Neural substrates and potential treatments for levodopa-induced dyskinesias in Parkinson's disease

Parkinson's disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodege...

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Elmentve itt :
Bibliográfiai részletek
Szerzők: Phillips Joseph R.
Eissa Abeer M.
Hewedi Doaa H.
Jahanshahi Marjan
El-Gamal Mohamed
Kéri Szabolcs
Moustafa Ahmed A.
Dokumentumtípus: Cikk
Megjelent: 2016
Sorozat:REVIEWS IN THE NEUROSCIENCES 27 No. 7
doi:10.1515/revneuro-2016-0009

mtmt:3092623
Online Access:http://publicatio.bibl.u-szeged.hu/11336
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520 3 |a Parkinson's disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodegenerative disease, with dopaminergic neuronal loss occurring in the substantia nigra pars compacta, thus disrupting basal ganglia functions. This leads to downstream effects on other neurotransmitter systems such as glutamate, gamma-aminobutyric acid, and serotonin. To date, one of the main treatments for PD is levodopa. While it is generally very effective, prolonged treatments lead to levodopa-induced dyskinesia (LID). LID encompasses a family of symptoms ranging from uncontrolled repetitive movements to sustained muscle contractions. In many cases, the symptoms of LID can cause more grief than PD itself. The purpose of this review is to discuss the possible clinical features, cognitive correlates, neural substrates, as well as potential psychopharmacological and surgical (including nondopaminergic and deep brain stimulation) treatments of LID. 
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700 0 1 |a Hewedi Doaa H.  |e aut 
700 0 1 |a Jahanshahi Marjan  |e aut 
700 0 2 |a El-Gamal Mohamed  |e aut 
700 0 2 |a Kéri Szabolcs  |e aut 
700 0 2 |a Moustafa Ahmed A.  |e aut 
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