Functional neuroanatomical correlates of eye movements during rapid eye movement sleep in depressed patients

2004 ◽  
Vol 130 (3) ◽  
pp. 259-268 ◽  
Author(s):  
Anne Germain ◽  
Daniel J. Buysse ◽  
Annette Wood ◽  
Eric Nofzinger
2003 ◽  
Vol 64 (2) ◽  
pp. 192-196 ◽  
Author(s):  
Ann L. Sharpley ◽  
Zubin Bhagwagar ◽  
Sepehr Hafizi ◽  
W. Richard Whale ◽  
Harm J. Gijsman ◽  
...  

1981 ◽  
Vol 1 (4) ◽  
pp. 253-260 ◽  
Author(s):  
Toshimasa Fukuda ◽  
Masato Wakakura ◽  
Satoshi Ishikawa

1991 ◽  
Vol 70 (3) ◽  
pp. 1194-1200 ◽  
Author(s):  
J. C. Hendricks ◽  
L. R. Kline

Simultaneous recordings of the diaphragmatic electromyogram (EMG) were made from two separate regions of the costal diaphragm in six normal cats. The diaphragmatic activities were always synchronous and the amplitudes and rates of rise were similar during slow-wave sleep. In contrast, during natural rapid-eye-movement (REM) sleep, different activity was often present in the two leads. These differences were in the time of onset and offset, as well as in the amplitude and spike patterns, and occurred in approximately 5-20% of the diaphragmatic bursts averaged over the entire REM sleep period. With respect to eye movement density, the rate of differential activation was higher during periods of high density (26%) than in the absence of eye movements (1%) in the four animals for which these data were available. Differential activation of portions of the costal diaphragm is apparently a normal event of REM sleep. This could result from descending state-specific phasic neuronal activity that bypasses the medullary respiratory generator. Differential activation of portions of the diaphragm could contribute to disordered ventilation during REM sleep.


1991 ◽  
Vol 38 (3) ◽  
pp. 237-246 ◽  
Author(s):  
Rafael J. Salin-Pascual ◽  
Daniel Granados-Fuentes ◽  
Juan Ramon de la Fuente ◽  
Rene Drucker-Colin

1999 ◽  
Vol 16 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Gérard Emilien ◽  
Jean-Marie Maloteaux

AbstractAbnormalities of circadian rhythms in depressed patients have been noted, including decreased amplitude, distorted waveform, day-to-day instability, and unusual 48 hour periods. Consistent electroencephalographic sleep recording in these patients show a shortened rapid eye movement latency and slow-wave sleep (stages 3 and 4), resulting in an increase in rapid eye movement sleep. This phenomenon appears to be a dependable, measurable marker for diagnosing primary depression. Total sleep deprivation appears to significantly improve mood in a high percentage of depressed patients. Current pharmacological research suggests that drug treatment such as lithium would not affect the intra sleep cycles of the REM stagebut would shift the phase backward and lithium would also shift the phase of circadian rhythm of the daytime sleepiness backward. This paper highlights some of the new approaches for investigating the molecular substrate for the control of circadian rhythmicity and sleep in man and critically examines the hypothesis of the alteration of this mechanism in psychopathology, particularly depression. What is known of the endogenous clock mechanism is discussed with known molecular circadian mechanisms with a view towards understanding how circadian information is transmitted to the rest of the central nervous system and how it is affected in depression.


2016 ◽  
Vol 25 (5) ◽  
pp. 576-582 ◽  
Author(s):  
María Corsi-Cabrera ◽  
Francisco Velasco ◽  
Yolanda del Río-Portilla ◽  
Jorge L. Armony ◽  
David Trejo-Martínez ◽  
...  

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