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To compare the efficacy of BF2.649 over placebo (12 week Double-Blind Phase) and assess the long term safety and the efficacy maintenance(9 months Open-Label Extension Phase) of BF2.649 in the improvement of excessive daytime sleepiness in patients diagnosed with Parkinson's Disease.
As measured by the change from baseline in the Epworth Scale Scores (ESS) at Week 12 and at Week 51, in patients diagnosed with EDS in Parkinson's Disease.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment
Not yet recruiting
Published on BioPortfolio: 2014-08-27T03:16:00-0400
The purpose of this study is to better define the absorption and elimination pathways, and circulating metabolites of Pitolisant at steady state using Pitolisant radiolabelled, in healthy ...
This EAP will be open to provide access to treatment with pitolisant while a U.S. New Drug Application (NDA) is being prepared and submitted for review for marketing approval. This program...
The purpose of this multicenter double blind study is to assess efficacy and safety of Pitolisant versus placebo in paediatric Narcoleptic patients with or without cataplexy.
The purpose of this study is to assess the abuse potential of single doses of pitolisant relative to phentermine HCl and placebo, when administered to healthy, non-dependent, recreational ...
Pitolisant (BF2.649) in the Treatment of Excessive Daytime Sleepiness in Patients With Obstructive Sleep Apnoea Syndrome, Treated or Not by Nasal Continuous Positive Airway Pressure, But Still Complaining of Excessive Daytime Sleepiness
The first objective of this study is to demonstrate the efficacy and safety of pitolisant given at 10, 20, or 40 mg per day versus placebo during 12 weeks of the Double Blind period, to tr...
Mild cognitive impairment is a common feature of Parkinson's disease, even at the earliest disease stages, but there is variation in the nature and severity of cognitive involvement and in the risk of...
To investigate whether diabetes mellitus is associated with Parkinson-like pathology in people without Parkinson disease and to evaluate the effect of diabetes mellitus on markers of Parkinson patholo...
Neuroimaging in Parkinson's disease is an evolving field, providing in-vivo insights into the structural and biochemical changes of the condition, although its diagnosis remains clinical. Here, we aim...
Multiple disease processes are associated with cognitive impairment in Parkinson disease (PD), including Lewy bodies, cerebrovascular disease, and Alzheimer disease. It remains unknown whether tau pat...
Common forms of Parkinson's disease have long been described as idiopathic, with no single penetrant genetic factor capable of influencing disease aetiology. Recent genetic studies indicate a clear as...
Proteins associated with sporadic or familial cases of PARKINSON DISEASE.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
Of all the types of Dementia, Alzheimer's disease is the most common, affecting around 465,000 people in the UK. Neurons in the brain die, becuase 'plaques' and 'tangles' (mis-folded proteins) form in the brain. People with Al...