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The study of brain in schizophrenia patients suggests that hallucination and amygdala have some connections. Schizophrenia is a neurobiological disorder diagnosed by a patient's inability to interpret a stimuli and select an appropriate response (i.e.: saying "good bye" instead of "thank you" when receiving a gift) (8). Other characteristics of this disorder include alterations of the senses, changes in emotions, movements and behavior, and most importantly, delusions and hallucinations (8). In one study, researchers have tested six hallucinating schizophrenics and have discovered the parts of brain activated when hallucination occurs (9). The active parts include bilateral thalamus, left hippocampus/parahippocampal gyrus, right anterior cingulate, and left orbitofrontal cortex, and they are responsible for generating mental activity and for integrating current and past cognitive/emotional experiences (9). The location of all these structures, deep inside the brain and very close to amygdala and hypothalamus (6), suggests that the active parts may have some interactions with amygdala during a hallucination state. Also, for amygdala plays important roles in emotions, especially fear, hallucination seems closely related to amygdala and terror.
The perception of fear integrated by amygdala activates "fight-or-flight" response, in which an animal respond quickly to a danger due to the function of hormone epinephrine and neurotransmitter norepinephrine (6, 10, 11, 12). Epinephrine, also called adrenaline, is primarily produced in the adrenal glands while norepinephrine, also called noradrenaline, is made in the brain and limbic system (10, 11). When the amygdala interprets fear, it stimulates the release of both epinephrine and norepinephrine into the body's system (7). The high concentration of epinephrine in the blood stream increases the heart and respiratory rates for more oxygen intake and constricts peripheral blood vessels for more blood flow into the large muscles, thereby preparing the body for fight or flight (7, 10, 11, 12). Norepinephrine, when released, mainly tenses the smooth muscles around the blood vessels, increasing the blood pressure (10, 11). The blood pressure in the brain probably increases tremendously in response to fear, too. The sudden increase in the blood pressure, then, may cause the membrane potential to change in the visual and/or auditory cortex, triggering hallucination to happen. Moreover, in the fear reaction, the pupils dilate to let more light and increase peripheral vision to observe threat (10, 12). This response may increase the chance of hallucination to happen, for a large amount of light enters the eye at one time.
In addition to epinephrine and norepinephrine, another neurotransmitter serotonin seems to play an important role in inducing the fight-or-flight response and hallucination. Like norepinephrine, serotonin affects broad range of conditions, such as depression, aggression, sleep regulation, anxiety, appetite control, temperature regulation, pituitary hormone secretion, pain reception, and blood vessel tone (13). It exists throughout the brain, but its most concentrated region lies in hypothalamus and the pineal gland (11). Hence, when the active potential carrying the information of fear reaches hypothalamus from amygdala, hypothalamus releases serotonin into the system, providing assists to epinephrine and norepinephrine to prepare the body for fight or flight. As a part of the process, serotonin causes the smooth muscles of the blood vessels to constrict. Consequently, the blood pressure rises in the brain, and the membrane potential in the optic/auditory cortex change, triggering hallucination.
The additional evidence for the "fight-or-flight" reaction's responsibility on hallucination comes from the hallucinogenic drugs. Hallucinogens, so called for their ability to induce visual/auditory hallucination, affect the hypothalamus and its regulation of hormones (14). Just like epinephrine, norepinephrine, and serotonin, they cause pupils to dilate, heart rate and breathing rate to increase, the body temperature to change, and/or the blood pressure to rise (14). Moreover, some common hallucinogens have similar structures to norepinephrine or serotonin and bind to the same receptors (14). For example, LSD looks very much like serotonin, and mescaline looks similar to norepinephrine (14). Thus, if the drugs that have very similar properties as epinephrine, norepinephrine, or serotonin can induce hallucination, the hormone or the neurotransmitters should be able to have the same effects. For the hallucinogens also stimulate the conditions produced by fight-or-flight response, the natural reaction to the fear enhanced by epinephrine, norepinephrine, and serotonin seems possible to cause hallucination under favorable conditions.
For a summary, a victim of a Sleep Paralysis feels extreme fear for he discovers he cannot move his body although he has consciousness. Integrating the fright, amygdala triggers the fight-or-flight response by stimulating the release of epinephrine, norepinephrine, and serotonin. These substances constrict the smooth muscles around the blood vessels, causing the blood pressure to rise in the brain. Consequently, the membrane potential in the visual/auditory cortex changes, triggering the firing of the neurons and hallucination to occur. The explanation above is only a hypothesis. There are more possibilities, too.
For another hypothesis, corollary discharge may trigger hallucination during sleep paralysis, as in the situation of phantom pain. In a phenomenon called phantom limb, a person who has lost an arm or leg perceives the position of the missing limb, often with a report of pain in specific parts of the limb (15). This abnormal observation can be explained in the terms of corollary discharge, or reafference. In order for a healthy person or an amputee to move a limb intentionally, a self-conscious part of brain, called I-function, sends a signal to another part of the brain that controls the movement of the limb (4). Then, the region that has just received a signal from I-function triggers the firing of neurons for the action potential to reach particular motor neurons, which then generate a movement (4). Simultaneously, the same region of the brain also sends corollary discharge signal; it transmits the information received from the I-function to many different brain parts (4, 15). As a result, the brain, or "neuromatrix" (15), knows what the limb has been ordered to do (4, 15). (The perception of the phantom limb may emerge due to the corollary discharge signals, spreading the information on the movement that limb is expected to produce (4).) In a healthy person, the neuromatrix receives a sensory input from the limb, which reports the limb's position and the muscle activity (4, 15). When I-function issues a signal to move a limb, the reafference allows the neuromatrix to expect what kind of sensory inputs it will receive even before the limb makes the required motion (4, 15). In an amputee with a phantom limb, the brain receives sensory message reporting that the limb is NOT moving at all (4, 15). In response, the neuromatrix, expecting a sensory input as the limb's motion, may send more frequent and stronger signals to urge the limb to move, and these output signals may cause the perception of cramping or phantom pain (15).
Like in phantom pain, the mismatch between the internal expectation and the sensory input may trigger hallucination in Sleep Paralysis. Unlike an amputee, a victim of Sleep Paralysis still has his limbs, but he cannot move them because of some errors in neurotransmission (1). When one wakes up and discovers himself under total body paralysis, he struggles to escape from the frightening immobile state. His I-function issues some messages urging the whole body to move, and the neuromatrix expects a certain sensory input, the action of skeletal muscle. However, with the body under the powerful control of inhibitors released during REM sleep, the neuromatrix receives a sensory input that the body is not moving, completely opposite from what it expects. As the I-function continues to send more and more signals trying to receive the expected input, somehow the frequent firing of the neurons may stimulate the release of particular substances, which eventually cause the change in membrane potential of optic and/or auditory nerves. Besides, the discrepancy caused by corollary discharge may strongly involve the stimulation of fear. As the neuromatrix keeps receiving a contradictory sensory input, it may perceive that something has gone wrong in the system. This realization may link to the arousal of fear, which then induce the pathway described earlier.
Also, as I have predicted in my previous paper, hallucinations during Sleep Paralysis may result from another error in neurotransmission, in which the brain continues to release the activators that trigger dreaming (1). During an episode of Sleep Paralysis, the nervous and endocrine systems keep releasing the inhibitors and "paralyzing" one's body even after some parts of his brain wakes up. As a result, his body continues to "sleep" even though his conscious part of brain is awake. Similarly, it may be possible for another part of the brain, which is responsible for dreaming, to stay in the state of REM sleep. Then, a person may continue to "see" the images and "hear" the noises produced in the dream that he has just had before conscious arousal.
