Dream Content and Cortical Activity Distribution

regional cortical acitivity associated with sleep
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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

Overview

In the recent decades, scientists are aiming to solve the mystery of dream contents. Not only are they interested in the meaning of each component within the dreams, they also focus mainly on the question “why do we dream?” Fortunately, through advanced technology, brain scans have been done on multiple experiment models which give us insight of how localized cortical activation can be linked to our dreams.

1.1 Cerebral imaging

In order to study neural activity, neuroscientists use a variety of imaging technologies to directly and indirectly visualize the living brains of model animals. While some techniques might be invasive and require injection of radioactive tracers, many others only scan based upon the distribution of brain composition in a rather moderate manner. Here, listing few of the most common imaging methods below will provide fundamental knowledge of how brain scans help scientists to decode unique dream features experienced by model individuals and will be further discussed in later sections.

1.1a fMRI

Introduction to fMRI

As the most well-known medical diagnose tool, functional magnetic resonance imaging (fMRI) has been widely applied to various fields of cerebral studies because it is not invasive and produces outstanding graphical representations of brain structure[3][4]. Since cerebral tissues rely heavily on oxidative metabolism for ATP generation and are vitally dependent on oxygenated blood circulation, fMRI helps neuroscientists to map the brain activity through measuring the change of magnetic strength of oxygenated and deoxygenated blood[3][4]. Depending on the oxygenation state of hemoglobin (oxygen-carrying protein found in red blood cell), dismagnetism (a repulsive property of an object against its external applied force) and paramagnetism (an attractive property of an object with its external applied force) characteristics are found in oxygenated blood and deoxygenated blood accordingly[4].Therefore a differentiated level of magnetic signal is used as an indirect indication of the strength of cortical activity, and this method is known as blood oxygen-level dependence or BOLD[3].

1.1b PET

PET, standing for positron emission tomography, is a nuclear imaging method that operates based on the decay characteristic of chemical tracer injected into patient’s bloodstream. Fluorodeoxyglucose(FDG) and many other options of radioactive tracers that resemble an analogue chemical feature of gluocse, emit positron upon positron emission decay in the body, they decelerate when interacting with electrons created by the PET scanner[5][6]. And since higher metabolic regions are highlighted by higher glucose uptake, 3D model of tissue can be reconstructed at different timeframes to compare different cerebral distributions. For example, via PET studies, increased overall metabolism and blood circulation in both of the cerebral hemispheres was found during complete wakefulness whereas declined blood flow was found in slow wave sleep in which the demand for nutrition and energy consumption is lower [5]. Besides its application of cerebral neuroimaging, PET has also been operated to scan for tumors and vascular diseases.

how SQUID sensor works
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1.1c MEG

Magnetoencephalograph, short for MEG, is a non-invasive imaging technique that detects the resulting magnetic fields from regional neuron electrical firings[7]. However, since the naturally occurring magnetic fields is extremely diminutive, a highly sensitive device called superconducting quantum interference device (SQUID) is used to isolate possible environmental noises and unnecessary disturbing signals from non-targeting body tissue[7]. It directly records simultaneous magnetic fields during dynamic neuron impulses with high spatial resolution and therefore plays a critical role in understanding cerebral functions and clinical analysis[7].

1.2 Dream content and cortical regions

After years of researches, elements of dream features are slowly getting revealed and coded topographically onto the cerebral map. Based on multiple comparisons and assessments, neuroscientists hypothesize known functions of target cerebral regions during full wakefulness to conduct experiments in order to study dreams[2]. And not surprisingly, brain scans done during wakefulness and dreams reveal strong correlated regional-specific responses. For example, activation of visual system observed in both states shows stable and consistent similarity in their cortical neuron firings while the auditory system also demonstrate good accordance[1].

And interestingly, one major finding of the cerebral studies is the reduced level of communication between two hemispheres while right hemisphere shows stronger dominance over the left one. This dominance is especially reflected on the deficit of dream features upon lesion studies of the right half of the brain[8]. In fact, even in the circumstance where communication between hemispheres is fully disconnected, right cerebral hemisphere’s still reported to perform independently without the involvement of left hemisphere and is thus concluded to be the major source of dreams[8].

1.2a Prefrontal cortex associated with dream lucidity

(also see lucid dreaming)

While most people probably share the same experience of getting confused with dreams and reality and feeling real within a dream, those two states of consciousness do in fact show converging brain activations such that lucid dreaming is made possible. Lucid dreaming is described as when dreamers are aware of the fact that they are dreaming and are able to exert manipulation over their participation in the dream to a certain degree[2]. However since the phenomenon of dream lucidity is a more complex concept and the degree of lucidity reported by dreamers often involves multiple subjective factors, it is difficult to clarify its occurrence solely based on few studies. To start off, it is critical to understand that lucid dreaming is most commonly reported following sleep that contains REM sleep(rapid eye movement) periods, and thus suspected to be the resulted sequential product of REM sleep[2][9]. Neuroscientists have demonstrated significant fluctuations of cortical activities during REM sleep via fMRI studies, areas such as lateral frontal cortex, posterior multimodal association areas, ventromedial prefrontal and anterior cingulate cortices have all been identified to experience either an inactivation or a hypoactivation[2]. Therefore they serve as excellent candidates for further researches.

Brain scan during lucid dreaming
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-Lateral frontal cortex and multimodal association areas:
When comparing lucid dreaming to normal dreaming, their greatest difference is the lack of awareness of one is dreaming in the later. And using PET scans, injected chemical tracer is used as a visual representation of tissue glucose reuptake and level of metabolism, and researchers have highlighted an observed deactivation of lateral frontal cortex and multimodal association areas in normal dreaming[2]. Such deactivation might serve to prone the working memory from previous experience, a possible adaptation to reserve potential neuronal space for future learning[2][5]. And finally, fMRI was done to suggest a strong correlation of increased dream lucidity and elevated frontal cerebral activity[2].

-Ventromedial prefrontal and anterior cingulate cortices:
Besides the two cortical areas previously mentioned, ventromedial prefrontal and anterior cingulate cortices are also involved in cognitive performance related to one’s self-awareness and even assisting decision making[2]. However, unlike lateral frontal cortex and multimodal association areas which are silenced, they become hypoactivated during REM sleep to levels which can even reach beyond the fully waking state. The reactivation and further activity in these localized areas are found during lucid dreaming[2], and based on their known functions, it is possible that their cortical neural distribution also contribute to the vividness and realistic characteristic of lucid dreaming[2].

1.2b Prefrontal cortex associated with visual distortion

(also see visual perception related to object recognition)

In order to achieve the complex experience of dreams, sensation often plays a critical role that auditory experience has been reported in about two thirds of the dreams whereas visual experience has been reported in almost all dreams. Indeed, a global increase of neuron firing in the right temporal (which is responsible for visual recognition) and parietal regions (which is responsible for visuospatial information) has been found responsible for visual dreaming[1]. However, why do dreams all share bizarre visual features? It is most likely due to heterogeneous activation of multiple brain regions while dreaming. Some of the visual distortions include misidentification syndromes of places, faces, and objects are triggered by anatomically segregated regions. For examples, the fusiform face area, located at the ventral surface of temporal lobe, is responsible for facial identity recognition while dreaming that it detects and verifies face structure and looks for familiarity[1]; and parahippocampal cortex, located medially in the temporal lobe, is responsible for spatial identification and it is activated for looking for environmental cues within dreams[1].

1.2c Other common association between dream features and cortical activation

Just like how sensation perception while asleep is in good accordance in terms of its cerebral activity distribution with wakening experience, the emotional component of dreaming shows similar pattern of localized neuron firing in regions responsible for sentiment. While nightmares are commonly experienced by individuals, the negative feeling of anxiety and stress in the dream is also triggered by the human limbic system[1]. Addition to that, the deficit of memory (also known as Amnesia
) and time perception generally reported by dreamers has been characterized by excess neuron firing within the prefrontal cortex[1].

1.3 Dreams and hallucination

Lysergic acid diethylamide
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serotonin projection in the brain
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Dreams are often confused with hallucination since both phenology share the same illusive features. However, to distinguish the two, one must first understand that hallucination occur between two states, sleeping and waking, while dreams on the other hand occur only when sleeping [10][11]. In other words, hallucination is achieved in the presence of consciousness whereas dream often lacks self-awareness (except for lucid dreaming). And despite the difference in terms of their diverging conscious awareness, they do however share some phenomenological similarities and both occur without stimuli from external environment[10][12].

One common feature shared by dreaming and hallucination is their mechanism of initiation-“inactivation of the neurochemical pathway for cerebral serotonin system” [10]. Serotonin is a type of neurontramsitter mainly found within brainstem nuclei that blocks processing of sensory modality and emotion and has been intensively studied for its behavioral influences across diverse mammalian species. Indeed, hallucination can be induced by drugs such as LSD (Lysergic acid diethylamide) that triggers depression of synaptic firing for serotonin-containing neurons, and low level of serotonin is associated with longer period of REM sleep[10]. And reciprocally, the opposite circumstance is observed, with increased serotonin concentration at the synapses, decreased hallucination related characteristics as well as shortening of REM sleep and dreams was reported[10]. Addition to that, level of serotonin is found to be concentrated in regions meditating hallucination-like experiences especially its visual perception and emotion component[10][13].

In the early 1950, LSD was first synthesized to disinhibit neurophysiological functions of the central nervous system. Like many other hallucinogens such as psilocybin, it’s a psychoactive drug that induces tremendous raise in their target neuron activity[10]. And specifically, for LSD, influence over sensation namely the visual component is highlighted resulting in visual hallucination and dream-like experience.

However, since cerebral functioning often doesn’t solely operate based on a single contributor, serotonin is not the only mechanism known that play a neuropsychological role in regulating dreams and hallucination activation. In other word, serotonin does not show dominant power over dreams/hallucination triggering but only facilitates their occurrence in a permissive fashion[10].

Bibliography
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3. Hoge, R. (2012). Calibrated fMRI. NeuroImage, 62,930-937.
4. Miller, K., Hargreaves, B., Lee, J., Ress, D., deCharms, R., & Pauly, J. (2003). Functional Brain Imaging Using a Blood Oxygenation Sensitive Steady State. Magnetic Resonance in Medicine, 50, 675-683.
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9. Sinton, C., & McCarley, R. (2004). Neurophysiological Mechanisms of Sleep and Wakefulnees: A Question of Balance. Seminar in neurology, 24(3), 211-223
10. Jacobs, B. (1978). Dreams and Hallucinations: A Common Neurochemical Mechanism Mediating Their Phenomenological Similarities. Neuroscience & Biobehavioral Reviews, 2, 59-69
11. Manni, R. (2005). Rapid Eye Movement Sleep, Non-Rapid Eye Movement Sleep, Dreams, and Hallucinations. Current Psychiatry Reports, 7, 196-200
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