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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
This phenomenon is thought to be caused by intrusion of the atonia of REM sleep into the wakeful state. Extraocular muscles and muscles of respiration are not affected. Attacks are often triggered by positive emotions, such as amusement, surprise, and elation, but may also occur with negative emotions such as anger or fear, though this is less common. The distribution of weakness from the atonia is variable, ranging from total postural collapse to minor forms involving focal muscle groups: buckling of the knees, dropping of the head, sagging of the face or jaw, or merely slurred speech. Consciousness is preserved and the duration is short, ranging from a few seconds to a few minutes. Recovery is rapid and complete. Cataplexy can be quite severe around the onset of the disease.
Extraordinary dreams
Published in Josie Malinowski, The Psychology of Dreaming, 2020
None of this is unusual, strange, or irregular in REM sleep, but what is irregular is that we aren’t supposed to suddenly wake up in our bed with all of these REM sleep physiological changes still occurring. But for some people, for various reasons, these aspects of REM sleep may intrude into wakefulness, and these physiological changes that we go through in REM sleep match up closely to the sleep paralysis experience. Muscle atonia accounts for the paralysis; hypoxia, and the effect on breathing of sleeping on your back, account for the feeling of suffocation or chest pressure; activation of the amygdala accounts for fear; excitation of the genitals accounts for the occasionally sexual nature of sleep paralysis; an active threat-detection system accounts for the harm that the entity often means.
Sleep Promoting Improvement of Declarative Memory
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
The medullary center inhibits the motor neurons and gives rise to atonia. A lateral locomotor strip, down the outside of the brain stem, plays an important role in the reduction of the motor drive. It is connected to structures in the spinal cord. In REM sleep the pons stimulates the inhibitory zone, turning off the locomotor strip and shutting down the motor drive.
Correlations with REM sleep behavior disorder severity in isolated rapid eye movement sleep behavior disorders patients
Published in International Journal of Neuroscience, 2023
Sang Jin Kim, Eun Ju Chung, Ki-Hwan Ji, Mi-Ri Kang, Jin Yong Hong, Sunseong Lee, Ji Sun Park, Jungsu S. Oh, Jae Seung Kim, Suk Yun Kang
Seventeen of 21 iRBD patients underwent one full-night of video-polysomnography (PSG) recording in the sleep laboratory, according to a standard protocol. The parameters for the percentage of tonic rapid eye movement (REM), percentage of phasic REM events, motor events, and vocalizations were assessed. Tonic and phasic REM were determined according to American Academy of Sleep Medicine (AASM) criteria [13]. Motor events, vocalizations, and REM sleep disorder severity scale (RBDSS) were defined as in a previously published study [14]. Motor events were rated according to movement locality and severity: 0, no visible movement but the presence of REM sleep without atonia (RWA); 1, slight movements including facial movements, jerks, or movements restricted to the distal extremities; 2, movements involving the proximal extremities and complex and/or violent behaviors; 3, any axial involvement with the possibility of falling or an observed fall. Vocalization was scored as 0 (no vocalization) or 1 (all sleep-associated sounds other than respiratory noises). The RBDSS is composed of each highest score for motor events and vocalizations. Motor and vocalization scores are separated by a full stop in behavior [14].
Pitolisant for the treatment of cataplexy in adults with narcolepsy
Published in Expert Opinion on Orphan Drugs, 2021
Gerard J. Meskill, Ulf Kallweit, Donna Zarycranski, Christian Caussé, Olivier Finance, Xavier Ligneau, Craig W. Davis
In the absence of adequate hypocretin activity, patients with NT1 experience not only EDS but also REM sleep dysregulation, which manifests as elements of REM sleep occurring during wakefulness or sleep-wake transitions (i.e. cataplexy, sleep paralysis, hypnagogic hallucinations) [2,9,10]. Muscle atonia is a normal characteristic of REM sleep [18]. During wakefulness, muscle tone is maintained by activity in several neural pathways, including REM sleep-suppressing neurons in the ventrolateral periaqueductal gray and lateral pontine tegmentum (vlPAG/LPT), norepinephrine neurons of the locus coeruleus, serotonin neurons of the dorsal raphe nucleus, and acetylcholine neurons in the lateral dorsal tegmental/pedunculopontine tegmental (LDT/PPT) nuclei [10,12,18–20]. Cataplexy is thought to result from the intermittent activation of REM sleep atonia circuitry, which allows the intrusion of this REM sleep manifestation (i.e. muscle atonia) into wakefulness [9,10,18,21]. Strong emotions activate neural pathways in the prefrontal cortex and amygdala, and hypocretin functions to suppress atonia during normal wakefulness [12,20,21]. Due to the lack of adequate hypocretin activity in patients with NT1, the experience of strong emotions can lead to disinhibition of neurons in the REM sleep atonia circuit and reduced activity in neural pathways that maintain normal muscle tone, which results in the occurrence of muscle atonia during wakefulness (i.e. cataplexy; Figure 1) [9,10,12,18,20,21].
Therapeutic approach to difficult-to-treat typical absences and related epilepsy syndromes
Published in Expert Review of Clinical Pharmacology, 2021
Giovanni Mastroianni, Michele Ascoli, Sara Gasparini, Francesco Brigo, Vittoria Cianci, Sabrina Neri, Emilio Russo, Umberto Aguglia, Edoardo Ferlazzo
Typical absences (TAs) are brief (~5–30 seconds) generalized epileptic seizures of abrupt onset and termination, clinically presenting with impairment of awareness combined or not with other manifestations (see below). Impairment of awareness is usually associated with sudden onset and interruption of ongoing activities, often with a blank stare, with immediate return to the baseline level of awareness and activity [1]. If the impairment of awareness is less severe, the patient may not stop ongoing activities, although reaction time and speech may be slow. Other common ictal manifestations include automatisms, myoclonia, tonic, atonic, or autonomic phenomena. Myoclonic jerks may be rhythmic or arrhythmic, single or repeated, and may involve the eyelids, mouth, trunk, and limbs, the most common being eyelid myoclonia. Atonic phenomena can manifest with head drop, dropping of the arms, and very rarely falls due to lower limb atonia. Tonic phenomena can involve facial and neck muscles. TAs are typically elicited by hyperventilation. Activation by photic stimulation or thinking may rarely occur [2].