Sleep Paralysis and Anxiety Disorders Studies have suggested that individuals who suffer from an anxiety disorder are more likely to experience isolated sleep paralysis. Sleep paralysis is the inability to make voluntary movements during the onset of sleep called hypnagogic sleep paralysis or upon awakening called hypnopompic sleep paralysis. During sleep, the body alternates between REM (rapid eye movement) and NREM (non-rapid eye movement). During REM sleep, the body goes into a state of paralysis to keep the person from acting out their dreams. A person experiences sleep paralysis when they become aware before the end of the REM cycle, therefore experiencing the inability to move or talk and often experiencing hallucinations.
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A study by Otto, Simon, Powers, Hinton, Zalta, & Pollack (2005) aimed to distinguish the rates of isolated sleep paralysis among those with panic disorder, social anxiety disorder, and generalized anxiety disorder (GAD). Sixty-one individuals between the ages of 30 and 56 took part in the study with 43% being women. Participants were outpatients seeking treatment for panic disorder with or without agoraphobia, social anxiety, or GAD. Researchers assessed the participants sleep paralysis using a self-report Sleep Experience Questionnaire. Results showed that 12 of the 61 (19.7%) participants reported symptoms consistent with sleep paralysis. The rates of isolated sleep paralysis were not significantly different by anxiety diagnosis. Also, while 16 patients were taking antidepressants during the time of assessment, there was no indication of association between medication use and isolated sleep …show more content…
The second study measured cortical functional activity in patients with GAD. Results showed the increase in D2 values in all cerebral regions especially the left cerebral region and right temporal lobe while those with mild anxiety showed increased D2 values in the left prefrontal regions. According to Muzur, Pace-Schott, & Hobson (2002) the transition from waking to NREM is characterized by deactivation in the frontal cerebral cortex. This deactivation increases with the deepening of NREM sleep and stays the same during the transition from NREM to REM. However, during the onset of REM portions of the ventromedial, limbic-related prefrontal cortex and closely associated medial subcortex are reactivated and sometimes reaching levels that are higher than those of waking (Muzur, Pace-Schott, & Hobson 2002). Defective frontal functioning was also observed after sleep deprivation by Muzur, Pace-Schott, & Hobson (2002). If Wang, et. al (2016) concluded that there is an increase in activity in the prefrontal region of those with anxiety, could there possibly be a correlation between the dysfunctional cortical activity from anxiety disorders and sleep paralysis? Future research focused on the cortical activity of those who suffer from anxiety disorder and its correlation between isolated sleep paralysis is needed to further understand the links between the
A study by Otto, Simon, Powers, Hinton, Zalta, & Pollack (2005) aimed to distinguish the rates of isolated sleep paralysis among those with panic disorder, social anxiety disorder, and generalized anxiety disorder (GAD). Sixty-one individuals between the ages of 30 and 56 took part in the study with 43% being women. Participants were outpatients seeking treatment for panic disorder with or without agoraphobia, social anxiety, or GAD. Researchers assessed the participants sleep paralysis using a self-report Sleep Experience Questionnaire. Results showed that 12 of the 61 (19.7%) participants reported symptoms consistent with sleep paralysis. The rates of isolated sleep paralysis were not significantly different by anxiety diagnosis. Also, while 16 patients were taking antidepressants during the time of assessment, there was no indication of association between medication use and isolated sleep …show more content…
The second study measured cortical functional activity in patients with GAD. Results showed the increase in D2 values in all cerebral regions especially the left cerebral region and right temporal lobe while those with mild anxiety showed increased D2 values in the left prefrontal regions. According to Muzur, Pace-Schott, & Hobson (2002) the transition from waking to NREM is characterized by deactivation in the frontal cerebral cortex. This deactivation increases with the deepening of NREM sleep and stays the same during the transition from NREM to REM. However, during the onset of REM portions of the ventromedial, limbic-related prefrontal cortex and closely associated medial subcortex are reactivated and sometimes reaching levels that are higher than those of waking (Muzur, Pace-Schott, & Hobson 2002). Defective frontal functioning was also observed after sleep deprivation by Muzur, Pace-Schott, & Hobson (2002). If Wang, et. al (2016) concluded that there is an increase in activity in the prefrontal region of those with anxiety, could there possibly be a correlation between the dysfunctional cortical activity from anxiety disorders and sleep paralysis? Future research focused on the cortical activity of those who suffer from anxiety disorder and its correlation between isolated sleep paralysis is needed to further understand the links between the