Tardive dyskinesia
Tardive dyskinesia | |
---|---|
Other names | Linguofacial dyskinesia, tardive dystonia, tardive oral dyskinesia |
Diagnostic method | Based on symptoms after ruling out other potential causes[1] |
Differential diagnosis | Huntington's disease, cerebral palsy, Tourette syndrome, dystonia[2] |
Prevention | Using lowest possible dose of neuroleptic medication[3] |
Treatment | Stopping neuroleptic medication if possible, switching to clozapine[1] |
Medication | Valbenazine, tetrabenazine, botulinum toxin[1][4] |
Prognosis | Variable[1] |
Frequency | 20% (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.
Tardive dyskinesia occurs in some people as a result of long-term use of
Efforts to prevent the condition include either using the lowest possible dose or discontinuing use of
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]
- 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.[8]
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
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
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
Risk factors
An increased risk of tardive dyskinesia has been associated with smoking in some studies,
Diagnosis
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Prevention
Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a
Studies have tested the use of
Treatment
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]
References
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- ^ a b c d "Tardive Dyskinesia". Medscape Reference. WebMD. 9 February 2012. Archived from the original on 3 December 2013. Retrieved 25 November 2013.
- ^ a b National Institutes of Health, National Institute of Neurological Disorders and Stroke. (2011). Ninds tardive dyskinesia information page. Retrieved from website: "Tardive Dyskinesia Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Archived from the original on 2012-04-27. Retrieved 2012-05-01.
- ^ Nasrallah, H. (2003, Sept). Tardive dyskinesia. Retrieved from "NAMI | Tardive Dyskinesia". Archived from the original on 2012-04-21. Retrieved 2012-05-01.
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