15 Nightmare Disorder and Effect on the Brain

Meadow Leech

Learning Objectives

  • Define nightmare disorder.
  • Compare and contrast nightmare disorder to other types of parasomnias.
  • Describe the causes of nightmare disorder.
  • Compare and contrast nightmare disorder treatment options.
  • Explain what brain regions are involved, and how their involvement in other functions might explain nightmares.

Nearly everybody can recall having a nightmare at some point in their lives. One study done by the American Academy of Family Physicians found that 47% of surveyed undergraduate students had a nightmare in the last two weeks [4]. Nightmares are unpleasant, vivid, and upsetting dreams, typically occurring during the REM stage of sleep, and can be recalled being awoken. The main distinction between a nightmare and a bad dream is that the latter does not wake you up, despite both containing frightening content [1]. What separates a nightmare from night terrors is that night terrors result in screaming or flailing but affected people won’t recall the event. When an individual has nightmares that occur frequently, to the extent that their daily lives are affected, they may have a type of parasomnia called nightmare disorder [1].

The aetiology of nightmare disorder is still being researched, the leading theories suggest hyperarousal and impaired fear extinction are what causes the disorder. Individuals with nightmare disorder often have a hyperactivity to negative stimuli, even when the stimuli may be considered mild to somebody else [2]. The accumulation of hyperarousal throughout the day and carries into night, triggering nightmares [1]. Hyperarousal is also a primary pathophysiological factor in other disorders, such as PTSD and insomnia [1,2]. Patients with PTSD often report frequent nightmares, and they also typically display a reduced tolerance and hypersensitivity to stimuli that could be perceived as a threat, without the stimuli being explicitly negative [2], for example, loud noises. While nightmare disorder patients report less distress than PTSD patients, the similarities can still be useful in identifying the aetiology [2].

Healthy sleepers with normally functioning fear extinction are able to recombine negative memories with novel and dissociated contexts [1]. In contrast, individuals who can’t supress the arousing memories, and reinforce the fear memories by activate them in fragments during sleep [1], could be described as having impaired fear extinction. Afferent load is the determinant for the ongoing need to develop new fear extinction memories, and maintaining fear extinction memories [5], in other words, it is a determinant of how negative and stressful events influence our ability to regulate our emotions. Contrastingly, afferent distress is the tendency to react to negative and stressful events with distress [1]. People with high afferent load and afferent distress are more likely to have impaired fear extinction [2], and people with impaired fear extinction are more likely to have nightmares that constitute a clinical problem such as nightmare disorder [1]. Additionally, certain medications and drugs can cause frequent nightmares, particularly substances that influence norepinephrine, serotonin, and dopamine neurotransmitters. This suggests that there may be chemosensory pathways facilitating nightmares, though more research is required as not all results are consistent [1].

One study collected fMRI data of four men and eleven women with nightmare disorder experiencing an episode of frequent nightmares. The anterior cingulate cortex (ACC) plays an important role in mood regulation, and when fMRI data is collected during the REM stage of sleep, the ACC is intensely activated, along with the ventromedial prefrontal cortex, and the amygdala [2]. This suggests that the inability to regulate emotions is related to nightmare disorder. There was also high activation of the inferior parietal lobule in the fMRI data. The inferior parietal lobule plays a role in mediating spatial perception, which is involved in allowing us to recognize and react to some threats. Patients with PTSD also have high activation inferior parietal lobule during episodes of intrusive thought or intense nightmares. This suggest that the hyperarousal experienced by people with nightmare disorder, as well as PTSD, is linked to the high activation of the inferior parietal lobule [2].

There are a few different approaches to treatment of nightmare disorder, and they all treat nightmares as an overlearned behavior that needs to be unlearned [1]. One technique is desensitization and exposure therapy. The technique works by instructing the patient to visualize the nightmare(s) while awake, and relax their muscles whenever they experience tension, or asked to visualize the nightmare(s) while awake without the muscle relaxation [1]. This technique is controversial because of the potential for patient distress. Medication and imagery rehearsal treatment are two of the more commonly used methods. Imagery rehearsal treatment works by instructing patients to alter the ending of their nightmare while they are conscious to a more pleasant conclusion, so that it no longer resembles a nightmare and begins to resemble a normal or good dream. They are then asked to rehearse this dream in their head a few times a day, so it will occur while sleeping. Patients undertaking imagery rehearsal treatment report fewer and less intense dreams, as well as no adverse effects. [1]. Lucid dreaming may also be used as treatment [1], though lucid dreaming is rare without a great deal of practice and training. Like imagery rehearsal therapy, patients change the script of their story to a pleasant one, though they can consciously influence the dream as they are having it rather than rehearsing beforehand [1]. 

References

[1] Gieselmann, A., Ait Aoudia, M., Carr, M., Germain, A., Gorzka, R., Holzinger, B., Kleim, B., Krakow, B., Kunze, A. E., Lancee, J., Nadorff, M. R., Nielsen, T., Riemann, D., Sandahl, H., Schlarb, A. A., Schmid, C., Schredl, M., Spoormaker, V. I., Steil, R., … Pietrowsky, R. (2019). Aetiology and treatment of nightmare disorder: State of the art and future perspectives. Journal of Sleep Research, 28(4). https://doi.org/10.1111/jsr.12820

[2] Nielsen, T., & Levin, R. (2007). Nightmares: A new neurocognitive model. Sleep Medicine Reviews, 11(4), 295–310. https://doi.org/10.1016/j.smrv.2007.03.004

[3] Pagel, J. F. (2000). Nightmares and Disorders of Dreaming. American Academy of Family Physicians, 2037–2042.

[4] Shen, C., Wang, J., Ma, G., Zhu, Q., He, H., Ding, Q., Fan, H., Lu, Y., & Wang, W. (2016). Waking-hour cerebral activations in nightmare disorder: A resting-state functional magnetic resonance imaging study. Psychiatry and Clinical Neurosciences, 70(12), 573–581. https://doi.org/10.1111/pcn.12455

 

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