What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more?

I'm really interested to know when we are sleeping how a series of stories come to our mind that we called this process dreaming. If you know a useful article on this topic, please tell me thanks.

Dreams are hallucinations that occur during certain stages of sleep. They're strongest during REM sleep, or the rapid eye movement stage, when you may be less likely to recall your dream. Research is yet to reveal the true reason of dreams. But we know for sure it is not one reason.

Speculated Reasons:

1. Dreams as fight-or-flight training

One of the areas of the brain that's most active during dreaming is the amygdala. The amygdala is the part of the brain associated with the survival instinct and the fight-or-flight response.

One theory suggests that because the amygdala is more active during sleep than in your waking life, it may be the brain's way of getting you ready to deal with a threat.

2. Dreams as memory aides

One widely held theory about the purpose of dreams is that they help you store important memories and things you've learned, get rid of unimportant memories, and sort through complicated thoughts and feelings.

Research shows that sleep helps store memories. If you learn new information and sleep on it, you'll be able to recall it better than if asked to remember that information without the benefit of sleep.

How dreams affect memory storage and recall isn't clearly understood yet.

3. Creative times!

One theory for why we dream is that it helps facilitate our creative tendencies. Artists of all kinds credit dreams with inspiring some of their most creative work. You may have awakened at times in your life with a great idea for a movie or a song, too. Without the logical part of the brain working, emotional and illogical thoughts take over your mind!

Eectroencephalography (EEG), electro-oculography (EOG), and electromyography (EMG) are used to monitor neurological data from the brain to reveal information about neurological activities in the sleeping brain.

Here is a scientific literature (pdf) you can go through for in-depth study ( this link leads to ResearchGate page, you can read it there or download the pdf) :

Chapter 3 AP Psych

Ernest Hilgard believes that hypnosis involves social influence and special dual processing state or dissociation
------viewed hypnotic dissociation as a vivid from or everyday mind splits
------similar to doodling while listening to a lecture

------PET scans show that hypnosis reduces brain activity in a region that processes painful stimuli
but not in the sensory cortex which receives the raw sensory input

hypnosis doesn't block sensory input, but blocks attention to stimuli

explains why injured athlete feels no pain when caught up with competition until game ends

focusing of conscious awareness on a particular stimuli

our awareness focuses on a minute aspect of all that you experience

much or our behaviours occurs on auto pilot

can lead form the ever increasing doses or toleration

talking substance longer or more than intended

much time devoted to obtaining substance

normal activities abandoned or deuced

people given morphine to control pain rarely develop cravings

but 10% do have a hard time using a psychoactive drug in moderation or stopping altogether

but recovery rates or treated and untreated groups differ less than one might guess

addiction as a disease needing treatment has been suggested for excessive behaviour
------shopping, gambling, work, sex
------but labeling behaviour doesn't explain the impulses

alcohol works as a disinhibitor
------slows brain activity that control judgement and inhibition

equal opportunity drug
------increases (disinhibits) helpful tendencies, like drunks leave huge tips
------increases harmful tendencies, as when sexually aroused men become more disposed to sexual aggression
------drinking- more seuxal assaults

in larger doses, alcohol can become a staggering problem: slow reactions, speech slur, skilled performance deteriorates

paired with sleep deprivation, alcohol is a potent sedative

many people are killed from the influence of alcohol

reduced self awareness and self control

heavy drinkers don't remember the person they met the night before

result from the way alcohol suppresses REM sleep, which helps fix the day's experience into memory

heavy drinking can also have long term effects on brain and cognition

in rats, at a developmental period corresponding to human adolescence, bring drinking contributes to nerve cell death and reduces the birth of new nerve cells
------also impairs the growth of synaptic connections

alcohol consumed peron- 2x likely to be caught mind wandering during a reading task, yet were less likely to notice that they zoned out

alcohol produces a "myopia"

focuses attention on arousing situation, such as provocation, and distracts attention from normal inhibitions and future consequences

when people believe that alcohol affects social behaviour in certain ways and that they've been drinking alcohol, they behave accordingly

------university men were given non alcoholic and alcoholic drinks
------½ on each group were told that they were drinking alcohol, and half not
------after watching erotic film, men who thought they drank alcohol were more likely to report having strong secual fantasies and feeling guilt free

depress nervous system activity

reduced anxiety but impairing memory and judgement

Nembutal, Seconal, Amytal are prescribed to reduce anxiety and induce sleep

in larger doses, they can impair memory and judgment

also depresses neural functioning

pupils constrict, breathing slows, lethargy sets in as blissful pleasure replaces pain and anxiety

long term price: gnawing craving for another fix, need for larger doses, extreme discomfort of withdrawal

pupils dilate, heart and breathing rates increase, blood sugar level rise, causing a drop in appetite

energy and self-confidence also rise

used to feel alert, lose weight, boost mood or athletic performance

may crash into fatigue, headaches, irritability, depression- if cut off from usual dose

psychoactive drug in tobacco

10,000 deaths from cigarettes

teen to grave smokers-> 50% chance of dying from cigarettes

as addictive as heroin and cocaine

attempts to quit even within the first weeks of smoking- fails

if in college or university, people won't start here

self conscious adolescents- vulnerable to smoking's allure
------imitate celebrity, project mature image, get social reward of acceptance by other smokers

teens whose friends smoke usually smokes, because offered a cigarette and suggests its pleasures

epinephrine and norepinephrine diminish appetite and boost alertness and mental efficiency

dopamines and opioids calm anxiety and reduces sensitivity to pain

fewer than 1/7 smokers who want to quit are able to

½ of americans who have smoked have quit

aided by nicotine replacement drug and encouragement from telephone counselor or a support group

success is equal of gradual quit or abrupt quit

acute craving and withdrawal symptoms gradually disappear over 6 months

after 1 year abstinence, only 10% will relapse

recipe for coca-cola used to have extract from coca plant, creating cocaine tonic for tired elderly people

cocaine is now snorted, injected or smoked

it enters the bloodstream quickly, producing a rush of euphoria that depletes the brain's supply of the neurotransmitters dopamine, serotonin, norepinephrine

adverse- cardiovascular stress, suspiciousness, depressive crash,in situations that trigger aggression, cocaine use may heighten reactions and fight

faster working crystallized from of cocaine

produces a briefer but more intense high followed by a more intense crash

craving for more wanes after several hours, only to return several days later

but greater effect than amphetamine

meth triggers the release of neurotransmitter dopamine, stimulating the brain cells that enhance energy and mood

result: 8 or so hours of heightened energy and euphoria

over time, may reduce baseline dopamine levels, leaving user with depressed functioning

very addictive drug that stimulated nervous system

major effect: releasing stored serotonin and blocking its reuptake, prolonging serotonin's feel good flood

users feel the effect about 30 minutes after taking the pill

3-4 hours experience high energy,
emotional elevation, and connectedness with those around- I LOVE EVERYONE
emotional elevation and disinhibition

so with dancing, can lead to overheating, increased blood pressure, and death

long term repeated leaching of brain serotonin can damage serotonin producing neurons, leading to decreased output and increased risk of permanently depressed mood

that distort perceptions and evoke sensory images in the absence of sensory input

LSD and MDMA are synthetic

made by albert hoffman, a chemist

can result in seeing stream of fantastic pictures, extraordinary shapes with intense kaleidoscope like play of colors

emotions of a trip: varies from euphoria to detachment to panic

people with loss of oxygen, extreme sensory deprivation, the brain hallucinates the same way

experience begins with geometric forms, the next phase has more meaningful images superimposed by tunnels, funnels and others at replay past emotional experience

altered state of consciousness

experienced by 15% of those who survive cardiac arrest

visions of tunnels, bright light of light, replay of old memories, out of body sensations

oxygen deprivation and other insults to the brain can cause hallucinations

after temporal lobe seizures, people see similar mystical stuff

has THC- delta-9-tetrahydrocannabinol
difficult drug to classify

smoke- reach brain in 7 seconds

eat- causing peak to reached at a slower, unexpected rate

marijuana can intensify anxious or depression

more a person uses marijuana especially during adolescence, greater risk for depression and anxiety

disrupts memory formation and interferes with immediate recall of information learned only a few minutes before

cognitive effects outlast the period of smoking

heavy use for over 20 years associated with a shrinkage of brain areas that process memories and emotions

relieve pain and nausea associated with AIDS and cancer

in some cases, the institute of medicine recommends delivering inhaling THC with medical inhalers

alcohol is eliminated from body within hours

heredity influences alcohol abuse problems, especially those appearing by early adulthood

adopted individuals are more susceptible to alcohol dependence if one or both biological parents have a history of it

identical twin with alcohol dependence puts one at increased risk of marijuana and alcohol problems
------not with fraternal twins

boys who are excitable, impulsive, fearless at age 6 tend to smoke, drink, use drugs at teens

------mice and rats who like alcohol than water have lower levels of brain chemical NPY
------mice with overproduces NPY are sensitive to alcohol, and drink little

varies within european countries

lower in african american teens

low in religious active orthodox jews, mormons, amish, mennonites

small towns and rural areas that are drug free
------constrained genetic disposition to drug use
------cities= more opportunities, less supervision

------throw parties with drugs
depends on friends if they do or do not
------comes from happy family
------don't begin drinking before 15
------do well in school
------don't do drugs- no association with druggies

common among school dropouts without privilege, job skills, and hope

significant stress, failure, depression

girls with depression, eating disorders, sexual physical abuse

youth going neighborhood/school transition

collegians without clear identity

drugs temporarily dulls pain of awareness, coping mechanism for depression, anger, anxiety or insomnia

Background to the hypothesis

Stages of sleep

There are two major types of sleep. The first, rapid eye movement or REM sleep, occurs in ∼90-min cycles and alternates with four additional stages known collectively as NREM sleep—the second type of sleep. Slow wave sleep (SWS) is the deepest of the NREM phases and is the phase from which people have the most difficulty being awakened. REM sleep is characterized by low-amplitude, fast electroencephalographic (EEG) oscillations, rapid eye movements (Aserinsky and Kleitman 1953), and decreased muscle tone, whereas SWS is characterized by large-amplitude, low-frequency EEG oscillations (Maquet 2001). More than 80% of SWS is concentrated in the first half of the typical 8-h night, whereas the second half of the night contains roughly twice as much REM sleep as does the first half. This domination of early sleep by SWS, and of late sleep by REM, likely has important functional consequences but also makes it difficult at this time to know which distinction is critical: NREM sleep versus REM sleep or early sleep versus late sleep. We will use the terms NREM/early sleep and REM/late sleep, where necessary, to reflect this current ambiguity.

Neurotransmitters, particularly the monoamines (largely serotonin [5-HT] and norepinephrine [NE]) and acetylcholine, play a critical role in switching the brain from one sleep stage to another. REM sleep occurs when activity in the aminergic system has decreased enough to allow the reticular system to escape its inhibitory influence (Hobson et al. 1975, 1998). The release from aminergic inhibition stimulates cholinergic reticular neurons in the brainstem and switches the sleeping brain into the highly active REM state, in which acetylcholine levels are as high as in the waking state. 5-HT and NE, on the other hand, are virtually absent during REM. SWS, conversely, is associated with an absence of acetylcholine and nearly normal levels of 5-HT and NE (Hobson and Pace-Schott 2002).

The distribution of dreams

In the study of dreams, a major distinction has been drawn between REM and NREM sleep. Until recently, virtually all dream research focused on REM sleep, and indeed, dreams are prevalent during REM. In a recent review of 29 REM and 33 NREM recall studies, Nielsen (2000) reported an average REM dream recall rate of 81.8%. Importantly, however, he also reported an average NREM recall rate of ∼50%. Some NREM dreams are similar in content to REM dreams the majority of these come from those few NREM periods occurring early in the morning, during the peak phase of the diurnal rhythm, when cortisol levels are at their zenith (Kondo et al. 1989). Foulkes (1985) has argued for the existence of NREM dreaming and against a simple “REM sleep = dreaming” view. By simply changing the question asked of awakened subjects from “Did you dream?” to “Did you experience any mental content?,” Foulkes was able to show a far higher percentage of dream reports from NREM stages than original studies had suggested. These dream reports after NREM awakenings led Foulkes and others to conclude that the stream of consciousness never ceases during sleep and that the brain engages in cognitive activity of some sort during all sleep stages (Antrobus 1990).

Dreams and episodic memory content

Typical REM and NREM dreams are quite distinct, particularly with respect to episodic memory content. Episodic memory refers to knowledge about the past that incorporates information about where and when particular events occurred. It is typically contrasted with semantic memory, which consists of knowledge (e.g., facts, word meanings) that has been uncoupled from place and time, existing on its own (Tulving 1983). When examining REM sleep dreams for memory content, one finds that episodic memories are rare (see Baylor and Cavallero 2001) and typically emerge as disconnected fragments that are often difficult to relate to waking life events (see Schwartz 2003). These fragmented REM dreams often have bizarre content (Stickgold et al. 2001 Hobson 2002). For example, the normal rules of space and time can be ignored or disobeyed, so that in REM dreams it is possible to walk through walls, fly, interact with an entirely unknown person as if she was your mother, or stroll through Paris past the Empire State Building. NREM dreams, however, are quite different (Cavallero et al. 1992). Here, episodic memories do appear in dream content (see Foulkes 1962 Cicogna et al. 1986, 1991 Cavallero et al. 1992 Baylor and Cavallero 2001). Recent episodes are predominant, but remote memories occasionally appear as well. This pattern of results suggests to us that the memory systems needed to generate complete episodic retrieval are functional in NREM sleep but not in REM sleep. Although we do not fully understand how nightly neurochemical fluctuations account for this difference, some clues are available.

Sleep and memory consolidation

One important clue is that different types of memory (e.g., procedural, episodic) appear to be best consolidated during specific stages of sleep. REM sleep may be preferentially important for the consolidation of procedural memories and some types of emotional information (see Karni et al. 1994 Plihal and Born 1999a Kuriyama et al. 2004 Smith et al. 2004), whereas NREM, especially SWS, appears to be critical for explicit, episodic memory consolidation (Plihal and Born 1997, 1999a,b Rubin et al. 1999 also see Peigneux et al. 2001). This role for SWS appears to apply both to verbal tasks (e.g., list learning, paired-associated learning tasks Plihal and Born 1997) and spatial tasks (e.g., spatial rotation Plihal and Born 1999a). For example, Plihal and Born (1997) tested both episodic and procedural memory after retention intervals defined over early sleep (dominated by SWS) and late sleep (dominated by REM). Subjects were trained to criterion in the recall of a paired-associate word list (episodic) and a mirror-tracing task (procedural) and were retested after 3-h retention intervals, during either early or late nocturnal sleep. Recall of paired associates improved significantly more after a 3-h sleep period rich in SWS than after a 3-h sleep period rich in REM or after a 3-h period of wake. Mirror tracing, on the other hand, improved significantly more after a 3-h sleep period rich in REM than after 3 h spent either in SWS or awake. The fact that memories for personal episodes only undergo effective consolidation early in the night, when NREM (SWS) is particularly prominent, provides another indication that episodic memory systems are functional during NREM sleep.

Summary of background

This brief review highlights several points:

Sleep stages vary across the night: Early sleep is rich in NREM, but late sleep is rich in REM. These stage changes relate to, and are caused by, neurochemical fluctuations during sleep.

Dream content varies as a function of sleep stage or time of night: There is considerable episodic content in dreams during NREM/early sleep, but little episodic content in dreams during REM/late sleep.

Sleep affects memory consolidation, but in a complex way: Procedural memory benefits from both REM/late sleep and NREM/early sleep, but episodic memory only benefits from NREM/early sleep.

These points raise two critical questions:

What can account for the differences in dream content and effectiveness of memory consolidation as an apparent function of NREM/early sleep versus REM/late sleep?

What underlying concomitants of this difference actually produce the variations in dream content and memory consolidation?

Are neurotransmitters the key, as some have suggested (see Hobson 1988)? Is it strictly the REM/NREM distinction, or alternatively, could it be fundamental differences in early versus late sleep? It is important to note that Plihal and Born's studies (1997, 1999a) used late versus early sleep as the manipulation, not REM versus NREM per se. Moreover, late night NREM dreams are more “dream-like” and are thus often indistinguishable from REM dreams (Kondo et al. 1989), so perhaps something about late night sleep accounts for differences in dream content and memory consolidation. These are just some of the issues that arise within the framework we propose.

Does the new study change that theory?

Animal studies should always be taken with a grain of salt, as they often do not translate directly to human behavior. And there are additional caveats to this particular paper, says Dr. Cathy Goldstein, a sleep specialist at Michigan Medicine. The researchers looked specifically at cones in the animals’ eyes, which detect color, instead of melanopsin, which senses light and is central to the issue of melatonin secretion.

They also kept light levels dim, regardless of color, which may not reflect the bright lights of electronics.

And finally, though mice are frequently used in sleep research, Goldstein notes that since the rodents are nocturnal, they may respond differently to light than humans do. Taken together, Goldstein says these conditions mean the study&rsquos results apply only to a very narrow set of circumstances and metrics. &ldquoFor this to get extrapolated to saying &lsquoblue light at night isn&rsquot bad for you&rsquo is a little bit of an extension,” Goldstein says.

But that doesn’t mean blue light is evil. “Blue light has become the gluten of the sleep world,” Goldstein says with a laugh. In other words, though it may be a potential trigger for health issues, its impact has been blown way out of proportion.

“We put the cart so far ahead of the horse” with blue light, agrees James Wyatt, who directs sleep disorders and sleep-wake research at Rush University Medical Center. In Wyatt&rsquos view, recommendations around limiting blue light have far outpaced science around its effects. There is a valid scientific basis to the idea that blue light interrupts sleep, since research consistently shows that light of any kind suppresses melatonin and blue light may do so to an especially extreme degree. But Wyatt says most human research done in this field hasn’t been representative of the way the average person is exposed to blue light. That is, most experimental conditions don’t correspond to the average person’s day, and even then they often result in only tiny changes in sleep.

Take that iPad study, for example. While it did show that bedtime exposure to blue light through an iPad can suppress melatonin, Wyatt notes that people who read on their devices for hours took only 10 minutes longer to fall asleep than paper book readers. “In over 20 years of practicing sleep medicine, I have never had a patient come to me and say, ‘Hey, doc, can you help me fall asleep 10 minutes faster?'” Wyatt says.

Goldstein adds that the spectrum of light isn’t the only thing that matters&mdashso do brightness, and duration of exposure. “You can&rsquot just worry about spectrum alone,” she says. “You can&rsquot have your blue light filter on, and then have your phone or your tablet at maximal brightness” and expect to drift right off with no problem.

Sleep Cycles

You typically go through all the sleep stages three to five times a night. The first REM stage may be just a few minutes, but gets longer with each new cycle, up to about a half an hour. The N3 stage, on the other hand, tends to get shorter with each new cycle. And if you lose REM sleep for whatever reason, your body will try to make it up the next night. Scientists aren’t sure of the purpose of any of this.

How can we use this to our advantage?

Clearly these homeostatic mechanisms aren’t the only basis for migraine, but it is logical to think that trying to maintain a well-balanced sleep-wake cycle may make triggering a migraine attack less likely. It is therefore perhaps important for migraine sufferers to observe something called good sleep hygiene, which is a set of suggestions designed to keep the sleep-wake cycle, and the quality of sleep, as even as possible.

Despite some rather compelling evidence of a close interaction between sleep and headache, there is clearly much to still be learnt and therapeutically exploited. Assessing both brain states in tandem, both scientifically and clinically, is likely to yield a much clearer view of this complex relationship in future.

Sleep hygiene

  • Try to go to bed and get up at the same time each day, as sleeping during the correct phase of your circadian cycle is important.
  • Understand your sleep need, including both the timing of sleep (when feels right for you to go to bed), and the duration of sleep (most adults need about 8 hours a night).
  • Do try and spend some time outdoors or in natural light during the daytime, as this provides an important cue to your brain for finetuning timing of the body clock.
  • Try and make your sleeping environment as restful as possible, including sufficient darkness and quiet, comfortable bedding and few devices around the bed, particularly those with lights.
  • Exercise, preferably before dinner rather than before bed, can be helpful as can stopping smoking as nicotine has a stimulant effect and suppresses melatonin.
  • It would be sensible to recommend that you don’t use your bed for activities that could be done elsewhere (such as watching TV, studying), and try to avoid staying in bed if you are wide-awake.
  • Avoiding caffeine before bed is recommended, as is avoiding alcohol, as this actually reduces the overall quality of your sleep rather than improving your sleep as is commonly assumed.

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Other Crazy Things That Happen

A number of unexpected things can happen when you are sleeping, either due to a medical condition or a complete fluke of luck! These include:


The Mayo Clinic explains that snoring happens when “air flows past relaxed tissues in your throat, causing the tissues to vibrate as you breathe.” A few factors play into this, including the anatomy of your mouth and throat, alcohol consumption, your sleep position, and nasal passage issues. If you find that snoring is waking you up at night or disturbing your partner, you can try sleeping on your side or speaking with a doctor to see if the snoring is associated with obstructive sleep apnea.


Getting out of bed at night and moving around while completely asleep doesn’t just happen in cartoons. In fact, research suggests that sleepwalking in adults is less rare than you might think — it affects around 3.6% of Americans, which is more than 8.4 million adults. “It is thought that medication use and certain psychological and psychiatric conditions can trigger sleepwalking, but the exact causes are unknown,” a Harvard Health report on sleepwalking explained. If you are prone to sleepwalking or live with someone who sleepwalks, there are potential safety risks like falling or accidental injuries — speak with a doctor about how to treat sleepwalking or make your home a safer place for sleepwalkers.

What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more? - Biology

The emotion of fear is perceived in a structure called amygdala in the brain (5, 6, 7). It is a small, almond looking structure deep inside the brain and has several distinct nuclei, including, medial, lateral, basal, and central (5, 6). The lateral nucleus seems to receive input from thalamus and cortical sensory and association areas (5). Then the basolateral nucleus integrate the input as fear and send the information to the central nucleus, from which a major output transmits through projections to the hypothalamus and brainstem autonomic areas (5).

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.

The origin of hallucinations during Sleep Paralysis is still not clear, but many neuroscientists supports that it has some connection to anxiety (16). So far, many studies on Sleep Paralysis and hallucinations have been done on neurobiological level, but there are many aspects and questions yet to be discovered, explained, or answered. Why do some people experience hallucination and others do not? Which factors determine the hallucinatory images that each victim sees or hears? Are they really hallucination or evil spirits? The hallucination during Sleep Paralysis remains mysterious.

WWW Sources

6)The Emotional Brain, by Mary Lynn Hendrix, National Institute of Mental Health

How Does Alcohol Affect Sleep?

After a person consumes alcohol, the substance is absorbed into their bloodstream from the stomach and small intestine. Enzymes in the liver eventually metabolize the alcohol, but because this is a fairly slow process, excess alcohol will continue to circulate throughout the body. The effects of alcohol largely depend on the consumer. Important factors include the amount of alcohol and how quickly it is consumed, as well as the person’s age, sex, body type, and physical shape.

The relationship between alcohol and sleep has been studied since the 1930s, yet many aspects of this relationship are still unknown. Research has shown sleepers who drink large amounts of alcohol before going to bed are often prone to delayed sleep onset, meaning they need more time to fall asleep. As liver enzymes metabolize the alcohol during their night and the blood alcohol level decreases, these individuals are also more likely to experience sleep disruptions and decreases in sleep quality.

To understand how alcohol impacts sleep, it’s important to discuss different stages of the human sleep cycle. A normal sleep cycle consists of four different stages: three non-rapid eye movement (NREM) stages and one rapid eye movement (REM) stage.

  • Stage 1 (NREM): This initial stage is essentially the transition period between wakefulness and sleep, during which the body will begin to shut down. The sleeper’s heart beat, breathing, and eye movements start to slow down and their muscles will relax. Brain activity also begins to decrease, as well. This phase is also known as light sleep.
  • Stage 2 (NREM): The sleeper’s heartbeat and breathing rates continue to slow down as they progress toward deeper sleep. Their body temperature will also decrease and the eyes become still. Stage 2 is usually the longest of the four sleep cycle stages.
  • Stages 3 (NREM): Heartbeat, breathing rates, and brain activity all reach their lowest levels of the sleep cycle. Eye movements cease and the muscles are totally relaxed. This stage is known as slow-wave sleep.
  • REM: REM sleep kicks in about 90 minutes after the individual initially falls asleep. Eye movements will restart and the sleeper’s breathing rate and heartbeat will quicken. Dreaming mostly takes place during REM sleep. This stage is also thought to play a role in memory consolidation.

These four NREM and REM stages repeat in cyclical fashion throughout the night. Each cycle should last roughly 90-120 minutes, resulting in four to five cycles for every eight hours of sleep. For the first one or two cycles, NREM slow-wave sleep is dominant, whereas REM sleep typically lasts no longer than 10 minutes. For later cycles, these roles will flip and REM will become more dominant, sometimes lasting 40 minutes or longer without interruption NREM sleep will essentially cease during these cycles.

Related Reading

Alcohol and Insomnia

Insomnia, the most common sleep disorder, is defined as “a persistent difficulty with sleep initiation, duration, consolidation, or quality.” Insomnia occurs despite the opportunity and desire to sleep, and leads to excessive daytime sleepiness and other negative effects.

Since alcohol can reduce REM sleep and cause sleep disruptions, people who drink before bed often experience insomnia symptoms and feel excessively sleepy the following day. This can lead them into a vicious cycle that consists of self-medicating with alcohol in order to fall asleep, consuming caffeine and other stimulants during the day to stay awake, and then using alcohol as a sedative to offset the effects of these stimulants.

Binge-drinking – consuming an excessive amount of alcohol in a short period of time that results in a blood alcohol level of 0.08% or higher – can be particularly detrimental to sleep quality. In recent studies, people who took part in binge-drinking on a weekly basis were significantly more likely to have trouble falling and staying asleep. These findings were true for both men and women. Similar trends were observed in adolescents and young adults, as well as middle-aged and older adults.

Researchers have noted a link between long-term alcohol abuse and chronic sleep problems. People can develop a tolerance for alcohol rather quickly, leading them to drink more before bed in order to initiate sleep. Those who have been diagnosed with alcohol use disorders frequently report insomnia symptoms.

Alcohol and Sleep Apnea

Sleep apnea is a disorder characterized by abnormal breathing and temporary loss of breath during sleep. These lapses in breathing can in turn cause sleep disruptions and decrease sleep quality. Obstructive sleep apnea (OSA) occurs due to physical blockages in the back of the throat, while central sleep apnea (CSA) occurs because the brain cannot properly signal the muscles that control breathing.

During apnea-related breathing episodes – which can occur throughout the night – the sleeper may make choking noises. People with sleep apnea are also prone to loud, disruptive snoring. Some studies have suggested that alcohol contributes to sleep apnea because it causes the throat muscles to relax, which in turn creates more resistance during breathing. This can exacerbate OSA symptoms and lead to disruptive breathing episodes, as well as heavier snoring. Additionally, consuming just one serving of alcohol before bed can lead to OSA and heavy snoring even for people who have not been diagnosed with sleep apnea.

The relationship between sleep apnea and alcohol has been researched somewhat extensively. The general consensus based on various studies is that consuming alcohol increases the risk of sleep apnea by 25%.

What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more? - Biology


ANXIETY RESEARCH (U.K.), Volume 4: Pages 199-212.

Harvard Medical School

(Received 23 December 1991)

The recognition that trauma is qualitatively different from stress and results in lasting biological emergency responses following traumatic experiences may account for the biphasic trauma response, and the accompanying memory disturbances. The advances in our understanding of the underlying biology of this "physioneurosis". In addition to classically conditioned physiological reactions, changes now have been demonstrated in startle response in people with post-traumatic stress disorder and in central nervous system catecholamine, serotonin, and endogenous opioid systems. This paper reviews the research data which have demonstrated changes in these systems and explores how these biological changes may be related to the characteristic hyper-reactivity, loss of neuromodulation, numbing of responsiveness, dissociative states, and memory disturbances seen in PTSD. There is growing evidence that trauma has different biological effects at different stages of primate human, development. This article relates these findings to the studies which have demonstrated clear linkages between childhood trauma, and a variety of psychiatric disorders, including borderline personality disorder, and a range of self-destructive behaviors.

KEY WORDS: Post-traumatic stress disorder, psychobiology, arousal, memory, self-destructive behavior., psychopharmacology

They will fail to cope psychologically with their problems until they have a sense of security in their bodies. In loosing control over their bodily functions they are not the competent people they were before.

(Kolb & Multipassi, 1982 p. 985).

The recognition that trauma is qualitatively different from stress and results in lasting biological change goes back to the dawn of contemporary psychiatry. A century ago, Pierre Janet (1889) taught that overwhelming experiences are accompanied by "vehement emotions" which interfere with proper information processing and appropriate action. He thought that this hyperarousal caused the characteristic memory disturbances that accompany traumatization, by interfering with information processing on a verbal, symbolic level. Hyperarousal causes memories to be split off from consciousness and to be stored as visual images or bodily sensations. Fragments of these "visceral" memories return later as physiological reactions, emotional states, nightmares, flashbacks, or behavioral reenactments (van der Kolk & van der Hart, 1989).

Janet thought that the original excessive physiological response to trauma accounted for the continued emergency responses to subsequent stresses. He claimed that fear needs to be tamed for proper cognitive appraisal and for appropriate action: experiences which overwhelmed people's coping mechanisms set the stage (or to use Pavlov's later concept "condition" them) to react automatically with excessive emotional reactions to current experiences rooted in the past.

Freud adopted these views from Janet and also suggested that the fixation on the trauma is biologically based: "After severe shock . . . the dream life continually takes the patient back to the situation of his disaster from which he awakens with renewed terror . . . the patient has undergone a physical fixation to the trauma" (Freud, 1919, 1954, p. 207). The feature of hyperactivity to external stimuli was described by Freud in the clearest neuropsychiatric terms that he knew: "I think that one may venture . . . the traumatic neurosis as the result of an extensive rupture in the barrier against stimuli . . . we seek to understand the effect of the shock by considering the breaking through of the barrier with which the psychic organ is provided (p. 207).

Pavlov's investigations continued the tradition of explaining the trauma response as the result of lasting physiological alterations (Pavlov, 1926). He, and others employing his paradigm, coined the term "defensive reaction" for a cluster of innate reflexive responses to environmental threat. Many studies have shown how the response to potent environmental stimuli (unconditional stimuli-US) becomes a conditioned reaction. After repeated aversive stimulation, intrinsically non-threatening cues associated with the trauma (conditional stimuli-US) becomes a conditioned reaction. After repeated aversive stimulation, intrinsically non-threatening cues associated with trauma (conditional stimuli-CS) become capable of eliciting the defensive reaction by themselves (conditional response-CR). A rape victim may respond to conditioned stimuli, such as the approach by an unknown man as if she were about to be raped again, and experience panic. Pavlov also pointed out that "constitutional factors", i.e. individual differences in temperament, accounted for the variability in the human approach to traumatic stimuli.

Abraham Kardiner (1941) who first systematically defined post-traumatic stress for American audiences, noted that sufferers from PTSD continue to live in the emotional environment of the traumatic event, with enduring vigilance for and sensitivity to environmental threat. He described the five principal features of PTSD as (1) persistance of startle response and irritability, (2) proclivity to explosive outbursts of aggression, (3) fixation on the trauma, (4) constriction of the general level of personality functioning, nad (5) atypical dream life. He suggested that the startle reaction probably was a conditioned reflex and considered it the central element of the post-traumatic stress reaction, relating it to the development of irritability and psychosomatic symptoms in these patients.

In War Stress and Neurotic Illness, Kardiner and Spiegal (1945) stated that a traumatic neurosis is a physical one, and that the physical sensation endures: "the nucleus of the neurosis is a physioneurosis. This is present on the battlefield and during the entire process of organization it outlives every intermediary accommodative device, and persists in the chronic forms. The traumatic syndrome is ever present and unchanged" (p. 38).

In Men under Stress, Grinker and Spiegel (1945) describe physical symptoms in the acute post-traumatic state that seem to reflect neurochemical changes of the catecholamine system: they describe flexor changes in posture, hyperkinesis, "violently propulsive gait", tremor at rest, masklike faces, absence of associated movement while walking, cogwheel rigidity, gastric distress, urinary incontinence, mutism, and a violent startle reflex. Grinker and Spiegal noted the similarity of many of these symptoms and those of diseases of the extrapyramidal motor system. They seem to depict an extraordinary stimulation of biological systems, implicating ascending amine projections in particular. Contemporary studies, generally unaware of this earlier research, have continued to scientifically test these conceptions and they confirm that the stress hormones of people with PTSD continue to react in minor stimuli as emergencies.


The phasic post-traumatic symptoms of hyperalertness, hyper-reactivity to stimuli and traumatic reexperiencing have been documented in a vast literature on combat trauma, crimes, such as rape (e.g., Burgess & Holstrom, 1974 Kilpatrick, Veronen, & Best, 1985), kidnapping (Terr, 1983), natural disasters (e.g., Shore, Tatum & Vollmer, 1986), accidents (e.g., Wilkinson, 1983) and imprisonment (Krystal, 1978). The human response to trauma is so constant across traumatic stimuli that it is safe to say that the central nervous system (CNS) seems to react to any overwhelming, threatening and uncontrollable experience in quite a consistent pattern. Regardless of these circumstances, traumatized people are prone to have intrusive memories of element of the trauma, to have a poor tolerance for arousal, to respond to stress in an all-or-nothing way, and to feel emotionally numb. All of these psychological phenonema must have a basis in biological functioning, some of these relationships between biological states are now ready to be explored. PTSD as defined in the DSM-III-R, highlights those post-traumatic symptoms that are most clearly biologically based (for reviews see van der Kolk, 1987 Krystal et al., 1989) the secondary post-traumatic changes in identity and interpersonal relations are slated to be classified in the separate category of Disorders of Extreme Stress Not Otherwise Specified (DESNOS) in the DSM IV. Since there are good reasons to assume that the current PTSD hyperarousal are, biologically speaking, intimately related, we will discuss them jointly throughout this paper.

Autonomic Hyperactivity and Intrusive Reexperiencing

Kardiner (1941) coined the term "physioneurosis" to describe post-traumatic stress. He pointed out that while people with PTSD tend to deal with their environment by emotional constriction, their bodies continue to react to certain physical and emotional stimuli as if there were a continuing threat of annihilation. Starting with studies by Dobbs and Wilson (1960), conditioned autonomic arousal to combat stimuli has repeatedly been documented in veterans with PTDS. Using a variety of different techniques, Mallow, Fairbank, and Keane (1983) Kolb and Multipassi (1982), Blanchard, Kolb, Geradi, Ryan, and Pallmyer (1986) and Pitman, Orr, Forque, deJong, and Claiborn (1987), all have found significant conditioned reactions in response to stimuli reminscent of the original trauma, as measured by heartrate, bloodpressure and electromyogram. More recent studies have shown that both traumatized children (Ornitz, & Pynoos, 1989) and adults (Shalev et al., submitted) lack habituation to acoustic startle.

A relationship between autonomic arousal and intrusive recollections has long been postulated, and in recent years has started to be confirmed by the work of such investigators as Rainey and Southwick. Rainey et al. (1987) showed that the administration of lactate, which stimulates the physiological arousal system, elicited PTSD-like flashbacks in 7/7 subjects and panic attacks in 6 in 7 patients with PTSD, 6 of whom also met panic disorder criteria. Southwick and his colleagues demonstrated that yohimbine injections (which stimulate NE release from Locus Coeruleus) were able to induce somatosensory flashbacks in people with PTSD (Southwick et al., submitted). These studies further suggest common biological underpinnings of flashbacks and panic attacks in PTSD.

The reliability and specificity of the studies of physiological reactions to traumatic stimuli are beginning to raise the possibility that in the future a psychophysiologically based diagnostic test for PTSD will be available to help make the diagnosis. However, it is still unclear how specific the hyperarousal is as a conditioned response to traumatic stimuli alone. Clinical experience suggests that the increased autonomic arousal can be rather non-specific, and may occur in response to a variety of stimuli. In fact, some research suggests that habituation may follow repeated exposure to the traumatic stimulus itself, but associated events continue to illicit hyperactivity (Strian & Klicpera, 1978). These findings can be used therapeutically in implosion therapy (Keane, Fairbanks, & Caddell 1989).

The loss of neuromodulation that is at the core of PTSD leads to intensification of emotional reactivity in general: traumatized people go immediately from stimulus to response without being able to make the intervening psychological assessment of the cause of their arousal, which causes them to overreact and intimidate others. Non-specific noises played into the rooms of sleeping people with post-traumatic stress may precipitate nightmares in which old traumatic occurrences are recreated in exact detail (Kramer, Schoen, & Kinney, 1984). Hyperorousal also interferes with psychotherapy, in preventing remembering and working through painful memories.

Numbing of Responsiveness Numbing of responsiveness, which may be registered as depression, as anhedonia and amotivational states, as psychosomatic reactions, or in dissociative states, is tonic and part of the patients' baseline functioning. It interferes with the ability to explore, remember and symbolize which are essential to finding good meaning. Throughout the literature numbing is all too unquestioningly described as a psychological defense against remembering painful affects. Below, we will argue that numbing is a core, biologically based, symptom of PTSD.


While most studies on PTSD have been done on adults, particularly on war veterans, in recent years, a small prospective literature has emerged which calls attention to the differential effects of trauma at various age levels. Anxiety disorders, chronic hyperarousal, and reenactments have now been described with some regularity in acutely traumatized children (Bowlby, 1969 Eth & Pynoos, 1985, Stoddard, 1989 Terr 1988). In addition to the reactions to discrete, one time, traumatic incidents documented in these studies, intrafamilial abuse must certainly be included among the most severe traumas encountered by human beings. This recognition opens up the boundaries between the current concept of PTSD and the what we have called "the trauma spectrum" (van der Kolk, 1988): other post-traumatic disorders ranging from those that result from brief traumatic exposure at an early age, such as phobias and panic, to Borderline Personality Disorder and Multiple Personality Disorder which are usually associated with chronic intrafamilial abuse (Herman, Perry, and van der Kolk, 1989). Specific neurobiological abnormalities are beginning to be identified along this spectrum: prospective studies by Putnam are showing neuroendrocrine disturbances in sexually abused girls compared with normals, while others (G. Gillette, personal communication, 1989) have demonstrated abnormalities of the hypothalamic-pituitary-throid axis in adult female psychiatric patients with childhood histories of incest. Non-brain damaged adult patients who mutilate themselves invariably seem to have a history of severe childhood trauma, and their behavior has been associated with abnormalities of the endogenous opioid and catecholamine systems (Bach-y-Rita, 1974), van der Kolk, Greenberg, Orr, & Pitman, 1989). Research in the last decade has shown that many children who have been victims of intrafamilial abuse have chronic problems with hyperarousal, and aggression against others and themselves (Green, 1980 Cicchetti & Rosen, 1984 van der Kolk, Perry & Herman, 1991).

The biological effects of developmental trauma has best been studied in young non-human primates, who in many ways resemble young human beings. Forty years of primate research has firmly established that early disruption of the social attachment bond reduces the long term capacity to cope with subsequent social disruptions and to modulate physiological arousal. These studies have demonstrated that trauma early in the life cycle has long term effects on the neurochemical response to stress, including the magnitude of the catecholamine response, the duration and extent of the cortisol response, as well as a number of other biological systems, such as the serotonin and endogenous opioid systems (Kraemer et al., 1984, Reite & Field, 1987, van der Kolk, 1987).


The limbic system plays an important role in guiding the emotions that stimulate the behavior necessary for self-preservation and survival of the species. It is responsible for such complex behaviors as feeding, fighting, fleeing and reproduction, and it also assigns free-floating feeling of significance, truth and meaning to experience (MacLean, 1985). Destruction of parts of the limbic system abolishes social behavior, including play, cooperation, mating, and care of the young. The apparent similarities between some aspects of Temporal Lobe Epilepsy (TLE), PTSD and some long term sequelae of childhood trauma continues to challenge us to further explore the effects of trauma on the limbic system. During this past decade, the relationships between environmental trauma and the organization and function of the limbic system are slowly beginning to be understood, in part because of the work on non-human primates, which has conclusively shown that disruption of early attachment directly affects the maturation of the limbic system (Kling & Steklis, 1976). The limbic system also is the primary area of the CNS where memories are processed, and the most likely place to find an explanation for the memory disturbances which follow trauma. The hippocampus, which records in memory the spatial and temporal dimensions of experiences, dose not fully mature until the third or fourth year of life. However, the system that subserves memories related to the quality (feel and sound) of experience (which is located in the amygdala) matures much earlier (O'Keefe & Nadel, 1978 Jacobs & Nadel, 1985). Thus, in the first few years of life only the quality of events, but not their context can be remembered. Even after that, the hippocampal localization system remains vulnerable to disruption: severe or prolonged stress can disrupt hippocampal functioning, creating context-free fearful associations which are hard to locate in space and time. This results in amnesia for the specifics of traumatic experiences, but not the feelings associated with them. (Sapolsky, Krey, & McEwen, 1984). These experiences then may be encoded on a sensorimotor level without proper localization in space or time. They therefore cannot be easily tranlated into the symbolic language necessary for linguistic retrieval.

A third trauma related function of the limbic system involves the issue of kindling. Intermittent stimulation of the limbic system with an electrical current that was initially too small to produce overt behavioral effects can eventually sensitize limbic neuronal circuits and lower neuronal firing thresholds: repeated stimulation of the amygdala causes long-term alterations in neuronal excitability (for a review, see van der Kolk, 1987). It is possible that similar kindling phenomena occur when people are repeatedly traumatized, or when one traumatic event is followed by intrusive reexperiences. Thus, trauma may lead to lasting neurobiological and behavioral (characterological) changes mediated by alterations in the temporal lobe. Kindling may also account for the frequent finding of soft neurological signs in trauma victims, especially in child victims of physical or sexual abuse (van der Kolk, 1987). Open studies claim that carbamezapine is an effective treatment for the intrusive symptoms of PTSD (Lipper et al., 1986) which lends some support for a role of the limbic system in codifying post traumatic reactions.


The Locus Coeruleus (LC) is at the anatomical core of the physiological arousal mechanism in the Central Nervous System (CNS). It is the principal source of noradrenaline (NE) in the CNS, the neurotransmitted responsible for delivering messages to the rest of the brain about the need to prepare for emergencies. These noradrenergic connections prepare the hypothalamic mechanisms which control defensive reactions to be ready for action. Another noradrenergic bundle connects the LC with the septo-campal system, the part of the limbic system involved in the evaluation of the incoming stimuli. This noradrenergic bundle does not carry specific information, only the general message: this in important (Gray, 1982). Impulses reaching the septo-hippocampal system influence the interpretation of incoming information. Several naturally occurring or exogenous biochemical agents influence noradrenergic activity: endogenous opiates inhibit the firing of the LC (Bird & Kuhar, 1977), while such pharmacological agents as clonidine and the beta adrenergic blockers produce the same effect by: reducing noradrenergic activity in the the LC neurons. Antianxiety drung interferer with LC activity by increasing GABA-ergic inhibition on the cell bodies of the LC.

The function of the septo-hippocampal system is to evaluate the rough meaning of incoming stimuli, and whether they are associated with reward, punishment, novelty, or non-reward. The hippocampus thus is thought to be the evaluation center involved in behavioral inhibition, obsessional thinking, exploratory behavior, scanning and construction of a spatial map (O'Keefe & Nadel, 1978). It fulfills the crucial function of storing and categorizing information. When categorization is complete, the hippocampus disengages from active control of behavior. External stress increases corticosterone production which decreases the firing rate of the hippocampuse (Pfaff, Silva, & Weiss, 1971). Lesions of the hippocampus lead to motor paralysis because of excessive interference from competing responses.

The signal that punishment is imminent activates two related mechanisms, one of which inhibits ongoing behavior, while the other increases the level of arousal. The behavioral facilitating system (BFS) (which is mediated by NE fibers emanating from the LC) activates the CNS structures necessary for emergency responses. The BFS is activated when specific goal-oriented aggressive attack patterns require motivated motor support (Dupre & Spoont, 1989). The opposing system, that of behavioral inhibition (BIS) is mediated by the septo-hippocampal system, primed by ascending serotonergic and cholingergic mechanisms. The crucial role of the septo hippocampal system is to activate a descending inhibatory pathway which prevents initiation of emergency responses until it is clear that they are needed. Numerous studies have shown that serotonergic antagonists also cause increased aggression in response to stress, and hyper-reactivity to stimuli. (Sheard & Davis, 1976). The suppression of behavior by punishment is reversed by serotonin receptor blockers (e.g., Cook & Sepinwall, 1975). The ascending serotonergic pathways are thought to signal the septo-hippocampus to distinguish punishment from reward. The introduction of the serotonin reuptake blockers fluvoxamine, fluoxetine and gepirone demonstrated how these agents reversed the continued emergency responses and repetitive behaviors following stress in animals, allowing a better understanding about the degree to which decreased serotonin seems to play a role in these behaviors. Current clinical trials of these drugs in people with PTSD suggest that they are by far the most effective biological treatments of PTSD currently available. This makes us believe that in traumatized individuals decreased serotonin decreases the influence of the Behavioral Inhibition System, thereby disposing the septo-hippocampal system to interpret ordinary stressors as recurrents of traumatic experiences. Thus we postulate that lowered serotonin activity in PTSD is responsible for the continuation of emergency responses to minor stresses long after the actual trauma has ceased.


Arousal The body responds to increased physical or psychological demands by releasing norepinephrine from the Locus Coerulus and adrenorcorticotrophin (ACTH) from the anterior pituitary. The precise interactions between the various stress hormones is extremely complex, and still is poorly understood, but both norepinephrine and epinephrine play a role in stimulating the release of CRF (Axelrod & Neisine, 1984). The Hypothalamus regulates ACTH release by the secretion of corticotrophin releasing factor (CRF). The hypothalamus also secretes throxin releasing hormone (TRH) which activates the secretion of Thyroid Stimulating Hormone (TSH) from the pituitary. CRF, as well as vasopressin, activates the release of ACTH and beta endorphin and stimulate adenylate cyclase activity and the formation of cyclic AMP. Peripherally, the body's stress response consists of the secretion of norepinephrine by the sympathetic nerves and of epinephine by the adrenal medulla, while, stimulated by ACTH, the adrenal cortex secretes glucocorticoids. These hormones help the body mobilize the energy necessary to deal with stressors, ranging from increased glucose release to enhanced immune function. In a well functioning organism stress produces rapid and pronounced hormonal responses. However persistent stress blunts this effective stress response and induces desensitization: after prolonged stress, CRF secretion produces less cylic AMP formation and ACTH release because of down regulation of CRF receptors (Axelrod & Neisine, 1984).

It therefore is not surprising that, in a study of the psychobiology of PTSD, stress hormones have figured most prominently, and that abnormalities of these systems are often found in patients with PTSD. Kosten, Mason, Giller, Ostroff, and Harkness (1987) found increased 24 hour norepinephrine and epinephrine secretions in veterans with PTSD compared with patients other psychiatric diagnoses. Mason, Giller & Kosten (1988) found low 24 hour urinary cortisol levels in Vietnam veterans with PTSD. In a different study, PTSD subjects showed blunted ACTH response to CRH stimulation: Smith et al. (1989) found that the severity of PTSD was directly related to baseline cortisol level. This supports the notion that there is chronically increased levels of cortisol in patients with PTSD. However, Smith et al. also suggested the alternative explanation of decreased pituitary function secondary to persistent elevations of endogenous CRH due to chronic HYPAC axis activity at the level of the hypothalamus.

Changes in receptor activity have been found in PTSD which are consistent with down regulation secondary to chronic exposure to elevated levels of circulating catecholamines: Perry and associates (Perry, Giller, & Southwick, 1987) have demonstrated a 40% decrease in the muber of platelet alpha2 adrenergic receptors in 25 patients with PTSD. Lerer, Ebstein, Shestatsky, Shemesh, and Greenberg (1987) recently reported evidence of desensitization of adenylate cyclase coupled adrenergic receptors on lymphocytes and platelets with PTSD.

However, persistent activation of stress response is not only a function of the stress hormones themselves, but also of the capacity of the organism to modulate arousal. We discussed before how serotonergic input into the septal-hippocamus decreases the relative strength of the noradrenergic input, allowing modulation of the emergency responses. The serotonin reuptake blockers fluvoxamine, fluextine and gepirone seem to have a dramatic beneficial effect on the capacity to modulate arousal and decrease Post-traumatic repetitions of images, behaviors, or somatic states. The clinical trials with these drugs suggest that they are by far the most effective biological treatments of PTSD currently available.

Numbing While the numbing in responsiveness in PTSD has generally been conceptualized only in psychological terms, as a defense against reliving memories of the trauma, our recent research may shed some light on the biological components of this aspect of PTSD. Stress induced analgesia (SIA) has been described in experimental animals following a variety of inescapable stressors as electric shock, fighting, starvation and cold water swim. (Kelly, 1982 for a review see van der Kolk, 1987). In these severely stressed animals, opiate withdrawal symptoms can be produced equally by termination of the stressful stimulus or by naxolone injections. Thus, severe, chronic stress in animals results in a physiological state which resembles dependence on high levels of exogenous opioids (Terman, Shavit, Lewis, Cannon, & Liebeskind, 1984 Maier & Seligman, 1976).

Stimulated by the finding that fear activates the secretion of endogenous opioid peptides and that SIA can be become conditioned to subsequent stressors, and to previously neutral events associated with the noxious stimuli, we tested the hypothesis that in people with PTSD, re-exposure to a stimulus resembling the original trauma will cause an endogenous opioid response that can be indirectly measured as naxolone reversible anesthesia (van der Kolk et al., 1989 Pitman, van der Kolk, Orr, & Greensburg, 1990). We found that two decades after the original trauma, people with PTSD developed opioid-mediated analgesia in response to a stimulus resembling the traumatic stressor, which we correlated with a secretion of endogenous opioids equivalent to 8 mg. of morphine. This change in pain response was the most significant factor differentiating the PTSD from the control groups' response to a traumatic stimulus. Self-reports of emotional responses to the combat videotape in the placebo condition indicated a relative blunting of emotional response to the traumatic stimulus and we interpreted this finding to indicate that opioid-mediated SIA may be involved in psychic numbing. Survivors of severee trauma have repeated described a triad of physical analgesia, psychic numbing and depersonalization. Our finding of SIA in PTSD may also be relevant to the phenomenon of self-mutilation. Patients who engage is such self-destructive behavior or neglect invariably have a history of severe childhood trauma and, in response to even relatively minor emotional stressors, they may experience physical analgesia, dissociative reactions and emotional numbing, which can be abolished b (1) an act of self-mutilation or (2) the administration of naloxone (Richardson & Zaleski, 1983 Sandman, Barron, Crinella, & Donnelly, 1987) Whether the analgesia, dissociative reactions, and emotional numbing reported in these patients are all functions of a conditioned endogenous opioid response to a traumatic stressor remains a subject for further investigation.

Memory disturbances in PTSD. One of the hallmarks of PTSD is the intrusive reexperiencing of elements of the trauma in nightmares, flashbacks, or somatic reactions. These traumatic memories seem to be triggered by autonomic arousal (Rainey et al., 1987) and are thought to be due to the hyperpotentiation of memory pathways and mediated by noradrenergic pathways originating the locus coeruleus (LC) (van der Kolk, Greenberg, Boyd, & Krystal, 1985). The innervation of the structures of the brain subserving memory functions originate in the LC from which noradrenergic projections go to the limbic system, cerebral cortex, and to a lesser degree the hypothalamus (Grant & Redmond, 1981). The LC also facilitates memory retrieval by means of the noradrenergic tracts in the hippocampus and amygdala (Delaney, Tussi, & Gold, 1983). We (van der Kolk et al., 1985) and Pitman (1989) have hypothesized that a long term augmentation of the LC pathways following trauma underlies the repetitive intrusive relieving of the trauma, particularly after renewed stress. Since autonomic arousal is mediated by the LC it is plausible that not only flashbacks, but also traumatic nightmares accur following autonomic nervous system activation, mediated by the potentiated pathways from the LC to the hippocampus and amygdala. This also could account for the eidectic (picure-like), rather than oneiric (dream-like) quality of traumatic nightmares (van der Kolk et al., 1984) Further evidence for the existence of such long-term potentiation of memory in patients with PTSD comes from the recent experimental work by Southwick et al. (submitted).

Sleep studies. Patients with PTSD have been found to have chronically disturbed sleep which appears to be related to chronic hypearousal. Both Kaminer and Lavie (1988) and van Kammen, Christiansen,, van Kammen, and Reynolds (1990) found increased sleep latency, more awakening, less total sleep time and less REM time. Several researchers have found PTSD patients to be exquisitely sensitive to non-specific auditory stimuli during sleep the resulting autonomic arousal seems to precipitate nightmares about traumatic experiences, a finding that appears to analogous to that of Soutwick et al. We (van der Kolk et al., 1984) found that post-traumatic nightmares occur during any stage of the sleep cycle that most tend to occur during 2 and 3 a.m. during Stage II or III sleep, possibly during a transition to REM sleep. When they occur during Stage II or III, patient report exact living experiences of traumatic material, while, during REM, they are more likely anxiety dreams.

Psychosomatic reactions. Numerous studies for the past one hundred years have established a causal relation between the inhibition of expression of traumatic experience and psychophysiological impairment. These studies have demonstrated a marked increase in symptoms of the respiratory, digestive, cardiovascular and endocrine systems in people with PTSD (Janet, 1989 Krystal, 1978). Recent studies have indicated that learning to express the memories and feelings related to the traumatic event can restore some of the psychophysiological and immunological competence to people with trauma histories (Pennebaker & Susman, 1988).


While giving voice to both the traumatic events and the affects related to them is generally considered the most effective treatment of PTSD, verbal therapies cannot proceed as long as the patient is unable to tolerate the feelings associated with the trauma and continues to experience subsequent emotionally stimulating event as an unmodified recurrence of the trauma. It often is necessary to supplement psychotherapy with medications which decrease autonomic arousal, or increase neuromodulation. Clinical studies of war veterans have show that the autonomic nervous system is centrally involved in many of the symptoms of PTSD, including startle reactions, irritability, nightmares and flashbacks ad explosive outbursts of aggression. It is therefore predictable that those medications which affect autonomic arousal would prove helpful in relieving the symptoms of PTSD. Autonomic arousal can be reduced at different levels in the central nervous system: although inhibition of noradrenergic activity, (clonidine and the beta adrenergic blockers), by increasing the inhibitory effect of the gaba-ergic system with gaba-ergic agonists (the benzodiazepines) and through enhancing the serotonergic inhibition system with agents such as Lithium and the serotonin uptake blockers, monomine oxidase inhibitors (Hogben & Cornfield, 1981 Frank, Kosken, Giller, & Dan, 1988), lithium carbonate (van der Kolk, 1983), beta adrenergic blockers and clonidine (Kolb, Burris, & Griffiths, 1984), carbamezapine (Lipper et al., 1986) and antipsychotic agents. However, no carefully controlled studies documenting the differential effects of various psychotropic medications on the symptoms of PTSD exist at this time. The only psychotropic medications whose efficacy in PTSD sympomatology have been evaluated in double blind studies are tricyclic antidepressants and MAO inhibitors Bleich, Siegel, Garb, Kettler, & Lerer, 1987 Davidson, Kudler, Smith, Mahorney, & Lipper, in press Frank et al., 1988). These studies indicate that tricyclic antidepressants are effective in treating affective disorders in patients with PTSD, but do no little for core PTSD symptomatology, including psychological numbing. Tricyclic antidepressants generally thought to be most effective in treating nightmares, depression, sleep disorders and startle reactions, but were less able to relieve numbing. Hogben and Cornfield (1981) found MAO inhibitors effective in the treatment in PTSD, but that anecdotal study has not consisently held up to subsequent investigation (e.g., Shetaksy, Greenberg, & Lerer, 1989). Current studies in our laboratory indicate that the serotonin reuptake blocker fluoxetine is markedly effective in treating both the intrusive and the numbing symptoms seen in patients with PTSD.

A rapidly expanding knowledge of the effects of traumatization on the functioning of the Central Nervous System, the dawning awareness that memory functions are central in understanding the nature of PTSD, combined with the availability of animal models for PTSD, makes the psychobiology of trauma one of the most promising areas in psychiatry. As long as the most effective therapy of PTSD has not been firmly established, a greater understanding of the biochemical and physiological correlates of traumatization should provide important clues about appropriate intervention. A variety of psychopharmacological agents that affect the physiological arousal system, including clonidine, benzodiazepines, monoamine oxidase inhibitors, and tricylic antidepressants decrease the long term effects of inescapable shock in animals, and seem to have varying degrees of use in the pharmacotherapy of PTSD. The recent discovery that serotonin reuptake inhibitors seem to act by quite a different mechanism and may be extremely effective in reducing both the intrusive and the numbing effects of PTSD needs to be carefully documented and understood. Further exploration during the coming decades of how trauma affects neuroendocrine emergency systems, neuromodulation, and memory should provide us with a much greater understanding about the interplay between soma and psyche in coping with potentially overwhelming experiences.