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Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
Pharmacologic stimulants for excessive daytime sleepiness. Dopamine enhancement is the mechanism of action of most of these agents, though the exact mechanism for modafinil and armodafinil remains unclear.
Test Protocols
Published in Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam, Clinical Atlas of Polysomnography, 2018
Ravi Gupta, S. R. Pandi Perumal, Ahmed S. BaHammam
Best measure to rule out the excessive daytime sleepiness is:MSLTDaytime diagnostic sleep studyNighttime diagnostic sleep studyMWT
Fatigue in chronic medical conditions: A psychosomatic perspective
Published in S.R. Pandi-Perumal, Meera Narasimhan, Milton Kramer, Sleep and Psychosomatic Medicine, 2017
M. Zalai Dora, Gottschalk Raymond, Shapiro Colin Michael
Many patients with excessive daytime sleepiness have coexistent complaints of decreased energy and fatigue. However, it is important to note that fatigue (without subjective sleepiness) can be the only symptom of sleep problems. For example, in a sleep clinic sample, 64% of patients reported high fatigue without excessive daytime sleepiness, whereas only 4% reported sleepiness without high fatigue.38
Narcolepsy Treatment: Voices of Adolescents
Published in Behavioral Sleep Medicine, 2022
Lena Xiao, Anna Chen, Arpita Parmar, Lucy Frankel, Alene Toulany, Brian J. Murray, Indra Narang
The main treatment for narcolepsy is pharmacotherapy addressing excessive daytime sleepiness and cataplexy. Excessive daytime sleepiness is often treated with stimulants such as amphetamine, dextroamphetamine, and methylphenidate, as well as wake-promoting agents including modafinil (Thorpy & Bogan, 2020). However, these medications may cause common side effects such as palpitations, anorexia, headache, nervousness, nausea, and insomnia (Black & Hirshkowitz, 2005; Clavenna & Bonati, 2017; Kingshott et al., 2001; Rammohan, 2002). Cataplexy is treated with sodium oxybate, selective serotonin reuptake inhibitors, selective norepinephrine reuptake inhibitors, and tricyclic antidepressants (Wise et al., 2007). Common adverse effects include headache, nausea, epigastric discomfort, weight gain, and dry mouth (Babiker & Prasad, 2015; Kotagal, 2018). Specifically, sodium oxybate is a powerful sedative with the potential for misuse and has an inconvenient dosing regimen requiring a dose in the middle of the night. Tricyclic antidepressants may also cause serious adverse events such as arrhythmias, parkinsonism, neuroleptic malignant syndrome or seizures (Houghton et al., 2004). Overall, the disadvantages of pharmacotherapy in narcolepsy are inconsistent efficacy, development of tolerance, dependence, and nonadherence (Houghton et al., 2004; Pérez-Carbonell et al., 2020). Although there are medications or combinations of medications that are efficacious for narcolepsy, these have to be balanced with side effects, which may negatively impact the adherence with daily treatment over the long-term (Taddeo et al., 2008).
Profile of Somryst Prescription Digital Therapeutic for Chronic Insomnia: Overview of Safety and Efficacy
Published in Expert Review of Medical Devices, 2020
Somryst uses sleep restriction, limiting the time a patient spends in bed to generally match the amount of time they sleep. This treatment technique can increase risks of excessive daytime sleepiness to some patients whose pathophysiology may be worsened by sleep restriction. Because of this, Somryst is not appropriate for everyone. Patients with the following conditions or disorders should not use Somryst: any disorder exacerbated by sleep restriction (eg, bipolar disorder, schizophrenia, other psychotic spectrum disorders), untreated obstructive sleep apnea, parasomnias, epilepsy, individuals at high risk of falls, individuals who are pregnant, individuals who have any other unstable or degenerative illness judged to be worsened by sleep restriction delivered as part of CBT-I.
Factors associated with the remission of insomnia after traumatic brain injury: a traumatic brain injury model systems study
Published in Brain Injury, 2020
Anthony H. Lequerica, Erica Weber, Marcel P. Dijkers, Kristen Dams-O’Connor, Stephanie A. Kolakowsky-Hayner, Kathleen R. Bell, Tamara Bushnik, Yelena Goldin, Flora M. Hammond
Daytime sleepiness showed a marginally significant main effect, with the Persistent group reporting greater sleepiness across time points. Within the Persistent group, a trend toward higher percentages of individuals with excessive sleepiness was noted. While excessive daytime sleepiness is not typical among individuals with primary insomnia who tend to be prone to hyperarousal (55,56), it is possible that the daytime effects of chronic insomnia may be different for individuals with TBI. Previous research has shown a tendency for daytime sleepiness among this group, with the symptom becoming chronic in 25% and 67% of two samples studied (57,58). Individuals with chronic insomnia after TBI may experience an exacerbation of an already existing excessive daytime sleepiness phenomenon. It should be noted that excessive daytime sleepiness may be the result of an undiagnosed sleep disorder such as obstructive sleep apnea (59).