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Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Absence of: Rest tremor.Levodopa-induced dyskinesias after several years or despite high levodopa dose.Typical nonmotor symptoms as the disease progresses.
Drug therapy
Published in Jeremy Playfer, John Hindle, Andrew Lees, Parkinson's Disease in the Older Patient, 2018
Amantadine is an unusual drug. Its anti-parkinsonian effect was discovered by chance when it was being used as an anti-viral agent.46 Pharmacologically amantadine resembles anticholinergic drugs. It also appears to have effects modulating dopamine re-uptake and the releasing of dopamine stores. More recently amantadine has been shown to have anti-NMDA receptor activity, blocking the action of glutamate within the basal ganglia circuitry.47 There are reports that it may be beneficial in reducing levodopa-induced dyskinesias.48 The recommended dose for amantadine is 100 mg daily, increased after one week to 100 mg twice daily to a maximum of 400 mg. The drug must be used in caution with the elderly and a daily dose over 200 mg has a significant risk of psychiatric side effects. Amantadine is best used as adjunct therapy. It can give a short-term boost to anti-Parkinson treatments on special occasions for the patient. There are many cautions and potential interactions with this drug. In particular, it should be avoided in patients with hepatic or renal impairment. It may cause significant fluid retention. Gastro-intestinal disturbances, insomnia and anxiety, vasculitis (livedo reticularis) and visual disturbance are side effects which frequently curtail the use of amantadine. In longer-term use it is difficult to withdraw and side effects such as weight loss, cognitive impairment and hallucinations become more evident.
Nardostachys jatamansi and levodopa combination alleviates Parkinson’s disease symptoms in rats through activation of Nrf2 and inhibition of NLRP3 signaling pathways
Published in Pharmaceutical Biology, 2023
Jiayuan Li, Jiahe Yu, Jianyou Guo, Jinfeng Liu, Guohui Wan, Xiaojia Wei, Xue Yang, Jinli Shi
It has been found that the combination of traditional Chinese medicine and levodopa can improve the anti-PD effect of levodopa and inhibit LID, which has the effect of ‘enhancing the effect and reducing the toxicity’ (Huang et al. 2017). Nardostachys jatamansi (D. Don) DC. [syn. Patrinia jatamansi D.Don, N. grandiflora DC.](Valerianaceae) (NJ) is a traditional Chinese Medicine which has the effects of regulating Qi and relieving pain, opening depression, and waking up the spleen. Studies have suggested that it also has anti-inflammatory and antioxidant effects (Lyle et al. 2009; Shin et al. 2015). Previous study from our group found that 80% ethanol extract of NJ can effectively alleviate PD symptoms in rats and protect dopaminergic neurons, and the effect is better than other extracts (Wan et al. 2022). Moreover, the combination of NJ and levodopa can reduce the side effects of excessive levodopa induced dyskinesia (Li et al. 2022). However, whether the combination of 80% ethanol extract of NJ and levodopa could bring a synergistic effect in the treatment of PD has not been tested. Therefore, the goal of the current study was to investigate whether an 80% ethanol extract of NJ combined with levodopa had synergistic effects in the ROT-induced PD rat model and any involvement of the Nrf2/NLRP3 pathway in the underlying synergy.
Present and future of subthalamotomy in the management of Parkinson´s disease: a systematic review
Published in Expert Review of Neurotherapeutics, 2021
Jorge U. Máñez-Miró, Rafael Rodríguez-Rojas, Marta Del Álamo, R. Martínez-Fernández, José A. Obeso
Regarding the classic fear of inducing hemichorea-ballism following subthalamotomy, with our approach, the risk of induced dyskinesia may be strikingly reduced with sustained antiparkinsonian effect when lesions enlarge dorsally and also impinge on pallidothalamic fibers. In the event that HCB would ensue, the practical approach is to reduce drastically or even stop levodopa and dopamine agonists for several days, until the dyskinesias wane in severity. This typically occurs over 1–3 weeks in the large majority of cases. A pallidotomy would be indicated in the rarer instance that chorea-ballism becomes a major source of disability [99]. Nonetheless, patients with severe levodopa-induced dyskinesias, even if unilateral, are not optimal candidates. Similarly, those with severe impulsivity and other behavioral disorders associated with dopaminergic medications.
In vitro and in vivo evaluation of levodopa-loaded nanoparticles for nose to brain delivery
Published in Pharmaceutical Development and Technology, 2020
Sema Arisoy, Ozgun Sayiner, Tansel Comoglu, Deniz Onal, Ozbeyen Atalay, Bilge Pehlivanoglu
PD is a progressive neurological disorder characterized by a large number of motor and non-motor features. Effective and well-tolerated DA replacement agent levodopa, a DA precursor, is the first option in treatment for PD. Dyskinesia and psychiatric problems are the treatment-related complications due to intermittent delivery of DA-replacing drugs to the brain may eventually limit the clinical use of levodopa. In this study, F1-1 formulation was developed to extend the release of levodopa up to 9 h. Consequently, frequent stimulation of the receptors which causes levodopa-induced dyskinesia was prevented. F1-1 surface was modified with WGA to enhance nasal adsorption of nanoparticles. WGA-F1-1 reached high target tissue concentration with the low DA level in blood and showed high clinical efficacy. The nanoparticle formulation was also found to be well tolerated in mice and showed lower cytotoxicity compared to levodopa alone. Taken together, these results indicate that drug-loaded PLGA nanoparticles could be a potential alternative to the existing levodopa therapy in PD.