How to manage daytime sleepiness associated with Parkinson's disease.
Summary of "How to manage daytime sleepiness associated with Parkinson's disease."
Excessive daytime sleepiness (EDS) is frequent in Parkinson's disease. It should be explored by an Epworth sleepiness scale, a nighttime sleep recording and multiple sleep latency tests. EDS can be secondary to disturbed nighttime sleep that should be explored first. The main reasons for nighttime sleep disturbances are pain, nycturia, restless legs syndrome, obstructive sleep apnea syndrome and depression. They should be treated step by step. EDS can also be secondary to antiparkinsonien dopaminergic treatments that can induce nighttime insomnia and/or daytime sleepiness sometimes with sleep attacks. Treatment modifications and, when indicated, deep brain stimulation can improve these symptoms. Furthermore, EDS can be secondary to the disease itself modifying the sleep wake regulation systems. When the treatment of disturbed nighttime sleep and adjustments of the dopaminergic treatments are not sufficient to improve EDS, wake promoting treatments can be used. Their efficacy is variable but new hopeful drugs are coming soon.
Unité des troubles du sommeil, service de neurologie, CHU Gui-de-Chauliac, 80, avenue Augustin-Fliche, 34295 Montpellier cedex 5, France.
This article was published in the following journal.
Name: Revue neurologique
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20813386
- DOI: http://dx.doi.org/10.1016/j.neurol.2010.07.015
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Medical and Biotech [MESH] Definitions
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)
A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.