Dyskinesia

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Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, [1] including movements similar to tics or chorea and diminished voluntary movements. [2] 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. [3] Dyskinesia is a symptom of several medical disorders that are distinguished by their underlying causes.

Contents

Types

Medication-induced dyskinesias

Acute dystonia is a sustained muscle contraction that sometimes appears soon after administration of antipsychotic medications. [4] 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. [4] 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. [4]

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. [5] 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%. [6] There remains some controversy as of 2017. [7] [ relevant? ]

Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa (L‑DOPA) 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 L‑DOPA: [8] [9]

Chronic or tardive

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. [11]

Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1. [12]

Non-motor

Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders.

Treatment

Antidyskinetic drugs can be used to treat dyskinesia. [13] [14] [15] Certain anticonvulsants can be used as antidyskinetic agents, among drugs acting at other targets. [13] [15] Amantadine is approved for treatment of levodopa-induced dyskinesia. [16] Dopamine depleting agents like tetrabenazine, deutetrabenazine, and valbenazine are used to treat tardive dyskinesia. [17]

See also

Related Research Articles

<span class="mw-page-title-main">Benzatropine</span> Medication for movement disorders

Benzatropine (INN), known as benztropine in the United States and Japan, is a medication used to treat movement disorders like parkinsonism and dystonia, as well as extrapyramidal side effects of antipsychotics, including akathisia. It is not useful for tardive dyskinesia. It is taken by mouth or by injection into a vein or muscle. Benefits are seen within two hours and last for up to ten hours.

<span class="mw-page-title-main">Tardive dyskinesia</span> Neurological disorder featuring involuntary, repetitive body movements

Tardive dyskinesia (TD) is an iatrogenic disorder that results in involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips, which occurs following treatment with medication. Additional motor symptoms include chorea or athetosis. In about 20% of people with TD, the disorder interferes with daily functioning. 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.

A stereotypy is a repetitive or ritualistic movement, posture, or utterance. Stereotypies may be simple movements such as body rocking, or complex, such as self-caressing, crossing and uncrossing of legs, and marching in place. They are found especially in people with autism spectrum disorders and visually impaired children, and are also found in intellectual disabilities, tardive dyskinesia and stereotypic movement disorder; however, they may also be encountered in neurotypical individuals as well. Studies have shown stereotypies to be associated with some types of schizophrenia. Frontotemporal dementia is also a common neurological cause of repetitive behaviors and stereotypies. A number of causes have been hypothesized for stereotypy, and several treatment options are available.

<span class="mw-page-title-main">Hyperkinesia</span> Excessive movements due to basal ganglia dysfunction

Hyperkinesia refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease.

<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">Dopaminergic</span> Substance related to dopamine functions

Dopaminergic means "related to dopamine", a common neurotransmitter. Dopaminergic substances or actions increase dopamine-related activity in the brain.

<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">Punding</span> Compulsive performance of repetitive, mechanical tasks

Punding is compulsive performance of repetitive, mechanical tasks, such as assembling and disassembling, collecting, or sorting objects. It can also apply to digital objects, such as computer files and data. The term was originally coined to describe complex, prolonged, purposeless, and stereotyped behaviour in phenmetrazine and chronic amphetamine users, by Swedish forensic psychiatrist G. Rylander, in 1968. It was later described in Parkinson's disease, but mainly in cases of patients being treated with dopaminergic drugs. It has also been described in methamphetamine and cocaine users, as well as in some patients with gambling addictions, and hypersexuality.

<span class="mw-page-title-main">Trihexyphenidyl</span> Antispasmodic drug

Trihexyphenidyl is an antispasmodic drug used to treat stiffness, tremors, spasms, and poor muscle control. It is an agent of the antimuscarinic class and is often used in management of Parkinson's disease. It was approved by the FDA for the treatment of Parkinson's in the US in 2003.

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.

Tourettism refers to the presence of Tourette-like symptoms in the absence of Tourette syndrome, as the result of other diseases or conditions, known as "secondary causes".

In the management of Parkinson's disease, due to the chronic nature of Parkinson's disease (PD), a broad-based program is needed that includes patient and family education, support-group services, general wellness maintenance, exercise, and nutrition. At present, no cure for the disease is known, but medications or surgery can provide relief from the symptoms.

<span class="mw-page-title-main">Levodopa</span> Dopaminergic medication

Levodopa, also known as L-DOPA and sold under many brand names, is a dopaminergic medication which is used in the treatment of Parkinson's disease and certain other conditions like dopamine-responsive dystonia and restless legs syndrome. The drug is usually used and formulated in combination with a peripherally selective aromatic L-amino acid decarboxylase (AAAD) inhibitor like carbidopa or benserazide. Levodopa is taken by mouth, by inhalation, through an intestinal tube, or by administration into fat.

<span class="mw-page-title-main">Paroxysmal exercise-induced dystonia</span> Episodes of involuntary movement triggered by exercise

Paroxysmal exercise-induced dystonia (PED) is a rare neurological disorder that belongs to the paroxysmal dyskinesias, a group of rare movement disorders that involve attacks of hyperkinesia with intact consciousness. It is characterized by sudden, transient, involuntary movements, often including repetitive twisting motions and painful posturing triggered by exercise or other physical exertion. The term paroxysmal indicates that the episodes are sudden and short lived and usually unpredicted, and return to normal is rapid. The number of reported cases of people with PED is very small leading to difficulty in studying and classifying this disease and most studies are limited to a very small number of test subjects.

Dopamine-responsive dystonia (DRD) also known as Segawa syndrome (SS), is a genetic movement disorder which usually manifests itself during early childhood at around ages 5–8 years.

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.

<span class="mw-page-title-main">Dopamine dysregulation syndrome</span> Neuralogical disorder caused by long-term use of dopaminergic drugs

Dopamine dysregulation syndrome (DDS) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It is characterized by severely disinhibited patterns of behavior, leading to problems such as addiction to the offending medication, gambling addiction, or compulsive sexual behavior, along with a general orientation towards immediate gratification. It typically occurs in people with Parkinson's disease or restless legs syndrome (RLS) who have taken dopamine agonist medications for an extended period of time.

Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis.

Dopamine supersensitivity psychosis is a hypothesis that attempts to explain the phenomenon in which psychosis (e.g., hallucinations, delusions) 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.

<span class="mw-page-title-main">Mesdopetam</span> Chemical compound

Mesdopetam (INNTooltip International Nonproprietary Name; developmental code names IRL-790, IPN60170) is a dopamine D2 and D3 receptor antagonist with preference for the D3 receptor which is under development for the treatment of Parkinson's disease, drug-induced dyskinesia, and psychotic disorders. It has been described by its developers as having "psychomotor stabilizing" properties.

References

  1. ↑ "Dyskinesia (Health Article)". Yahoo! Health. Retrieved 25 January 2014.
  2. ↑ "dyskinesia" at Dorland's Medical Dictionary
  3. ↑ Healy 2008, p. 29-30.
  4. 1 2 3 Brian K. Alldredge; et al., eds. (2013). Applied therapeutics : the clinical use of drugs (10th ed.). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 1937. ISBN   978-1609137137.
  5. ↑ Rusinyak, Daniel E. (2011). "Neurologic manifestations of chronic methamphetamine abuse". Neurologic Clinics. 29 (3): 641–655. doi:10.1016/j.ncl.2011.05.004. PMC   3148451 . PMID   21803215.
  6. ↑ Hanson, Glen R.; Fleckenstein, Annette E.; Curtin, Kare (1 January 2015). "Dependence on amphetamines increases Parkinson's disease: Effect of gender". Drug and Alcohol Dependence. 146: e134–e135. doi:10.1016/j.drugalcdep.2014.09.284 . Retrieved 28 November 2017.
  7. ↑ Kish, Stephen J.; Boileau, Isabelle; Callaghan, Russell C.; Tong, Junchao (2017). "Brain dopamine neurone 'damage': methamphetamine users vs. Parkinson's disease – a critical assessment of the evidence". European Journal of Neuroscience. 45 (1): 58–66. doi:10.1111/ejn.13363. PMC   5209286 . PMID   27519465.
  8. 1 2 3 4 Fabbrini G, Brotchie JM, Grandas F, Nomoto M, Goetz CG (April 2007). "Levodopa-induced dyskinesias". Movement Disorders. 22 (10): 1379–89. doi:10.1002/mds.21475. PMID   17427940. S2CID   20926751.
  9. 1 2 3 4 Thanvi B, Lo N, Robinson T (June 2007). "Levodopa-induced dyskinesia in Parkinson's disease: clinical features, pathogenesis, prevention and treatment". Postgraduate Medical Journal. 83 (980): 384–88. doi:10.1136/pgmj.2006.054759. PMC   2600052 . PMID   17551069. Open Access logo PLoS transparent.svg (full free text)
  10. ↑ Halje P, Tamtè M, Richter U, Mohammed M, Cenci MA, Petersson P (November 2012). "Levodopa-induced dyskinesia is strongly associated with resonant cortical oscillations". Journal of Neuroscience. 32 (47): 16541–51. doi:10.1523/JNEUROSCI.3047-12.2012. PMC   6621755 . PMID   23175810. Open Access logo PLoS transparent.svg (full free text)
  11. ↑ Healy 2008, p. 30–31.
  12. ↑ Gonzales GR (July 1992). "Postherpes simplex type 1 neuralgia simulating postherpetic neuralgia". J Pain Symptom Manage. 7 (5): 320–3. doi: 10.1016/0885-3924(92)90065-p . PMID   1624816.
  13. 1 2 Pranzatelli MR (September 1996). "Antidyskinetic drug therapy for pediatric movement disorders". J Child Neurol. 11 (5): 355–369. doi:10.1177/088307389601100503. PMID   8877602.
  14. ↑ Chase TN, Oh JD, Konitsiotis S (April 2000). "Antiparkinsonian and antidyskinetic activity of drugs targeting central glutamatergic mechanisms". J Neurol. 247 Suppl 2: II36–II42. doi:10.1007/pl00007759. PMID   10991664.
  15. 1 2 Rylander D (January 2012). "The serotonin system: a potential target for anti-dyskinetic treatments and biomarker discovery". Parkinsonism Relat Disord. 18 Suppl 1: S126–S128. doi:10.1016/S1353-8020(11)70039-6. PMID   22166409.
  16. ↑ Kwon DK, Kwatra M, Wang J, Ko HS (November 2022). "Levodopa-Induced Dyskinesia in Parkinson's Disease: Pathogenesis and Emerging Treatment Strategies". Cells. 11 (23): 3736. doi: 10.3390/cells11233736 . PMC   9736114 . PMID   36496996.
  17. ↑ Bashir HH, Jankovic J (May 2020). "Treatment of Tardive Dyskinesia". Neurol Clin. 38 (2): 379–396. doi:10.1016/j.ncl.2020.01.004. PMID   32279716.

Works cited

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