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Dyskinesia-ufrivillige-tungebevægelser-og-urolig-krop

Ochsner J. 2017 Summer; 17(2): 162–174.

Medication-Induced Tardive Dyskinesia: A Review and Update

Elyse M. Cornett, PhD,1 Matthew Novitch, BS,2 Alan David Kaye, MD, PhD,3 Vijay Kata, MS,3 and Adam M. Kaye, PharmD4

 

 

(Danske noter på grundlag af ovenstående kilde):

Såkaldt tardive dyskinesia (TD) er dvs. forsinket udvikling (tardiv = langsom) af fejlfunktion af kroppens bevægelser, med udvikling af ufrivillige bevægelser af tungen, evt. læber og ansigt, samt ben og arme og evt. uro i kroppen.

 

Skyldes medicin-bivirkning, såkaldt "dopaminergic antagonist medications", typisk antipsykotiske lægemidler (antipsychotic drugs [APD] – men også en række andre lægemidler, se nedenfor og se artiklens kilde ovenfor).

 

Tilstanden kan optræde efter kort tids brug eller længere tids brug af lægemidlet.

 

Det kan også optræde efter at man stopper med at tage lægemidlet.

 

Hvis det varer mindst 1 måned efter at man er ophørt med at tage lægemidlet har man en TD-diagnose.

 

I mange patienter er TD irreversibel.  Det er meget generende for patientens dagligdag og sociale liv og kan hæmme evnen til at læse mv.

 

Man kan læse om emnet ved at lave en søgning på "medication-induced TD" eller "tardive dyskinesia".

 

Årsagen tænkes at være blokering af de postsynaptiske dopamin-receptorer, hvilket kroppen søger at kompensere for ved at gøre dopamin-receptorerne alt for meget følsomme (dopamine receptor supersensitivity) samt nedsætte mængden af GABA (gamma-aminobutyric acid (GABA) depletion) samt fremkalde mangel på acetylcholin (cholinergic deficiency) samt medføre noget som kræver antioxidanter (tilstanden oxidative stress) og ved at ændre synapsernes forandringsparathed (altered synaptic plasticity) og ved at dræbe visse hjerneceller (neurotoxicity) og ved at give fejl i hjernecellernes signalkommunikation når de påvirkes (defective neuroadaptive signaling)..

 

Med hensyn til den forklaring, som går ud på at lægemidlets bivirkning, altså TD-tilstanden, skyldes at lægemidlet har blokeret for dopamin, hvorved kroppen har reageret ved at opregulere følsomheden hos dopamin-receptorerne, så vil resultatet altså være, at der kommer et for stort respons på dopamin, når dette dopamin rammer receptorerne (efter synapsekløften mellem to hjernenerveceller, dvs. postsynaptisk).

Man kan tænke sig, at kroppen (måske som kompensation) danner for meget dopamin.  Denne øgede "dopamin-metabolisme" medfører øget dannelse af frie radikaler. 

 

Enzymet Monoaminoxidase metaboliserer dopamin. Og dette kan fremkalde skadelig iltning af fedtmolekyler ((dvs. fremkalde lipid peroxidation og ændring af antioxidant-enzymer, hvilket kan dræbe celler i hjernen. Dopamin i sig selv kan også give disse virkninger. 

 

De såkaldte basalganglier (basal ganglia), og bestemte hjerneområder inde i hjernen, som kaldes "subcortical nuclei" og som bl.a. er områderne "striatum" og "substantia nigra" har mange nerveceller, som bruger dopamin som signalstof. Disse steder i hjernen er derfor særlig følsomme og udsatte for oxidativt stress og hvis det sker, opstår TD (de ufrivillige bevægelser).

 

Nedbrydningsprodukterne af psykofarm-lægemidler kan i sig selv være giftige for disse hjernenerveceller, igen formentlig fordi de fremkalder oxidativt stress. 

 

Nogle mennesker er mere følsomme herfor, det gælder f.eks.  ældre kvinder.

 

Der kan også være genetiske varianter, idet nogle mennesker har særlige varianter af dopamine D3 receptor Ser9Gly og i øvrigt er der også særlige varianter af serotonin 2A receptoren og serotonin 2C receptoren.

 

Der kan også være nogle mennesker med særlige varianter af neurotrophic factor Val66Met

 

Disse personer kan være særlig følsomme for disse typer af oxidativt stress.

 

TD opstår hos hver tredje som får såkaldt "typisk antipsykotisk medicin" (typical APD) får TD, dvs. ufrivillige bevægelser.

 

TD opstår hos hver 7. af dem, som får "atypisk antipsykotisk medicin (atypical APD)

 

Årsagen er at de atypiske (!) antipsykotiske lægemidler bindes svagere til dopamin-D2 receptor i "dorsal striatum"

 

Østrogen har en antioxidant virkning, som måske beskytter mod TD (derfor er ældre kvinder, der er ældre og altså lever efter den tid hvor kroppen danner meget østrogen, mere udsat for TD).

 

Blokering af dopamin-receptorer skyldes lægemidler, som virker som "dopamin antagonister", måske især "dopamin-D2 receptor antagonister, så basal-ganglierne bliver for supersensitive for dopamin-D2.

 

D3 og D5 receptorer, og ikke kun D2 dopaminreceptorer er også forbundet med TD på denne måde.

 

Ubalance mellem dopamin og acetylcholin kan sandsynligvis også give TD. 

 

Ubalance mellem dopamin og serotonin kan sandsynligvis også give TD. (idet for meget serotonin, fremkaldt af SSRI-lægemidler, hæmmer dannelsen af dopamin, og så bliver dopaminreceptorerne også supersensitive af denne grund). 

 

Ubalance mellem dopamin og GABA: GABA-nerveceller kan hæmme dopamin-nerveceller i visse hjerneområder.

 

risperidone, aripiprazole og amisulpride er såkaldt "atypiske" antipsykotiske lægemidler som kan give TD.

 

Personer som tager lithium har større risiko for at et antipsykotisk lægemiddel vil fremkalde TD. 

 

SSRI-lægemidler, såsom fluoxetine, kan medføre TD.  Det samme gælder sertraline, et andet SSRI.

 

Monoamine oxidase inhibitors (MAOI) bruges mod depression og Parkinson. Det hæmmer metabolismen af monoaminer. Derved kan niveauet af monoaminer øges. Der findes to typer af monoamine oxidase (MAO) Type A og type B. De laves i hypothalamus, hippocampus og cingulate cortex og striatum samt globus pallidus (de sidste to er især type B). Hjernebarken har kun høje niveauer af type A. Dette forklarer at det er lægemidler som virker på type B som kan fremkalde TD (da type B laves i hjerneområder hvor der er meget dopamin, såsom striatum-hjerneområdet).

 

Selegiline bindes f.eks. kun til MAO-type B hvorved enzymet inaktiveres så dets aktivitet hæmmes altså.

 

Rasagiline, har samme historie, men giver TD i mildere grad.

 

Phenelzine, bindes både til type A og til type B. Den giver også TD.

 

TD kan også opstå fra lægemidler mod kvalme, mod malaria, mod allergi, og mod Parkinson og mod frygt mv. se artiklen ifølge kilden ovenfor.

 

Ikke godt, når man har TD:

histamine, serotonin, norepinephrine, dopamine, and epinephrine.

tyramine  i gammel ost, kød, fermenterede madvarer, alkohol, chokolade.

 

Lav dosis (100 mg) caffein nedsætter TD (men høj dosis caffein er dårligt og øger TD).

 

Donepezil, en reversibel acetylcholinesterase-hæmmer, nedsætter TD-bivirkningerne.

 

Clozapine, en serotonin  og dopamine receptor antagonist, er bedste valg når en patient skal have antipsykotisk medicin og vil undgå TD.  Det kan også stoppe TD-bivirkningerne.

 

quetiapine, er en dopamine antagonist, kan lindre TD-symptomer

 

olanzapine, er en dopamine og  serotonin receptor antagonist, kan lindre TD-symptomer

 

Apomorphine, en dopamine receptor antagonist, kan lindre TD-symptomer når det gives sammen med L-DOPA

En tetrabenazine-analog såsom valbenazine, (og tetrabenazine selv har samme virkning, men det nedbrydes for hurtigt i kroppen til at virke godt) kan lindre TD,  og synes at være særlig velegnet til at lindre TD.

 

Lav dosis af propranolol lindrer TD.

 

Amantadine lindrer TD når det gives til Parkinsonpatienter som får L-DOPA (og som får TD af L-DOPA)

 

Branched-chain amino acids (BCAAs) lindrer TD. De nedsætter blodets indhold af phenylalanin ved at stimulere proteinsyntesen og insulin-frigivelsen.  De nedsætter også ophobningen af tyrosin som er forstadie til dopamin. Derved nedsættes dopamin-syntesen i hjernen.  BCAA kan købes i helsekostforretninger, såsom forretningen "The Touch" på 2. sal th i Frederiksbergcenteret. 

 

2 mg/dag clonazepam lindrer TD

 

Ginkgo Biloba lindrer TD.

 

Da oxidativt stress medvirker til TD (formentlig) kan antioxidanter gives som tilskud og derved lindre TD, f.eks.  zonisamide, yi gan san (en kinesisk urt, herb), levetiracetam, melatonin, omega-3 fedtsyrer, piracetam, resveratrol, vitamin B6 og vitamin E.

 

Vigtigt: Undgå store doser af antipsykotisk medicin, og brug medicinen i kortest mulig tid. Undgå det evt. helt om muligt. Vær opmærksom på tidligere tegn på TD. Trap ikke hurtigt, men derimod langsomt ud af behandlingen med antipsykotisk medicin (da hurtig stop kan fremkalde TD).

 

=====================

2. artikel:

https://www.medicalnewstoday.com/articles/320175.php

 

Sometimes switching or reducing the medication relieves the symptoms of tardive dyskinesia, but this is not always the case.

Until recently, there were no FDA-approved treatments for tardive dyskinesia. In 2017, two medications were approved to treat this condition:

  • valbenazine (Ingrezza)
  • deutetrabenazine (Austedo)

Anyone wanting to try these medications to reduce the symptoms of tardive dyskinesia should speak to their doctor.

The American Academy of Neurology suggest that ginkgo biloba extract may also help relieve tardive dyskinesia symptoms in some people. It is worth noting, however, that its effects were only studied in people hospitalized with schizophrenia.

They also noted that there is not enough evidence to show whether other natural remedies, such as vitamin E and melatonin, work for tardive dyskinesia.

However, there is some evidence that an anti-anxiety drug known as clonazepam can help treat tardive dyskinesia, but this drug can be habit-forming.

===========

 

Akathisia = urolighed, har svært ved at sidde stille, skal helst bevæge sig. Meget vanskelig form for TD at behandle.

Men følgende (VMAT2 inhibitors) kan lindre akathisia-TD:

propranolol

anticholinergics

clonazepam

mirtazapine

 

. Symptoms typically begin with an insidious
onset, evolving to a full syndrome over days to weeks following
onset. This is followed by a stabilization of symptoms in a chronic, but
sometimes waxing and waning [= øge og falde, komme og gå, variere over tid] course [11].

TS can persist for years after discontinuation of the offending agent,
although some patients can experience partial or complete remission [= bedring] of
symptoms a few years after discontinuation of the causative agent.

 

Tungebevægelserne kan mindskes under tale og spisning eller når man sætter en finger på læben. Distraktion som når patienten bliver bedt om at udføre bevægelser med hænderne vil øge tungebevægelserne. Tungemusklen bliver større på grund af den stadige aktivering (macroglossia).

 

O-B-L betyder , oral-buccal-lingual (dvs. mund, mundhule og tunge

DRBA = dopamine receptor blocking agent.

Når tungen bevæges ud af munden kaldes dette for fly-catchers tongue.

Kun 2% bliver helt raske af TD.

TD kan udløses af blot 2 uger på medicinen.  (kilde 3: https://www.jns-journal.com/article/S0022-510X(18)30063-7/pdf)

 

kilde 4: https://emedicine.medscape.com/article/1151826-overview#a2

Increased dopamine transport (DAT) uptake after treatment with quetiapine has been reported with the amelioration of TD

Curcumin, an antioxidant, may prevent the development of dyskinesias

 

Haloperidol induced vacuous chewing movements, orofacial movements, and facial stereotypies in rats. These changes were reversed after treatment with adenosine or caffeine; The prevalence of TD is higher in cigarette smokers

 

The prevalence of TD is 29% in elderly patients receiving dopamine antagonist treatment for 3 months and 26-67% in patients undergoing long-term treatment.

 

MENNESKER DER HAR HAFT TD SKAL ADVARES MOD AT FÅ DOPAMIN-RECEPTOR BLOKERENDE LÆGEMIDLER I FREMTIDEN!  Advise the patient to avoid receiving dopamine-receptor blocking drugs. Advise the patient to obtain a medical alert bracelet to warn against the administration of dopamine-receptor blocking drugs

 

Diagnosis of neuroleptic-induced TD generally requires exposure to neuroleptics for at least 3 months. At least 1 month of exposure is typically required if the patient is aged 60 years or older.

 

Antiparkinsonism agents usually do not improve neuroleptic-induced dyskinesias.

Neuroleptic-induced TDs are absent during sleep.

 

Test for TD:

Have the patient sit in a chair with hands on knees, legs slightly apart, and feet flat on the floor. Examine the entire body for movements while the patient is in this position, then ask the patient to count backwards from 30.

 

Ask the patient to sit with hands hanging unsupported (between the legs if male, or hanging over the knees if female and wearing a dress). Observe the hands and other body areas, then request that the patient describe in detail the path traveled that day. Ask the patient where the trip started, what streets were traveled, where turns were made, where the trip terminated, and what floor and room were entered. These procedures stimulate the patient and may provoke the appearance of movement disorders.

 

If asked to hold the tongue in a protruded position, the person may be unable to maintain protrusion for longer than 1 second. Although the individual may attempt to disguise the movements by placing the hand to the mouth, in time, the movements become constant during waking hours and cannot be suppressed by the patient.

 

ask the individual to remove shoes and socks so that the movements of the toes and feet can be observed fully. Movements typically become constant during waking hours. Often, the individual cannot suppress them for longer than 1 second.

 

Neuroleptic-induced TD is present at rest and diminishes or subsides when the affected body part is activated. For example, squeezing the hand of another person often eliminates finger dyskinesias, tongue protrusion commonly reduces tongue dyskinesias, and mouth opening diminishes orofacial dyskinesias. Simply pointing out these movements and asking the patient to stop can reduce the movements. For example, orofacial movements may be stopped by placing the patient’s fingers on his or her lips.

 

Asking the patient to repeatedly touch the thumb to each finger sequentially in both hands may amplify TD in the tongue and the face. Provocative distracting movements may be necessary to induce movement in mild TD.

 

Tardive akathisia includes the presence of subjective symptoms of restlessness and the urge to move. It refers to the inability to sit down or remain still. People with tardive akathisia exhibit constant pacing and moving of the hands and feet. They typically shift their weight from one foot to the other when standing and swing their legs when sitting.

 

Examine the patient with his or her feet bare and hands exposed so that movements of the extremities can be observed. Ask the patient to sit, stand, and lie still for 2 minutes in each position.

After the patient has maintained the designated position for a full minute, ask, “Do you feel restless inside? Do you have the urge to move? Are you able to keep your feet still?” If the patient responds that these sensations are present, ask him or her to quantify the magnitude of the urge to move as mild, moderate, or severe.

 

Unlike TDs, withdrawal dyskinesias remit within a month after discontinuance of neuroleptics.

 

Amelioration of TD resulting from the administration of quetiapine (dvs. at stoffet lindrer TD)

 

Proton magnetic resonance spectroscopy has demonstrated neural damages in the left lenticular nucleus in a group of patients with TD.

 

The evidenced-based guidelines of the American Academy of Neurology recommend the use of clonazepam and ginkgo biloba for TD. [

 

FDA has approved valbenazine(Ingrezza), the first drug to treat tardive dyskinesia. Valbenazine is a selective vesicular monoamine transporter 2 (VMAT2) inhibitor. These drugs modulate the presynaptic packaging and release of dopamine into the synapse, and may offset the movement-related effects of antipsychotics and other dopaminergic blockers.

Deutetrabenazine (Austedo) is a novel, highly selective vesicular monoamine transporter type 2 (VMAT2) inhibitor. FDA has approved deutetrabenazine tablets for the treatment of adults with tardive dyskinesia (TD). 24 mg/day and 36 mg/day—were associated with statistically significant improvement in patients’

 

Clonazepam (1-4.5 mg/day) showed a decrease of TD symptoms by 35%

 

TD may worsen initially after neuroleptics are discontinued.

 

In particular, clozapine has been recommended as treatment for patients with TD who require antipsychotics. Although clozapine has been associated with TD, [64the incidence of TD with this and other atypical agents appears markedly less than that of traditional neuroleptics. The benefits of clozapine may result from its affinity for the D4 receptor. Treatment with clozapine requires regular hematologic evaluation to avoid fatal agranulocytosis.

 

Other therapeutic agents for which there is some anecdotal support include vitamin E, levodopa (see carbidopa/levodopa), benzodiazepines, botulinum toxinreserpinetetrabenazine, propranolol, [66and dopamine-depleting agents. Ondansetron, a selective 5-hydroxytryptamine-3 antagonist, has helped some individuals with TD. Discontinuance of anticholinergic therapy may relieve TD. A controversial strategy for treating TD is to continue or increase the dose of the dopamine antagonist.

 

Clozapine has treated tardive tremor successfully.

 

Propranolol is useful for tardive akathisia.

 

it is preferable to taper the dose slowly (by 10% increments of the original dose) while closely observing the patient for exacerbation of psychotic symptoms.

 

 

 

 

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