Propranolol therapy for Tardive dyskinesia: A retrospective examination

Hatcher-Martin, Jaime M.; Armstrong, Karen; Scorr, Laura; Factor, Stewart A.

doi:10.1016/j.parkreldis.2016.09.004

Cited by 23 publications

(11 citation statements)

References 13 publications

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“…While our study has focused on propranolol, the anti-dyskinetic effect of this drug is likely related to its efficacy as a β-blocker that promotes a secondary anticholinergic action. Propranolol has been traditionally used to treat a variety of neurological and systemic symptoms [29,30], but with broad anticholinergic properties, propranolol may not be suitable for the elderly. However, centrally-acting β-blockers or drugs that might specifically target β-ARs or other G-protein coupled receptors on ChIs might also be expected to improve LID.…”

Section: Discussionmentioning

confidence: 99%

Propranolol Relieves L-Dopa-Induced Dyskinesia in Parkinsonian Mice

et al. 2020

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Background: Parkinsonism is caused by dopamine (DA) insufficiency and results in a hypokinetic movement disorder. Treatment with L-Dopa can restore DA availability and improve motor function, but patients can develop L-Dopa-induced dyskinesia (LID), a secondary hyperkinetic movement disorder. The mechanism underlying LID remains unknown, and new treatments are needed. Experiments in mice have shown that DA deficiency promotes an imbalance between striatal acetylcholine (ACh) and DA that contributes to motor dysfunction. While treatment with L-Dopa improves DA availability, it promotes a paradoxical rise in striatal ACh and a further increase in the ACh to DA ratio may promote LID. Methods: We used conditional Slc6a3DTR/+ mice to model progressive DA deficiency and the β-adrenergic receptor (β-AR) antagonist propranolol to limit the activity of striatal cholinergic interneurons (ChIs). DA-deficient mice were treated with L-Dopa and the dopa decarboxylase inhibitor benserazide. LID and motor performance were assessed by rotarod, balance beam, and open field testing. Electrophysiological experiments characterized the effects of β-AR ligands on striatal ChIs. Results: LID was observed in a subset of DA-deficient mice. Treatment with propranolol relieved LID and motor hyperactivity. Electrophysiological experiments showed that β-ARs can effectively modulate ChI firing. Conclusions: The work suggests that pharmacological modulation of ChIs by β-ARs might provide a therapeutic option for managing LID.

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Section: Discussionmentioning

confidence: 99%

Propranolol Relieves L-Dopa-Induced Dyskinesia in Parkinsonian Mice

et al. 2020

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“…NE may also largely serve to activate a wide range of physiological processes, many of which are not well characterized at this time, including: embryonic development (and possibly postnatal development, leading up to adulthood), consistent with the NE-lowering HDAC inhibitor valproic acid having teratogenic properties [ 82 ]; noradrenergic promotion of hunger, feeding, and weight gain or loss, including a potential relationship with cachexia in cancer; flashbulb memories and learning associated with surprise [ 83 ] which historically have been more attributed to DA, where beta adrenergic and DA D1 receptors may have differential effects [ 84 ]; tardive dyskinesia, L-DOPA induced dyskinesia, and neuroleptic malignant syndrome [ 85 ]; postural sway associated with schizophrenia and other disorders; locomotion stimulating NE release and NE release stimulating locomotion, with a neural correlate of enhanced theta (and possibly gamma) oscillations; and focusing the “spotlight” of attention, including spatial attention focused on different areas of one’s body, where NE plays a role in pupillary dilation during orienting of attention [ 86 ]. It is suggested here that this general “activational” role for NE, in the brain and periphery, is not limited to functional opposition of the parasympathetic nervous system by sympathetic signaling.…”

Section: Consequences Of the Hypothesismentioning

confidence: 99%

Norepinephrine May Oppose Other Neuromodulators to Impact Alzheimer’s Disease

Fitzgerald

2021

IJMS

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While much of biomedical research since the middle of the twentieth century has focused on molecular pathways inside the cell, there is increasing evidence that extracellular signaling pathways are also critically important in health and disease. The neuromodulators norepinephrine (NE), serotonin (5-hydroxytryptamine, 5HT), dopamine (DA), acetylcholine (ACH), and melatonin (MT) are extracellular signaling molecules that are distributed throughout the brain and modulate many disease processes. The effects of these five neuromodulators on Alzheimer’s disease (AD) are briefly examined in this paper, and it is hypothesized that each of the five molecules has a u-shaped (or Janus-faced) dose-response curve, wherein too little or too much signaling is pathological in AD and possibly other diseases. In particular it is suggested that NE is largely functionally opposed to 5HT, ACH, MT, and possibly DA in AD. In this scenario, physiological “balance” between the noradrenergic tone and that of the other three or four modulators is most healthy. If NE is largely functionally opposed to other prominent neuromodulators in AD, this may suggest novel combinations of pharmacological agents to counteract this disease. It is also suggested that the majority of cases of AD and possibly other diseases involve an excess of noradrenergic tone and a collective deficit of the other four modulators.

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“…Pro pra no lo lis yra be ta ad re ner gi niø re cep to riø an ta go nistas, var to ja mas aka ti zi jai, aukð tam krau jo spûdþiui, ðir dies rit mo su tri ki mams ir mig re nai gy dy ti. Ret ros pek ty vi nis 47 pa cien tø, ser gan èiø VD, ty ri mas, ku ris tae së si 17 më nesiø po an ti psi cho ti kø nu trau ki mo, pa ro dë, kad ma þa propra no lo lio do zë ðio je pa cien tø gru pë je bu vo ge rai to le ruoja ma ir 64 % pa cien tø pa ste bë jo sa vo simp to mø pa ge rë jimà [45].…”

Section: Propranololisunclassified

Treatment of tardive dyskinesia caused by long-term antipsychotic use: case reports and literature review

Pabarčiūtė¹,

Karnickas²

2020

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Įvadas. Vėlyvoji diskinezija – judėjimo sutrikimas, prasidedantis bent keletą mėnesių vartojant dopamino receptorių blokatorius. Šie vaistai apima daugumą vaistų nuo psichozės, kurių vartojimas plačiai taikomas gydant psichikos ligas. Ši neįgalumą sukelianti būklė išliks klinikine šiuolaikinės psichiatrijos dalimi, o pastaraisiais metais literatūroje pasirodęs didelis publikacijų apie vėlyvąją diskineziją skaičius yra didžiulis postūmis šioje srityje. Atvejų aprašymai. 43 metų moteris, serganti paranoidine šizofrenija, 2018 m. hospitalizuota dėl viso kūno nuolatinių nevalingų judesių, itin išreikštų apie 2 metus. Pacientė antipsichotikus vartoja apie 20 metų, pirmieji diskineziniai judesiai pastebėti prieš 10 metų (įvairūs trūkčiojimai) ir aprašyti 2014 m. (čepsėjimas). Pacientei diagnozuota vėlyvoji diskinezija, paskirtas gydymas tetrabenazinu. Pacientės būklė stacionare akivaizdžiai gerėjo, stereotipiški distoniniai-hiperkineziniai galūnių ir liemens judesiai bei kiti simptomai išnyko. Kita pacientė – 55 metų moteris, 2019 m. hospitalizuota dėl nevalingų judesių, reguliariai antipsichotikus vartojusi apie 10 metų dėl kliedesinio sutrikimo. Akatizija ir rankų diskinezijos atsirado prieš 7 metus, pamažu progresavo iki veido, kaklo, rankų, liemens choreoatetoidinių judesių. Hospitalizacijos metu diagnozuota paranoidinė šizofrenija, vėlyvoji diskinezija, paskirtas gydymas tetrabenazinu. Gydant sumažėjo nevalingų judesių amplitudė, pacientė tapo labiau funkcionali. Literatūros apžvalga. Vienas sunkumų psichiatrijoje, gydant vėlyvąją diskineziją, – poreikis tęsti būklę sąlygojusius antipsichotikus. Geriausias pasirinkimas būtų antros kartos atipiniai antipsichotikai. Pirmo pasirinkimo vaistai vėlyvajai diskinezijai gydyti yra VMAT2 inhibitoriai – deutetrabenazinas, valbenazinas, jei šie vaistai neprieinami – tetrabenazinas. Išvados. Norint pateikti patikimas, įrodymais pagrįstas vėlyvosios diskinezijos gydymo rekomendacijas, geriau suprasti jos patofiziologiją, genetinę predispoziciją ir gydymui skirtus preparatus, reikėtų atlikti daugiau, didesnių imčių ir vienodesnių sąlygų tyrimų.

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Propranolol therapy for Tardive dyskinesia: A retrospective examination

Cited by 23 publications

References 13 publications

Propranolol Relieves L-Dopa-Induced Dyskinesia in Parkinsonian Mice

Propranolol Relieves L-Dopa-Induced Dyskinesia in Parkinsonian Mice

Norepinephrine May Oppose Other Neuromodulators to Impact Alzheimer’s Disease

Treatment of tardive dyskinesia caused by long-term antipsychotic use: case reports and literature review

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