Cerebral
A. Sahib El-Radhi in Paediatric Symptom and Sign Sorter, 2019
Children require sufficient sleep, but the amount required as sufficient varies. Young infants need on average 14 hours of sleep per 24 hours, which is almost evenly distributed throughout the day and night due to incompletely developed circadian rhythm. Children aged 6–12 years require about 10–11 hours and teens about 9 hours. Insomnia is characterised by difficulty in initiating and/or maintaining sleep, waking too early or having restless sleep. It is fairly normal for infants to wake several times at night; some 30% of infants do this. Older children (4–12 years) commonly present with bedtime resistance. Insufficient sleep at night is likely to affect the child's mood and behaviour during the day, leading to school problems such as reduced attention span, aggressiveness and poor performance. Sleep-related breathing disorders include central sleep apnoea and obstructive sleep apnoea. Parasomnia is disruptive sleep-related disorders occurring during the non-rapid eye movement (NREM) sleep such as sleepwalking, sleep terrors and confusional arousal. Those disorders occurring during rapid eye movement (REM) sleep include absent sleep paralysis. Hypersomnia, or excessive sleep, includes narcolepsy.
Sleep, sedation and coma
Ad (Sandy) Macleod, Ian Maddocks in The Psychiatry of Palliative Medicine, 2018
There is a normal circadian propensity to feel sleepy in the early to mid afternoon. In the general population, 11% of women and 6.7% of men reported daytime sleepiness most days.10 Drowsiness, mental blunting or torpidity (a mild reduction in alertness) may be disease related, symptomatic of early delirium, or a consequence of medicinal oversedation. Dissociative type disorders of consciousness are not usually encountered in palliative care practice. Disease burden and fatigue cause excessive daytime sleep. Cerebral injury and degenerative disorders usually cause hypersomnia (and REM behavioural disorders) rather than insomnia. The fatigue associated with CNS damage is profound, accounting for excessive sleep. Returning to infantile sleeping patterns can occur in the twilight of life. Hypersomnia is a symptom of atypical (hibernatory) depression. Sedative adverse effects of medications are potentially correctable, and should be considered in all such clinical situations. Tricyclic antidepressants, anti-emetics (cyclizine, metoclopramide), antipsychotics (levomepromazine), benzodiazepines and opioids can all have residual daytime effects. SSRIs occasionally are associated with daytime sleepiness, perhaps in part because of insufficient sleep. A few escape the worries of life by sleeping (and requesting sedation) and withdrawing (often an indication of depression). Excess sleep, more than 10 hours in normal persons, can be associated with the ‘blah’ syndrome, which consists of tiredness, lethargy and difficulties in thinking and getting going in the morning.11 Oversleeping does not refresh.
Classification of sleep disorders
S.R. Pandi-Perumal, Meera Narasimhan, Milton Kramer in Sleep and Psychosomatic Medicine, 2017
Idiopathic hypersomnia is now a single entity with elimination of the two ICSD-2 hypersomnia disorders that had specific sleep duration criteria. Idiopathic hypersomnia disorder requires sleepiness for at least 3 months and either an MSLT mean sleep latency of 8 minutes or less or a nocturnal sleep duration of at least 660 minutes. The ICSD-2 category of recurrent hypersomnia has been reduced to a single entry of Kleine–Levin syndrome, with a subtype of menstrual-related Kleine–Levin syndrome.8 The sleepiness must persist for 2 days to 5 weeks, and at least once every 18 months. There can be only one symptom with sleepiness consisting of cognitive dysfunction, altered perception, eating disorder, or disinhibited behavior. Normal alertness and cognitive function must be present between episodes. Hypersomnia due to a medical disorder requires an association of sleepiness with any underlying medical or neurological disorder. Seven subtypes are mentioned: hypersomnia secondary to Parkinson’s disease; posttraumatic hypersomnia; genetic disorders associated with primary central nervous system somnolence; hypersomnia secondary to brain tumors, infections, or other central nervous system lesions; hypersomnia secondary to endocrine disorder; hypersomnia secondary to metabolic encephalopathy; and residual hypersomnia in patients with adequately treated OSA.
Pharmacological options for narcolepsy: are they the way forward?
Published in Expert Review of Neurotherapeutics, 2023
Vivien C. Abad
Lack of clear understanding of the neurobiological mechanisms associated with the various central hypersomnia disorders underlies the imprecision in current diagnostic criteria. Diagnostic criteria (ICSD-3) for narcolepsy have been criticized for being imprecise in terminology and consistency (e.g., hypersomnolence describing both a symptom and a group of disorders) [30] and in the identification of cataplexy and the exclusion of disease mimics; they are cumbersome to use and insufficiently distinguish between various clinical phenotypes and etiologies of narcolepsy [14]; and they rely significantly on the MSLT results, even though the test has low sensitivity and specificity from the diagnostic standpoint [30]. Maski et al. indicate that inadequate definitions in ICSD-3 and inconsistent standards for performing tests are challenging, that the MSLT is often unreliable in differentiating NT2 from idiopathic hypersomnia, and that diagnostic uncertainty and limited access to treatments may cause patients to suffer [31]. There is also a proposal to combine idiopathic hypersomnia without long sleep time with NT2 [32]. Using a data driven approach, Gool et al. identified distinct patient subgroups within the central hypersomnia population, and their results challenge the inclusion of sleep onset rapid eye movement periods (SOREMPs) in diagnostic criteria for patients without cataplexy; they suggest a cluster-guided classification [33].
A Latent Profile Analysis of Sleep, Anxiety, and Mood in Youth with Craniopharyngioma
Published in Behavioral Sleep Medicine, 2022
Sara M. Witcraft, Molly E. Wickenhauser, Kathryn M. Russell, Belinda N. Mandrell, Heather M. Conklin, Thomas E. Merchant, Valerie McLaughlin Crabtree
The novel findings of the present study contribute to the understanding of craniopharyngioma-related morbidity but have not yet uncovered how these varying sleep profiles may be related to daytime functioning. Although we did not find a significant relationship between disrupted sleep and anxiety or depression in patients with craniopharyngioma, our patients would still likely benefit from interventions to improve nighttime sleep and daytime sleepiness. Preliminary evidence suggests that cognitive behavioral therapy for hypersomnia (CBT-H) is efficacious for reducing hypersomnia (Ong et al., 2020). CBT-H is a modular and idiographic intervention for daytime sleepiness that uses behavioral (e.g., scheduled naps) and cognitive strategies (e.g., enhancing cognitive flexibility) to maintain valued living and improve health-related quality of life (Ong et al., 2020). Although CBT-H has only been examined in an adult population to date, the individual components are efficacious in the treatment of sleep disturbance (Harvey, 2016) in youth. Providers may consider incorporating individual or group CBT-H for youth with craniopharyngioma to reduce daytime sleepiness and enhance quality of life. Further research implementing cognitive-behavioral interventions for hypersomnia in youth is needed to provide pertinent information about the benefits of targeting sleep on daily functioning.
How Does Narcolepsy Impact Health-Related Quality of Life? A Mixed-Methods Study
Published in Behavioral Sleep Medicine, 2021
Jason C. Ong, Rina S. Fox, Rylee F. Brower, Sophia Mazurek, Cameron Moore
Currently, there are no formal interventions directly aimed at improving HRQoL in PWN. To address this clinical need, our lab has begun work on developing a psychosocial intervention for PWN following a phased approach recommended for behavioral treatment development (Czajkowski et al., 2015; Rounsaville, Carroll, & Onken, 2001). In an early Phase I study, we examined the need and potential interest in non-pharmacological approaches to help improve psychosocial functioning and symptom management in people with hypersomnia (Neikrug et al., 2016). Between 61% and 91% endorsed at least one cardinal symptom of depression and anxiety. Furthermore, 73.9% reported being “somewhat” or “extremely” interested in learning cognitive and behavioral strategies for improving psychosocial functioning and managing symptoms of narcolepsy. These data provide support for the interest and acceptability of a psychosocial intervention for narcolepsy.
Related Knowledge Centers
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