832 Dose-Dependent Quetiapine-Induced Somnambulism and Sleep-Related Eating Disorder

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A324-A324
Author(s):  
Tuyet Pham ◽  
Sonal Malhotra

Abstract Introduction Parasomnias are abnormal sleep-related movements that can occur during non-rapid eye movement sleep, rapid eye movement sleep, or transition of sleep. The prevalence of parasomnias in young children ranges from 9–40% which may be underestimated as this relies on parental recall. There are multiple reported cases of pharmacologically-induced parasomnias. Quetiapine is an atypical antipsychotic medication associated with somnambulism and sleep-related eating disorder. Report of case(s) A 9-year-old female with a history of attention deficit hyperactivity disorder, post-traumatic-stress disorder, depression, and sexual abuse during childhood presented to the Sleep Medicine Clinic for two years of worsened sleepwalking and sleep eating. Her medications included Methylphenidate, Quetiapine, Clonidine, and Duloxetine. She has had parasomnias since she was 3-years-old, initially presenting as abnormal sleeping positions (standing or sitting). She was initiated on Seroquel at 4-years-old, but parasomnias worsened over the last two years when Quetiapine was increased from 50 mg to 200 mg for behavioral and mood issues. Her somnambulism began to occur nightly. The family was required to remove all items from her bedroom except for the bed to prevent major injuries. She also had significant changes to her eating habit: she would eat two to three times her normal quantity as well as eating while asleep. The family would find her eating ice cream, chips, grapes, cold tortillas, or anything she was able to access. Fortunately, she did not consume raw meat or other frozen foods. The child did not have any recollection of eating at night. Psychiatry worked with her to cross-taper Quetiapine and Topiramate. At the lower dose of Quetiapine, she had exacerbation of her mood symptoms, paranoia, and insomnia; therefore, Topiramate was discontinued and Quetiapine was titrated to 150 mg with improvement in mood symptoms, insomnia, and resolution of sleep-related eating disorder. She continues to have somnambulism. Conclusion This case illustrates that quetiapine-induced somnambulism and sleep-related eating disorder can be dose-dependent; thus, important for clinicians to educate patients and/or family members of adverse effects while titrating quetiapine. Support (if any):

PEDIATRICS ◽  
1985 ◽  
Vol 75 (5) ◽  
pp. 832-835
Author(s):  
William C. Orr ◽  
Monte L. Stahl ◽  
James Duke ◽  
Mary Anne McCaffree ◽  
Paul Toubas ◽  
...  

Sixty-four infants with a history of apnea were studied to determine the effects of sleeping position and sleep state (rapid eye movement [REM]) v (nonrapid eye movement [NREM]) on the occurrence of central and obstructive apneas. All-night polysomnographic studies were conducted on each infant, and the spontaneous occurrence of central and obstructive apneic events was determined in the prone, supine, and side positions. Sleeping position did not significantly affect the rate or duration of central or obstructive apneas. Furthermore, neither central nor obstructive apneic episodes were significantly altered by sleep state. These data suggest that, in spite of an ostensible predisposition to upper airway obstruction in the supine position and during rapid eye movement sleep, neither sleeping position nor sleep state appears to affect the rate of duration of apneic events.


1993 ◽  
Vol 74 (2) ◽  
pp. 545-548 ◽  
Author(s):  
T. Sato ◽  
M. Tadokoro ◽  
H. Kaba ◽  
H. Saito ◽  
K. Seto ◽  
...  

The presence of endogenous digitalis-like factors in the central nervous system suggests their functional significance in the central nervous system. Three-day infusions of three-stepped doses of the digitalis agent ouabain (1–100 ng.kg body wt-1.h-1) into the lateral cerebral ventricle of freely moving rats caused a dose-dependent increase in the number of central-apneic episodes during rapid-eye-movement sleep without affecting the time spent in rapid-eye-movement sleep or basic respiratory rate. These results suggest that endogenous digitalis-like factors may be involved in the genesis of central sleep apneas.


2009 ◽  
Vol 110 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Matthias Eikermann ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
Carl Rosow ◽  
...  

Background Anesthetics depress both ventilatory and upper airway dilator muscle activity and thus put the upper airway at risk for collapse. However, these effects are agent-dependent and may involve upper airway and diaphragm muscles to varying degrees. The authors assessed the effects of pentobarbital on upper airway dilator and respiratory pump muscle function in rats and compared these results with the effects of normal sleep. Methods Tracheostomized rats were given increasing doses of pentobarbital to produce deep sedation then light and deep anesthesia, and negative pressure airway stimuli were applied (n = 11). To compare the effects of pentobarbital with those of natural sleep, the authors chronically instrumented rats (n = 10) with genioglossus and neck electromyogram and electroencephalogram electrodes and compared genioglossus activity during wakefulness, sleep (rapid eye movement and non-rapid eye movement), and pentobarbital anesthesia. Results Pentobarbital caused a dose-dependent decrease in ventilation and in phasic diaphragmatic electromyogram by 11 +/- 0.1%, but it increased phasic genioglossus electromyogram by 23 +/- 0.2%. Natural non-rapid eye movement sleep and pentobarbital anesthesia (10 mg/kg intraperitoneally) decreased respiratory genioglossus electromyogram by 61 +/- 29% and 45 +/- 35%, respectively, and natural rapid eye movement sleep caused the greatest decrease in phasic genioglossus electromyogram (95 +/- 0.3%). Conclusions Pentobarbital in rats impairs respiratory genioglossus activity compared to the awake state, but the decrease is no greater than seen during natural sleep. During anesthesia, in the absence of pharyngeal airflow, phasic genioglossus activity is increased in a dose-dependent fashion.


2021 ◽  
Vol 11 (1) ◽  
pp. 1-5
Author(s):  
Harinder Jaseja

Epilepsy is one of the commonest and oldest neurological diseases in the history of mankind, the exact pathophysiology of the evolution of which still remains elusive. The intimate and intriguing relation between epilepsy and sleep has been known for a long time. Rapid eye movement sleep (REMS) is well documented to exert potent antiepileptic action in human epilepsies and the underlying mechanism of which is largely based on its property to induce widespread electroencephalogram (EEG)-desynchronization. The pedunculopontine nucleus (PPN) owing to its property to enhance REMS has recently been under study for its potential role in intractable epilepsy (IE) and has been proposed as a novel deep brain stimulation target in IE. This brief paper unfolds the existing role of PPN, REMS, and EEG-desynchronization (PRED) in the evolution of epilepsy in an axial manner, the realization and comprehension of which is likely to open new avenues for further understanding of epileptogenesis, improved treatment of epilepsy and reducing the risk of IE.


Sign in / Sign up

Export Citation Format

Share Document