Chronic s.c. Lisuride in Parkinson’s disease — motorperformance and avoidance of psychiatric side effects

1988 ◽  
pp. 35-54
Author(s):  
S. Bittkau ◽  
H. Przuntek
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Psychiatric Side Effects

Psychiatric side-effects of medications: recent developments

2005 ◽  
Vol 11 (1) ◽  
pp. 58-70 ◽  
Author(s):  
Nora Turjanski ◽  
Geoffrey G. Lloyd
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Hiv Infection ◽  
Recent Developments ◽  
Psychiatric Side Effects ◽  
Neuropsychiatric Side Effects

Medications often induce neuropsychiatric side-effects. This article reviews psychiatric side-effects that are well known and describes those induced by recently developed medications. Therapeutic innovations have been prominent in the treatment of HIV infection, Parkinson's disease and epilepsy and therefore psychiatric side-effects caused by these agents are described in more detail.

Liposomes: Novel Drug Delivery Approach for Targeting Parkinson’s Disease

2020 ◽  
Vol 26 (37) ◽  
pp. 4721-4737 ◽  
Author(s):  
Bhumika Kumar ◽  
Mukesh Pandey ◽  
Faheem H. Pottoo ◽  
Faizana Fayaz ◽  
Anjali Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Drug Delivery ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Targeting ◽  
Neural Cells ◽  
Blood Brain ◽  
The Brain

Parkinson’s disease is one of the most severe progressive neurodegenerative disorders, having a mortifying effect on the health of millions of people around the globe. The neural cells producing dopamine in the substantia nigra of the brain die out. This leads to symptoms like hypokinesia, rigidity, bradykinesia, and rest tremor. Parkinsonism cannot be cured, but the symptoms can be reduced with the intervention of medicinal drugs, surgical treatments, and physical therapies. Delivering drugs to the brain for treating Parkinson’s disease is very challenging. The blood-brain barrier acts as a highly selective semi-permeable barrier, which refrains the drug from reaching the brain. Conventional drug delivery systems used for Parkinson’s disease do not readily cross the blood barrier and further lead to several side-effects. Recent advancements in drug delivery technologies have facilitated drug delivery to the brain without flooding the bloodstream and by directly targeting the neurons. In the era of Nanotherapeutics, liposomes are an efficient drug delivery option for brain targeting. Liposomes facilitate the passage of drugs across the blood-brain barrier, enhances the efficacy of the drugs, and minimize the side effects related to it. The review aims at providing a broad updated view of the liposomes, which can be used for targeting Parkinson’s disease.

scholarly journals Blood-brain barrier opening with focused ultrasound in Parkinson’s disease dementia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Carmen Gasca-Salas ◽  
Beatriz Fernández-Rodríguez ◽  
José A. Pineda-Pardo ◽  
Rafael Rodríguez-Rojas ◽  
Ignacio Obeso ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Drug Delivery ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Neurodegenerative Disorders ◽  
Focused Ultrasound ◽  
Temporal Cortex ◽  
Clinical State ◽  
Cognitive Improvement ◽  
Bbb Opening

AbstractMR-guided focused ultrasound (MRgFUS), in combination with intravenous microbubble administration, has been applied for focal temporary BBB opening in patients with neurodegenerative disorders and brain tumors. MRgFUS could become a therapeutic tool for drug delivery of putative neurorestorative therapies. Treatment for Parkinson’s disease with dementia (PDD) is an important unmet need. We initiated a prospective, single-arm, non-randomized, proof-of-concept, safety and feasibility phase I clinical trial (NCT03608553), which is still in progress. The primary outcomes of the study were to demonstrate the safety, feasibility and reversibility of BBB disruption in PDD, targeting the right parieto-occipito-temporal cortex where cortical pathology is foremost in this clinical state. Changes in β-amyloid burden, brain metabolism after treatments and neuropsychological assessments, were analyzed as exploratory measurements. Five patients were recruited from October 2018 until May 2019, and received two treatment sessions separated by 2–3 weeks. The results are set out in a descriptive manner. Overall, this procedure was feasible and reversible with no serious clinical or radiological side effects. We report BBB opening in the parieto-occipito-temporal junction in 8/10 treatments in 5 patients as demonstrated by gadolinium enhancement. In all cases the procedures were uneventful and no side effects were encountered associated with BBB opening. From pre- to post-treatment, mild cognitive improvement was observed, and no major changes were detected in amyloid or fluorodeoxyglucose PET. MRgFUS-BBB opening in PDD is thus safe, reversible, and can be performed repeatedly. This study provides encouragement for the concept of BBB opening for drug delivery to treat dementia in PD and other neurodegenerative disorders.

Dopamine agonists for parkinson’s disease

1991 ◽  
Vol 29 (2) ◽  
pp. 7-8
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Therapeutic Efficacy ◽  
Dopamine Agonists ◽  
Dopa Decarboxylase ◽  
Decarboxylase Inhibitor ◽  
Duration Of Action ◽  
Motor Disability ◽  
The Uk

Bromocriptine, lysuride (formerly lisuride, Revanil – Roche) and pergolide (not yet marketed in the UK) are dopamine agonists developed for use in the treatment of patients with Parkinson’s disease. Combination of a dopamine agonist with levodopa plus a dopa-decarboxylase inhibitor (‘co-dieldopa’)* may have advantages at all stages of the disease. The aim of combined co-dieldopa + agonist treatment is to limit some of the problems with prolonged co-dieldopa use alone; especially fluctuations in motor disability.1 It is still not clear how the three agonists compare with each other for therapeutic efficacy, duration of action, and side effects, nor how they are best combined with co-dieldopa.

Side effects of treatment for Parkinson's disease

2012 ◽  
Vol 14 (5) ◽  
pp. 230-233 ◽  
Author(s):  
Daiga Heisters ◽  
John Bains
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects

scholarly journals TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson’s Disease

2020 ◽  
Vol 21 (2) ◽  
pp. 590 ◽  
Author(s):  
Mª Muñoz ◽  
Nerea de la Fuente ◽  
Amelia Sánchez-Capelo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Side Effects ◽  
Pathological Features ◽  
Therapeutic Approaches ◽  
Brain Nuclei ◽  
Dopaminergic Neurodegeneration ◽  
Cognitive Alterations ◽  
Gaba Neurotransmission

γ-Aminobutiryc acid (GABA) is found extensively in different brain nuclei, including parts involved in Parkinson’s disease (PD), such as the basal ganglia and hippocampus. In PD and in different models of the disorder, an increase in GABA neurotransmission is observed and may promote bradykinesia or L-Dopa-induced side-effects. In addition, proteins involved in GABAA receptor (GABAAR) trafficking, such as GABARAP, Trak1 or PAELR, may participate in the aetiology of the disease. TGF-β/Smad3 signalling has been associated with several pathological features of PD, such as dopaminergic neurodegeneration; reduction of dopaminergic axons and dendrites; and α-synuclein aggregation. Moreover, TGF-β/Smad3 intracellular signalling was recently shown to modulate GABA neurotransmission in the context of parkinsonism and cognitive alterations. This review provides a summary of GABA neurotransmission and TGF-β signalling; their implications in PD; and the regulation of GABA neurotransmission by TGF-β/Smad3. There appear to be new possibilities to develop therapeutic approaches for the treatment of PD using GABA modulators.

scholarly journals CQA 206-291 in Parkinson's Disease: An Acute Single Escalating Dosage Study

1990 ◽  
Vol 17 (4) ◽  
pp. 416-419 ◽  
Author(s):  
Anthony E. Lang ◽  
David E. Riley ◽  
Luc Vachon ◽  
Xavier Lataste
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Parent Compound ◽  
Term Treatment ◽  
Effective Dosage ◽  
Dopamine Antagonist ◽  
Peak Response ◽  
Dosage Study ◽  
Ergot Derivative

ABSTRACT:CQA 206-291, a new ergot derivative with a “biphasic” dopaminergic profile, was studied in 6 patients with longstanding Parkinson's disease suffering from pronounced fluctuations in hourly mobility. On alternate days, up to seven single doses, escalating from 0.2 to 20 mg, were given as replacement for the usual first morning dose of levodopa. At the most effective dosage, four of the six patients obtained as good a peak response to CQA (8-20 mg) as to L-dopa. Side effects were common and similar to other ergot derivatives, suggesting that the initial weak dopamine antagonist properties of the parent compound, documented in animals, may be of little clinical significance. However, comparative studies will be needed to confirm this suspicion. The addition of domperidone successfully reduced the incidence and severity of side effects. CQA 206-291 has potent anti-parkinsonian properties; further longer-term treatment trials are indicated.

scholarly journals Receptor Ligands as Helping Hands to L-DOPA in the Treatment of Parkinson’s Disease

Biomolecules ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 142 ◽  
Author(s):  
Fabio Bello ◽  
Mario Giannella ◽  
Gianfabio Giorgioni ◽  
Alessandro Piergentili ◽  
Wilma Quaglia
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Elevated Liver Enzyme ◽  
Therapeutic Potential ◽  
Motor Complication ◽  
Receptor Ligands ◽  
Dopaminergic Drugs ◽  
The Many ◽  
Non Motor Symptoms

Levodopa (LD) is the most effective drug in the treatment of Parkinson’s disease (PD). However, although it represents the “gold standard” of PD therapy, LD can cause side effects, including gastrointestinal and cardiovascular symptoms as well as transient elevated liver enzyme levels. Moreover, LD therapy leads to LD-induced dyskinesia (LID), a disabling motor complication that represents a major challenge for the clinical neurologist. Due to the many limitations associated with LD therapeutic use, other dopaminergic and non-dopaminergic drugs are being developed to optimize the treatment response. This review focuses on recent investigations about non-dopaminergic central nervous system (CNS) receptor ligands that have been identified to have therapeutic potential for the treatment of motor and non-motor symptoms of PD. In a different way, such agents may contribute to extending LD response and/or ameliorate LD-induced side effects.

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