Modafinil treatment of pramipexole-associated somnolence

Hauser, Robert A.; Wahba, Mervat; Zesiewicz, Theresa A.; Anderson, William

doi:10.1002/1531-8257(200011)15:6<1269::aid-mds1036>3.0.co;2-r

Cited by 55 publications

(20 citation statements)

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“…Recent evidence indicates that modafinil is effective in the treatment of excessive day-time sleepiness (and fatigue) in disorders other than narcolepsy, e.g. idiopathic hypersomnia (Ivanenko et al 2003), night-shift sleep disorder (Walsh et al 2004), obstructive sleep apnoea (Pack et al 2001), multiple sclerosis (Rammohan et al 2002), Parkinson's disease (Adler et al2003), myotonic dystrophy (MacDonald et al 2002), depression (DeBattista et al 2003), schizophrenia (Rosenthal and Bryant 2004) and drug-induced sedation (Hauser et al 2000;Webster et al 2003;Larijani et al 2004). It has been shown that modafinil's action is different from that of the psychostimulant amphetamine: whereas excessive day-time sleepiness is effectively alleviated by modafinil, there is little psychomotor agitation or interference with night-time sleep (Saletu et al 1989;Buguet et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Does modafinil activate the locus coeruleus in man? Comparison of modafinil and clonidine on arousal and autonomic functions in human volunteers

et al. 2005

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Section: Introductionmentioning

confidence: 99%

Does modafinil activate the locus coeruleus in man? Comparison of modafinil and clonidine on arousal and autonomic functions in human volunteers

et al. 2005

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“…It has also been shown to alleviate the EDS associated with a number of other conditions (Parkinson's disease: Nieves and Lang, 2002;idiopathic hypersomnia: Ivanenko et al, 2003;night shift sleep disorder: Walsh et al, 2004; obstructive sleep apnoea: Pack et al, 2001; multiple sclerosis: Rammohan et al, 2002;myotonic dystrophy: MacDonald et al, 2002;depression: DeBattista et al, 2003;schizophrenia: Rosenthal and Bryant, 2004;sleep deprivation: Pigeau et al, 1995; and drug-induced sedation: Webster et al, 2003). Interestingly, in a case study of a PD patient, modafinil was found to reverse the sedative effect of pramipexole (Hauser et al, 2000b). The mode of action of modafinil is unclear, but it appears to involve dopaminergic and/or noradrenergic arousal pathways (Saper and Scammell, 2004) and has been found to increase extracellular levels of dopamine (Wisor et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Comparison of pramipexole and modafinil on arousal, autonomic, and endocrine functions in healthy volunteers

Samuels

Hou²,

Langley³

et al. 2006

J Psychopharmacol

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The noradrenergic locus coeruleus is a major wakefulness-promoting nucleus of the brain, which is also involved in the regulation of autonomic and endocrine functions. The activity of the locus coeruleus is believed to be tonically enhanced by a mesocoerulear dopaminergic pathway arising from the ventral tegmental area of the midbrain. Both modafinil, a wakefulness-promoting drug, and pramipexole, a D(2)/D(3)receptor agonist with sedative properties, may act on this pathway, with modafinil increasing and pramipexole decreasing locus coeruleus activity. The aim of this study was to compare the two drugs on alertness, autonomic and endocrine functions in healthy volunteers. Pramipexole (0.5mg), modafinil (200mg), and their combination were administered to 16 healthy males in a double-blind, placebo-controlled design. Methods included tests of alertness (pupillographic sleepiness test, critical flicker fusion frequency, visual analogue scales), autonomic functions (resting pupil diameter, light and darkness reflex responses, heart rate, blood pressure, salivation, core temperature), and endocrine functions (blood concentrations of prolactin, growth hormone, and thyroid stimulating hormone). Data were analysed by ANOVA. Pramipexole reduced alertness, caused pupil dilatation, increased heart rate, reduced prolactin and thyroid stimulating hormone, and increased growth hormone level. Modafinil caused small increases in blood pressure and core temperature, and reduced prolactin levels. The sedative effect of pramipexole and the autonomic effects of modafinil are consistent with altered activity in the mesocoerulear pathway; the pupil dilatation following pramipexole suggests reduced dopaminergic excitation of the Edinger-Westphal nucleus.

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“…Prescribing wake promoting agents such as modafinil, bupropion, or traditional psychostimulants seems justified upon identification of a narcolepsy-like phenotype or an MSL score of less 8 minutes. Initial open-label experiences with modafinil in PD patients with drug-related drowsiness were encouraging [59][60][61][62]. Two double-blind, randomized, placebo-controlled studies demonstrated improvements in a subset of patients [63,64], but these could not be corroborated by objective MWT testing [64].…”

Section: General Approach and Managementmentioning

confidence: 99%

“…Modafinil appears to promote wakefulness by improving dopaminergic transmission [71], although its precise mechanism of action is unknown. Experience and success with modafinil for parkinsonian-related sleepiness includes several case reports [59,61,62], including one open-label trial in 10 patients [60], and two larger double-blind, placebocontrolled trials [63,64]. Modafinil is well tolerated by older patients, has no apparent interactions with antiparkinsonian medications, and adverse effects upon the clinical severity of PD have not been reported.…”

Section: Modafinilmentioning

confidence: 99%

Excessive daytime sleepiness and unintended sleep in Parkinson’s disease

Rye

2006

Curr Neurol Neurosci Rep

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Patients with Parkinson's disease and parkinsonian syndromes (eg, dementia with Lewy body disease, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. This sleepiness is common and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, namely narcolepsy/cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Male patients with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics exacerbate sleepiness in a small subset of patients in a dose-dependent fashion. Nonetheless, the primary pathologies involved in parkinsonism appear to be the greatest contributors to daytime sleepiness. Sleepiness in parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents such as bupropion, modafinil, or traditional psychostimulants.

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Modafinil treatment of pramipexole-associated somnolence

Cited by 55 publications

References 12 publications

Does modafinil activate the locus coeruleus in man? Comparison of modafinil and clonidine on arousal and autonomic functions in human volunteers

Does modafinil activate the locus coeruleus in man? Comparison of modafinil and clonidine on arousal and autonomic functions in human volunteers

Comparison of pramipexole and modafinil on arousal, autonomic, and endocrine functions in healthy volunteers

Excessive daytime sleepiness and unintended sleep in Parkinson’s disease

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