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 the 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. [14] [15]

Causes

Tardive dyskinesia was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs. [16] However, the exact mechanism of the disorder remains largely uncertain. The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia. [17] The D2 hypersensitivity hypothesis is also supported by evidence of a dose–response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research. [17]

Given similar doses of the same neuroleptic, differences among individuals still exist in the likelihood of developing tardive dyskinesia. Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, intellectual disability, alcohol and drug use, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics. [17] Antipsychotic drugs can sometimes camouflage the signs of tardive dyskinesia from occurring in the early stages; this can happen from the individual having an increased dose of an antipsychotic drug. Often the symptoms of tardive dyskinesia are not apparent until the individual comes off of the antipsychotic drugs; however, when tardive dyskinesia worsens, the signs become visible. [18]

Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine, used to treat gastrointestinal disorders. Atypical antipsychotics are considered lower-risk for causing TD than their typical counterparts, with incidence rates of 13.1% and 32.4% respectively in short-term trials primarily utilising Haloperidol as the typical antipsychotic. [19] Quetiapine and clozapine are considered the lowest risk agents for precipitating TD. [19] From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia. [20] As of 2013, reports of tardive dyskinesia in aripiprazole have grown in number. [21] The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the person more sensitive to tardive dyskinesia. Since 1973 the use of these drugs has been found to be associated with the development of tardive dyskinesia. [22] [23]

Risk factors

An increased risk of tardive dyskinesia has been associated with smoking in some studies, [24] [25] although a negative study does exist. [26] There seems to be a cigarette smoke-exposure-dependent risk for TD in people who are antipsychotic-treated . [27] Elderly people are also at a heightened risk for developing TD, [7] as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia. [19] TD is also more common in those that experience acute neurological side effects from antipsychotic drug treatment. [19] Racial discrepancies in TD rate also exist, with Africans and African Americans having higher rates of TD after exposure to antipsychotics. [7] Certain genetic risk factors for TD have been identified including polymorphisms in the genes encoding the D3, 5-HT2A and 5-HT2C receptors. [28]

Diagnosis

Prevention

Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. However, with diseases of chronic psychosis such as schizophrenia, this strategy must be balanced with the fact that increased dosages of neuroleptics are more beneficial in preventing recurrence of psychosis. If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal of the drug for months, years or even permanently. [29] [30] Some studies suggest that practitioners should consider using atypical antipsychotics as a substitute to typical antipsychotics for people requiring medication. These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia. [31]

Studies have tested the use of melatonin, high dosage vitamins, and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current rate of people for those taking antipsychotic drugs. [32] Tentative evidence supports the use of vitamin E for prevention. [33]

Treatment

Valbenazine was approved by the FDA for tardive dyskinesia in April 2017. [34] Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders (e.g. Huntington's chorea). [8] Deutetrabenazine, an isotopic isomer of tetrabenazine, was approved by the FDA for tardive dyskinesia in August 2017. [35] Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials, [36] [37] but the overall evidence for its effectiveness is considered "weak." [38] Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage. [39] Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia. [7] As of 2018 evidence is insufficient to support the use of benzodiazepines, baclofen, progabide, sodium valproate, gaboxadol, or calcium channel blockers (e.g. diltiazem). [40] [41] [42]

Epidemiology

Tardive dyskinesia most commonly occurs in people with psychiatric conditions who are treated with antipsychotic medications for many years. The average rate of people affected has been estimated to be around 30% for individuals taking antipsychotic medication, such as that used to treat schizophrenia. [43] A study being conducted at the Yale University School of Medicine has estimated that "32% of people develop persistent tics after 5 years on major tranquilizers, 57% by 15 years, and 68% by 25 years." [44] More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs. According to this research study, 26% of people developed tardive dyskinesia after just one year on the medication. Another 60% of this at-risk group developed the disorder after 3 years, and 23% developed severe cases of tardive dyskinesia within 3 years. [45] According to these estimates, the majority of people will eventually develop the disorder if they remain on the drugs long enough. [46]

Elderly people are more prone to develop tardive dyskinesia, and elderly women are more at-risk than elderly men. The risk is much lower for younger men and women, and also more equal across the sexes. [47] Several studies have recently been conducted comparing the number of people affected of tardive dyskinesia with second generation, or more modern, antipsychotic drugs to that of first generation drugs. The newer antipsychotics appear to have a substantially reduced potential for causing tardive dyskinesia. However, some studies express concern that the number of people affected has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics. [32] [48]

A practitioner can evaluate and diagnose a person with tardive dyskinesia by conducting a systematic examination. The practitioner should ask the person to relax, and look for symptoms like facial grimacing, eye or lip movements, tics, respiratory irregularities, and tongue movements. In some cases, people experience nutritional problems, so a practitioner can also look for a gain or loss in weight. [31]

Apart from the underlying psychiatric disorder, tardive dyskinesia may cause afflicted people to become socially isolated. It also increases the risk of body dysmorphic disorder (BDD) and can even lead to suicide. Emotional or physical stress can increase the severity of dyskinetic movements, whereas relaxation and sedation have the opposite effect. [49]

Related Research Articles

<span class="mw-page-title-main">Antipsychotic</span> Class of medications

Antipsychotics, previously known as neuroleptics and major tranquilizers, are a class of psychotropic medication primarily used to manage psychosis, principally in schizophrenia but also in a range of other psychotic disorders. They are also the mainstay, together with mood stabilizers, in the treatment of bipolar disorder. Moreover, they are also used as adjuncts in the treatment of treatment-resistant major depressive disorder.

<span class="mw-page-title-main">Neuroleptic malignant syndrome</span> Medical condition

Neuroleptic malignant syndrome (NMS) is a rare but life-threatening reaction that can occur in response to antipsychotic (neuroleptic) medications. Symptoms include high fever, confusion, rigid muscles, variable blood pressure, sweating, and fast heart rate. Complications may include rhabdomyolysis, high blood potassium, kidney failure, or seizures.

<span class="mw-page-title-main">Haloperidol</span> Typical antipsychotic medication

Haloperidol, sold under the brand name Haldol among others, is a typical antipsychotic medication. Haloperidol is used in the treatment of schizophrenia, tics in Tourette syndrome, mania in bipolar disorder, delirium, agitation, acute psychosis, and hallucinations from alcohol withdrawal. It may be used by mouth or injection into a muscle or a vein. Haloperidol typically works within 30 to 60 minutes. A long-acting formulation may be used as an injection every four weeks by people with schizophrenia or related illnesses, who either forget or refuse to take the medication by mouth.

<span class="mw-page-title-main">Typical antipsychotic</span> Class of drugs

Typical antipsychotics are a class of antipsychotic drugs first developed in the 1950s and used to treat psychosis. Typical antipsychotics may also be used for the treatment of acute mania, agitation, and other conditions. The first typical antipsychotics to come into medical use were the phenothiazines, namely chlorpromazine which was discovered serendipitously. Another prominent grouping of antipsychotics are the butyrophenones, an example of which is haloperidol. The newer, second-generation antipsychotics, also known as atypical antipsychotics, have largely supplanted the use of typical antipsychotics as first-line agents due to the higher risk of movement disorders in the latter.

<span class="mw-page-title-main">Atypical antipsychotic</span> Class of pharmaceutical drugs

The atypical antipsychotics (AAP), also known as second generation antipsychotics (SGAs) and serotonin–dopamine antagonists (SDAs), are a group of antipsychotic drugs largely introduced after the 1970s and used to treat psychiatric conditions. Some atypical antipsychotics have received regulatory approval for schizophrenia, bipolar disorder, irritability in autism, and as an adjunct in major depressive disorder.

<span class="mw-page-title-main">Quetiapine</span> Atypical antipsychotic medication

Quetiapine, sold under the brand name Seroquel among others, is an atypical antipsychotic medication used for the treatment of schizophrenia, bipolar disorder, and major depressive disorder. Despite being widely used as a sleep aid due to its sedating effect, the benefits of such use may not outweigh its undesirable side effects. It is taken orally.

<span class="mw-page-title-main">Olanzapine</span> Atypical antipsychotic medication

Olanzapine, sold under the brand name Zyprexa among others, is an atypical antipsychotic primarily used to treat schizophrenia and bipolar disorder. For schizophrenia, it can be used for both new-onset disease and long-term maintenance. It is taken by mouth or by injection into a muscle.

<span class="mw-page-title-main">Akathisia</span> Movement disorder involving a feeling of inner restlessness

Akathisia is a movement disorder characterized by a subjective feeling of inner restlessness accompanied by mental distress and an inability to sit still. Usually, the legs are most prominently affected. Those affected may fidget, rock back and forth, or pace, while some may just have an uneasy feeling in their body. The most severe cases may result in aggression, violence, and/or suicidal thoughts. Akathisia is also associated with threatening behaviour and physical aggression that is greatest in patients with mild akathisia, and diminishing with increasing severity of akathisia.

<span class="mw-page-title-main">Perphenazine</span> Antipsychotic medication

Perphenazine is a typical antipsychotic drug. Chemically, it is classified as a piperazinyl phenothiazine. Originally marketed in the United States as Trilafon, it has been in clinical use for decades.

Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements. Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower extremities. Discoordination can also occur internally especially with the respiratory muscles and it often goes unrecognized. Dyskinesia is a symptom of several medical disorders that are distinguished by their underlying cause.

<span class="mw-page-title-main">Dopamine antagonist</span> Drug which blocks dopamine receptors

A dopamine antagonist, also known as an anti-dopaminergic and a dopamine receptor antagonist (DRA), is a type of drug which blocks dopamine receptors by receptor antagonism. Most antipsychotics are dopamine antagonists, and as such they have found use in treating schizophrenia, bipolar disorder, and stimulant psychosis. Several other dopamine antagonists are antiemetics used in the treatment of nausea and vomiting.

<span class="mw-page-title-main">Progabide</span> Pharmaceutical drug

Progabide is an analogue and prodrug of γ-aminobutyric acid (GABA) used in the treatment of epilepsy. Via conversion into GABA, progabide behaves as an agonist of the GABAA, GABAB, and GABAA-ρ receptors.

<span class="mw-page-title-main">Amisulpride</span> Atypical antipsychotic and antiemetic medication

Amisulpride is an antiemetic and antipsychotic medication used at lower doses intravenously to prevent and treat postoperative nausea and vomiting; and at higher doses by mouth to treat schizophrenia and acute psychotic episodes. It is sold under the brand names Barhemsys and Solian, Socian, Deniban and others. At very low doses it is also used to treat dysthymia.

<span class="mw-page-title-main">Sulpiride</span> Atypical antipsychotic

Sulpiride, sold under the brand name Dogmatil among others, is an atypical antipsychotic medication of the benzamide class which is used mainly in the treatment of psychosis associated with schizophrenia and major depressive disorder, and sometimes used in low dosage to treat anxiety and mild depression. Sulpiride is commonly used in Asia, Central America, Europe, South Africa and South America. Levosulpiride is its purified levo-isomer and is sold in India for similar purpose. It is not approved in the United States, Canada, or Australia. The drug is chemically and clinically similar to amisulpride.

Extrapyramidal symptoms (EPS) are symptoms that are archetypically associated with the extrapyramidal system of the brain's cerebral cortex. When such symptoms are caused by medications or other drugs, they are also known as extrapyramidal side effects (EPSE). The symptoms can be acute (short-term) or chronic (long-term). They include movement dysfunction such as dystonia, akathisia, parkinsonism characteristic symptoms such as rigidity, bradykinesia, tremor, and tardive dyskinesia. Extrapyramidal symptoms are a reason why subjects drop out of clinical trials of antipsychotics; of the 213 (14.6%) subjects that dropped out of one of the largest clinical trials of antipsychotics, 58 (27.2%) of those discontinuations were due to EPS.

<span class="mw-page-title-main">Tiapride</span> Antipsychotic medication

Tiapride is a drug that selectively blocks D2 and D3 dopamine receptors in the brain. It is used to treat a variety of neurological and psychiatric disorders including dyskinesia, alcohol withdrawal syndrome, negative symptoms of psychosis, and agitation and aggression in the elderly. A derivative of benzamide, tiapride is chemically and functionally similar to other benzamide antipsychotics such as sulpiride and amisulpride known for their dopamine antagonist effects.

Tardive psychosis is a term for a hypothetical form of psychosis caused by long-term use of neuroleptics. It was first proposed in 1978 but was questioned by the late 1980s. It was hypothesized that psychosis could arise as neuroleptic medication become decreasingly effective, requiring higher doses, or when not responding to higher doses.

Pleurothotonus, commonly known as Pisa syndrome, is a rare neurological disorder which occurs due to prolonged exposure to antipsychotic drugs. It is characterized by dystonia, and abnormal and sustained involuntary muscle contraction. This may cause twisting or jerking movements of the body or a body part. Although Pisa syndrome develops most commonly in those undergoing long-term treatment with antipsychotics, it has been reported less frequently in patients receiving other medications, such as an acetylcholinesterase inhibitor. However, it has also been seen in those with other diseases causing neurodegeneration and in those who are not receiving any medication. The characteristic development of Pisa syndrome consists of two types of dystonia: acute dystonia and tardive dystonia. The underlying pathology of drug-induced Pisa syndrome is very complex, and development may be due to an underlying dopaminergic-cholinergic imbalance, or serotonergic/noradrenergic dysfunction.

Dopamine supersensitivity psychosis is a hypothesis that attempts to explain the phenomenon in which psychosis occurs despite treatment with escalating doses of antipsychotics. Dopamine supersensitivity may be caused by the dopamine receptor D2 antagonizing effect of antipsychotics, causing a compensatory increase in D2 receptors within the brain that sensitizes neurons to endogenous release of the neurotransmitter dopamine. Because psychosis is thought to be mediated—at least in part—by the activity of dopamine at D2 receptors, the activity of dopamine in the presence of supersensitivity may paradoxically give rise to worsening psychotic symptoms despite antipsychotic treatment at a given dose. This phenomenon may co-occur with tardive dyskinesia, a rare movement disorder that may also be due to dopamine supersensitivity.

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  37. ↑ Lerner, V; Miodownik, C; Kaptsan, A; Bersudsky, Y; Libov, I; Sela BA; Witztum, E (November 2007). "Vitamin B6 treatment for tardive dyskinesia: a randomized, double-blind, placebo-controlled, crossover study". Journal of Clinical Psychiatry. 68 (11): 1648–154. doi:10.4088/jcp.v68n1103. PMID   18052557.
  38. ↑ Adelufosi, Adegoke Oloruntoba; Abayomi, Olukayode; Ojo, Tunde Massey-Ferguson (13 April 2015). "Pyridoxal 5 phosphate for neuroleptic-induced tardive dyskinesia". Cochrane Database of Systematic Reviews (4): CD010501. doi:10.1002/14651858.CD010501.pub2. PMID   25866243.
  39. ↑ Aia, Pratibha G; Revuelta, Gonzalo J; Cloud, Leslie J; Factor, Stewart A (2011). "Tardive Dyskinesia". Current Treatment Options in Neurology. 13 (3): 231–241. doi:10.1007/s11940-011-0117-x. PMID   21365202. S2CID   24308129.
  40. ↑ Bergman, H; Bhoopathi, PS; Soares-Weiser, K (20 January 2018). "Benzodiazepines for antipsychotic-induced tardive dyskinesia". The Cochrane Database of Systematic Reviews. 1 (1): CD000205. doi:10.1002/14651858.CD000205.pub3. PMC   6491128 . PMID   29352477.
  41. ↑ Alabed, S; Latifeh, Y; Mohammad, HA; Bergman, H (17 April 2018). "Gamma-aminobutyric acid agonists for antipsychotic-induced tardive dyskinesia". The Cochrane Database of Systematic Reviews. 2018 (4): CD000203. doi:10.1002/14651858.CD000203.pub4. PMC   6513215 . PMID   29663328.
  42. ↑ Essali, Adib; Soares-Weiser, Karla; Bergman, Hanna; Adams, Clive E (26 March 2018). "Calcium channel blockers for antipsychotic-induced tardive dyskinesia". Cochrane Database of Systematic Reviews. 2018 (3): CD000206. doi:10.1002/14651858.CD000206.pub4. PMC   6494274 . PMID   29578611.
  43. ↑ Llorca, Pierre-Michel; Chereau, Isabelle; Bayle, Frank-Jean; et al. (2002). "Tardive dyskinesias and antipsychotics: A review". European Psychiatry. 17 (3): 129–138. doi:10.1016/S0924-9338(02)00647-8. PMID   12052573. S2CID   40761404.
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  45. ↑ Jeste, Dilip V.; Caligiuri, Michael P.; Paulsen, Jane S.; et al. (1995). "Risk of Tardive Dyskinesia in Older Patients: A Prospective Longitudinal Study of 266 Outpatients". Archives of General Psychiatry. 52 (9): 756–765. doi:10.1001/archpsyc.1995.03950210050010. PMID   7654127.
  46. ↑ Whitaker, Robert (2002). Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill . Perseus. ISBN   978-0738203850.[ page needed ]
  47. ↑ Marshall, DL; Hazlet, TK; Gardner, JS; et al. (2002). "Neuroleptic drug exposure and incidence of tardive dyskinesia: A records-based case-control study". Journal of Managed Care Pharmacy. 8 (4): 259–265. doi: 10.18553/jmcp.2002.8.4.259 . PMID   14613418.
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