Narcoleptics not only experience pronounced sleep disturbances, but they also experience cataplexy – the sudden unwanted loss of muscle tone during otherwise normal wakefulness. This review will describe our current understanding of the cells and circuits that mediate REM sleep in both health and disease.ĭisturbances in the normal control of REM sleep underlie cataplexy/narcolepsy and RBD, which are two common and serious sleep disorders. A distributed network of micro-circuits within the brainstem, forebrain, and hypothalamus is required for generating and sculpting REM sleep. Rapid eye movement (REM) sleep is characterized by rapid eye movements, cortical activation, vivid dreaming, skeletal muscle paralysis (atonia), and muscle twitches ( 1– 3). This review synthesizes our current understanding of mechanisms generating healthy REM sleep and how dysfunction of these circuits contributes to common REM sleep disorders such as cataplexy/narcolepsy and RBD. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie narcolepsy/cataplexy and REM sleep behavior disorder (RBD). REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. All rights reserved.Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Since inception of the concept there has been question about the appropriateness of the term "giggle incontinence." This review encourages discussion among readers/clinicians about the term and the essential qualities of the diagnosis.Įnuresis risoria Giggle incontinence Giggle micturition Laughter incontinence.Ĭopyright © 2017 Journal of Pediatric Urology Company. Comprehensive treatment of children with laughter incontinence requires an appreciation of both concepts.
The second emphasizes urologic dysfunction, with biofeedback and bladder retraining as the recommended therapy. The first emphasizes the neurologic origin of the cascade of events during laughter and urination, and draws a likeness to cataplexy and other CNS disorders, and emphasizes treatment with methylphenidate.
There is disagreement about the pathophysiology of laughter incontinence, with two differing explanations. This review provides a historical context for the diagnosis, a summary of what is known about its etiology, and a summary of current treatments. Decades of case studies and small research studies have formed the basis of what is known about giggle incontinence however, much remains unknown about this type of incontinence, leaving the recommendations for clinical management somewhat unguided.Ī systematic review of 22 articles on the topic of "giggle incontinence" and related terms was conducted, including all published articles and commentaries since the term was first seen in print in 1959. Giggle incontinence is a sudden and involuntary episode of urinary incontinence that is provoked by an episode of laughter.
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