Dreams and Hallucinations

Hallucinations are perceptual experiences in visual, motor, auditory and, in rarer cases, multisensory modalities that occur in the absence of external stimuli [1]. Researchers believe that these experiences have meaningful foundations in the brain's physiology [1]. The causes and subjective experiences are very heterogeneous, and research is attempting to identify the brain substrates responsible for both endogenous and induced hallucinations. Brain imaging studies of hallucinations often reveal activation of cortical areas during hallucinations, for example the frontal and temporal cortices in schizophrenic patients [1], the amygdala, forebrain, and spinal motor mechanisms during sleep states [3], [4], and the serotonin pathway in induced hallucinations [5], [6]. Neurotransmitter activity and dysfunction are commonly implicated as the underlying causes. This includes cholinergic dysfunction [7] and serotonin receptor binding [8], as found in some Parkinson’s
patients. In addition, compounds such as LSD (lysergic acid diethylamide) and DMT (dimethyltryptophan) interact with the central nervous system, inducing intense multimodal perceptual experiences [9]. Various articles have also looked at the psychotherapeutic effects of meditation induced hallucinations [10], [11] both for psychotic disorders as well as the psychological aspect of physical disorders. In sleep, hallucinations are caused by REM states during a physiological phenomenon called sleep paralysis [12], which is confirmed by PET neural activity in specific brain regions [13]. This provides some evidence that activation during REM sleep and wakefulness is quite similar and the content of dreams is not arbitrary.

1. Hobson J.A., Stickgold R., & Pace-Schott E.F. The neuropsychology of REM sleep dreaming. NeuroReport. (1998). (9) 3. R1- R14.
2. Ford, J.M., et al. (2012). Neurophysiological studies of auditory verbal hallucinations. Schizophrenia Bulletin, 38(4).
3. Cheyne, J. A., Newby-Clark, I. R., & Rueffer, S. D. (in press). Sleep paralysis and associated hypnagogic and hypnopompic experiences. Journal of Sleep Research
4. Chase, M. H., & Morales, F. R. (1989). The control of motoneurons during sleep. In M. H. Kryger, T.
5. Krall, C.M., Richards, J.B., Rabin, R.A., & Winter, J.C. (2008). Marked decrease of LSD-induced stimulus control in serotonin transporter knockout mice. Pharmacology biochemistry and behaviour. 88(3), 349-57.
6. Krebs-Thompson, K., Ruiz, E.M., Masten, V., Buell, M., & Geyer, M.A. (2006). The roles of 5-HT1A and 5-HT2 receptors in the effects of 5-MeO-DMT on locomotor activity and prepulse inhibition in rats. Psychopharmacology. 189(3), 319-29.
7. Manganelli, F., et al. (2009). Functional involvement of central cholinergic circuits and visual hallucinations in Parkinson’s disease. Brain, 132(9), 2350-5.
8. Ballanger, B., et al. (2010). Serotonin 2A receptors and visual hallucinations in Parkinson’s disease. Archives of neurology, 67(4), 416-21.
9. Strassman, R. (2001). DMT: The spirit molecule. Rochester, Vermont: Park Street Press.
10. Shapiro, D.H., Jr., Giber, D. (1978). Meditation and psychotherapeutic effects. Self-regulation strategy and altered states of consciousness. Archives of General Psychiatry, 35(3), 294-302.
11. Kelly, B.D. (2008). Buddhist psychology, psychotherapy and the brain: a critical introduction. Journal of Transcult Psychiatry, 45(1), 5-30.
12. Cheyne, J.A. (2005). Sleep paralysis episode frequency and number, types, and structure of associated hallucinations. Journal of Sleep Research, 319-24.
13. Grenell, G. (2008). Affect Integration in Dreams and Dreaming. Journal of the American Psychoanalytic Association, 56(1), 223-251

Dream Content and Cortical Activity Distribution

main article: Dream Content and Cortical Activity Distribution
author: Le-Keng Lin

regional cortical acitivity associated with sleep
Image Unavailable

Significant increase of regional cerebral blood flow(red) in temporo-occipital cortex,
motor cortex, anterior cingulate gyrus, occipital-lateral cortex, parahippocampic gyrus,
and amygdala; Significant decrease of regional cerebral blood flow(blue) in parietal
supramarginal cortex, prefrontal cortex, posterior cingulate gyrus and precuneus.

Retrieved from[1]

Regional cortical activity has always been suspected to be associated with the content of dreams[1] , and through recording its distribution, scientists are hoping to decode the functional meaning of sleep and dreams. And to do so, several techniques imaging neuronal activation such as fMRI
(functional magnetic resonance imaging), PET(positron emission tomography) and MEG(magnetoencephalography) are frequently used. While each identifies a unique set of information based on their method of measurement, the data collected from neural scanning are often combined to be processed as critical insights that lead to educated hypothesis. And by appliying modern cortical imaging techniques, researchers have identified many unique correlations between dream features and localized neuronal activation such as evaluated firing in prefrontal cortex leading to increased lucidity of dreams[2] and hypoactivation of the same area leading to profound temporal disturbance in dreams as well as the result of amnesia[1]. Expanding the area of interest from dreams to hallucination, many neurologists are now interested in comparing the two in terms of their content, brain stimulation and activation mechanism in order to solve the mystery of their phenomenology

1. Schwartz, S., & Maquet, Pierre. (2002). Sleep imaging and the neuropsychological assessment of dreams. Trends in Cognitive Science, 6(1), 23-30.
2. Neider, M., Pace-Schoot, E., Forselius, E., & Morgan, P. (2011). Lucid dreaming and ventromedial versus dorsolateral prefrontal task performance. Consciousness and Cognition, 20(2), 234-244.

Hallucinations During Sleep Paralysis

main article: Hallucinations During Sleep Paralysis
author: Afrin Chowdhury
Sleep paralysis (SP) is a physiological phenomenon that occurs during REM sleep[1]. Researchers claim that sleep paralysis has physiological importance, as during SP, muscle atonia causes the skeletal muscles to paralyse the body, only allowing the eyes to move during REM sleep[1],[2],[3]. This muscle atonia prevents the sleeper from enacting their dreams and harming themselves during REM sleep states[1]. Studies of sleep paralysis and its hallucinations can help researchers to further understand the workings of the human brain. Sleeping individuals experience SP as they transition from REM sleep state to wakefulness[4]. As they transition, most individuals experiencing SP will experience vivid hallucinations. These perceptual experiences can occur at sleep onset and during awakening; these situations are labelled hypnogagic and hypnopompic hallucinations, respectively[4]. The hallucinations are categorized in three ways: Intruder, Incubus and Vestibular- Motor (V- M), which activate the limbic system, parietal operculum , the parietal lobe, and other neurophysiological structures. Recent studies show that trauma, anxiety disorders, sleep disturbances, supine position[2], [4], [5], [7] and the fear emotion [5] play a role in triggering sleep paralysis, while other studies show that the blockage of the GABA and glycine receptors, simultaneously, inhibit muscle atonia during sleep paralysis[1].

Documentary: The Entity
Scientists explanation of sleep paralysis.
ZeEthiopia. (2012, September). Sleep Paralysis. Retrieved from
1. Brooks P.L., Peever J.H. (2012). Identification of the transmitter and receptor mechanisms responsible for REM sleep paralysis. The Journal of Neuroscience. (32)(29). 9785- 9795.
2. Cheyne J. A., Girard T. A. (2009). The body unbound:vestibular- motor hallucinations and out of body experiences. Cortex. (45). 201- 215.
3. Lavigne G. J., Kato A., Kolta A., Sesle B.J. (2003). Neurobiological mechanisms involved in sleep bruxism. (14)(1). 30- 46.
4. McCarthy D. E., Chesson A. L. (2008). A case of sleep paralysis with hypnopompic hallucinations. Journal of Clinical Sleep Medicine. 83- 84.
5. Chayne J.A. (2003). Sleep paralysis and the structure of waking- nightmare hallucinations. Dreaming. (13)(3). 163- 179.
6. McNally R. J., Clancy S.A. (2005). Sleep paralysis, sexual abuse, and space alien abduction. Transcultural Psychiatry. 113-122.
7. Otto M. W., Simon N. M., Powers M., Hinton D., Zalta A. K., Pollack M. H. (2005). Rates of isolated sleep paralysis in outpatients with anxiety disorders. Anxiety Disorders. 687- 693.

Hallucinations in Psychopathologies

main article: Hallucinations in Psychopathologies
author: Djurdja D

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Naturally occurring hallucinations in the waking state (i.e. not induced by drug effects, sleep or meditation) arise from a variety of physiological and psychological conditions. These include Schizophrenia, Parkinson's disease, Narcolepsy and epileptic seizures. Hallucinations also may occur in peripheral nervous system disorders, such as Guillain-Barré syndrome . The neurological bases for these hallucinations are diverse, however in many cases share commonalities. These may include activation of the primary sensory cortices [1], involvement of neurotransmitter systems such as cholinergic dysfunction [2], and abnormal cortical connections [3]. Sleep disorders and dreaming have also been associated with hallucinations in many of these pathologies, including abnormal REM sleep [4] and hypocretin-1 deficiency [5]. Research continues to examine the neurological bases of hallucinations in a variety of pathologies, which will provide insight not only into the causes and potential interventions for these abnormal experiences, but also the general processes of perception in the human brain.

Sacks talks hallucinations
Discussion of hallucinations by acclaimed author and neuroscientist Oliver Sacks,
particularly in patients with Charles Bonnet syndrome.
1. Dierks, T., Linden, D.E.J., Jandl, M., Rofmisano, E., Goebel, R., Lanfermann, H. & Singer, W. (1999). Activation of Heschl’s Gyrus during auditory hallucinations. Neuron, 22(3), 615-621.
2. Manganelli, F., Vitale, C., Santangelo, G., Pisciotta, C., Iodice, R., Cozzolino, A., Dubbioso, R., Picollo, M., Barone, P. & Santoro, L. (2009). Functional involvement of central cholinergic circuits and visual hallucinations in Parkinson’s disease. Brain, 132(9), 2350-5.
3. Hubl, D., Koenig, T., Strik, W., Federspiel, A., Kreis, R., Boesch, C., Maier, S.E., Schroth, G., Loyblad, K. & Dierks, T. (2004). Pathways that make voices: white matter changes in auditory hallucinations. Arch. Gen. Psychiatry, 61(7), 658-668.
4. Cochen, V., Arnulf, I., Neulat, M.L., Gourlet, V., Drouot, X., Moutereau, S., Derenne, J.P., Similowski, T., Willer, J.C., Pierrot-Deseiligny, C. & Bolgert, F. (2005). Vivid dreams, hallucinations, psychosis and REM sleep in Guillain–Barré syndrome. Brain, 128(11), 2535-2545.
5. Leu-Semenescu, S., de Cook, V.C., le Masson, V.D., Debs, R., Lavault, S., Roze, E., Vidailhet, M. & Arnulf, I. Hallucinations in narcolepsy with and without cataplexy: Contrasts with Parkinson’s disease. (2011). Sleep Medicine, 12(5), 497-504.

Meditation-Induced Hallucinations

main article: Meditation-Induced Hallucinations
author: Harshita Jagadeesh

the practice of meditation in a peaceful setting
Image Unavailable
retrieved from Fusionwellness

Meditation is the common practice of concentrating one’s attention upon a single aspect of life[1]. It can be performed for many reasons, including reduction of stress, coping with illness, and promoting personal growth. Common behaviours during meditation include a detachment from external sensory information and an increase in the effects of suggestion[2]. As a result, out of body experiences and hallucinations are frequently reported. Meditation induced hallucinations are even encouraged in some cultures[3] which leads to a different cultural outlook on certain psychotic disorders and therefore differences in patient outcomes of the disorders[3]. Many studies have looked at the psychotherapeutic effects of mediation-induced hallucinations[4][5]both for psychotic disorders as well as the psychological aspect of physical disorders. It has commonly been found that meditation helps to reduce the negative emotions that result from various mental and physical illnesses[4][5]. However, a new study looks at the potential of adverse effects of meditation-induced hallucinations[2]. Although many studies dealing with the topic of meditation tend to be cross-cultural studies or case studies, a novel study by Lehmann et. al (2001)[6] took EEG recordings for five different meditation induced hallucination states to examine which brain areas are involved in these processes. Since then, more research has been made examining brain changes during meditation with fMRI technology. A recent paper displays changes in neural plasticity after mindful-meditation training[7]. Meditation-induced hallucinations are a relatively under-researched area and more still needs to be looked at before the full effects and benefits can be understood.

1. meditation. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved March 7 2013 from http://medical-dictionary.thefreedictionary.com/meditation
2. Kuijpers, HJ, van der Heijden, FM, Tuinier, S, Verhoeven, WM. (2007). Meditation-induced psychosis. Journal of Psychopathology, 40(6):461-4.
3. Castillo, RJ. (2003). Trance, functional psychosis, and culture. Journal of Psychiatry, 66(1):9-21.
4. Shapiro, DH, Giber, D. (1978). Meditation and psychotherapeutic effects. Self-regulation strategy and altered states of consciousness. Archives of General Psychiatry, 35(3):294-302.
5. Kelly, BD. (2008). Buddhist psychology, psychotherapy and the brain: a critical introduction. Journal of Transcult Psychiatry, 45(1):5-30.
6. Lehmann, D, Faber, PL, Achermann, P, Jeanmonod D, Gianotti, LR, Pizzagalli, D. (2001). Brain sources of EEG gamma frequency during volitionally meditation-indued, altered states of consciousness, and experience of the self. Journal of Psychiatry Res, 108(2):111-21.
7. Allen, M, Dietz, M, Blair, KS, van Beek, M, Rees, G, Vestergaard-Poulsen, P, Lutz, A, Roepstorff, A. (2012). Cognitive-affecive neural plasticity following active-controlled mindfulness intervention. Journal of Neuroscience, 32(44):15601-10.

Natural, Synthetic, and Endogenous Psychedelic Compounds

main article: Natural, Synthetic, and Endogenous Psychedelic Compounds
author: Michael Aiello

Image Unavailable
Retrieved at Merapoetics

Numerous plants, animals, and fungi produce organic compounds that can act on the central nervous system to distort sensory and perceptual reality. For thousands of years hallucinogenic substances have been used by many different cultures to inspire creativity, practice spirituality, and induce euphoria. With the discovery of lysergic acid diethylamide (LSD) in 1943, the use of these “mind-altering” drugs gradually increased, spiking in popularity around the 1960’s [1]. During this time numerous studies were carried out to further investigate these compounds, but much of the momentum of this research ceased when the government made LSD illegal in 1968 [1]. Now more than 40 years later, there is a renewed interest in these drugs and their effects on the human body [1]. Modern techniques, such as the use of competitive radioligand binding, or creation of genetically altered knock out (KO) mice, are now providing us with increased insight into the internal mechanisms of these substances [2]. Of specific interest are the serotonin (5-HT) receptors, which seem to be common targets for many hallucinogenic ligands [2]. Evidence has shown that both phenylalanine and tryptamine based psychedelic drugs act on several 5-HT subtypes, binding with varied affinity [3]. When activated, the g-protein coupled receptors initiate a molecular cascade that is believed to be partly responsible for the intoxicating effects of the drugs [3]. These findings have strong implications for the treatment of psychopathology, as many of these receptors are targets for the treatment of schizophrenia and mood disorders [3].

1. Dyck, E. (2005). Flashback: Psychiatric Experimentation with LSD in Historical Perspective. Canadian Journal of Psychiatry 50 (7): 381-8
2. Titeler, M., Lyon, R.A., & Glennon, R.A. (1988). Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens. Psychopharmacology 94 (2): 213-6
3. Porter, R.H.P., et al. (1999). Functional characterization of agonists at recombinant human, 5-HT2A, 5-HT2-B and 5-HT2C receptors in CHO-K1 cells. British Journal of Pharmacology 128: 13-20

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