Audio-Visual Entrainment as a Treatment Modality

for Post-Traumatic Stress Disorder (Part One)


By David Siever 


Abstract: Post-traumatic stress disorder (PTSD) is the aftermath of trauma. Trauma spans a diverse spectrum of unfortunate life experiences such as sexual abuse, assault, car accidents, war, and natural disasters. PTSD occurs when the inflicted can no longer mentally cope with the situation. Following trauma, permanent changes occur within the brain that increases “racy-headedeness,” guardedeness, anxiety, depression, insomnia, plus memory and cognitive impairments. The behavioral aftermath of PTSD also typically involves increased aggression and drug and alcohol abuse. Audio-visual entrainment (AVE) has been shown to reduce anxiety, insomnia and improve coping for police officers and military. AVE has also been shown to reduce depression and anxiety among vets with chronic fatigue syndrome and fibromyalgia.



The American Psychiatric Association defines psychological trauma as “the development of characteristic symptoms of intense fear, helplessness, or horror following exposure to an extreme traumatic stress or involving direct personal experience of an event that involves actual or threatened death or serious injury, or other threat to one’s physical integrity; or witnessing an event that involves death, injury, or a threat to the physical integrity of another person; or learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate,” (American Psychiatric Association, 1994).

The ensuing brain damage from severe and chronic stress further brings about a host of trauma-related psychiatric disorders or trauma spectrum disorders, which include impairments in learning, reasoning, rationalizing, impaired alertness and increased destructive behavior including smoking, alcoholism, drug abuse, family violence and reckless risk taking (Bremner, 2002). Psychological trauma affects about half of all Americans sometime in their lives. As described by Bremner, Post Traumatic Stress Disorder (PTSD) comes about from acquiring the knowledge or “wisdom” that the world is not a safe place, as once believed.

Every year, in the USA, more than 1 million children are confirmed as victims of child abuse (Teicher, 2002) and close to 50 million American adults have suffered from childhood abuse. Somewhere between 25% and 50% of all Americans are exposed to a psychological trauma, related to a wide variety of incidents including child abuse, assault, rape, car accidents, house fires, natural disasters, etc., at some time in their lives (Acierno, et al, 1999). Of these, about 15% will develop PTSD, roughly comprising 5% to 8% of the American population, making it one of the most common illnesses in the USA. PTSD is twice as common in women as men (Kessler, et al, 1995). PTSD is 10 times more common than cancer, yet society dedicates only one tenth the funding in PTSD research as it does for cancer research (Bremner, 2002).

The Aftermath of War

About one million young men experienced the stress of the Vietnam War between 1963 and 1971 and several hundred thousand were deployed in the Gulf War from 1990 to 1991 (Bremner, 2002). Currently, U.S. Service Members serving overseas in theaters of operation in Afghanistan and Iraq are continually subjected to direct and indirect traumatic effects of combat, which includes shelling, artillery, missile attacks, improvised bombs, watching people die and dealing with burnt, charred bodies. Service members assigned to combat support and service support units that are not on the front lines are just as exposed to the effects of PTSD, since rear echelon units no longer have the traditional distinction of being non-combative. The individual service member’s physical condition, training and experience for combat will certainly prepare him or her for these various traumatic experiences often encountered during military missions, but no matter how trained an individual is to deal with the tragedy of war, trauma is inevitable.

For all groups responding after deployment, there was a strong reported relation between combat experiences, such as being shot at, handling dead bodies, knowing someone who was killed, or killing enemy combatants, and the prevalence of PTSD. For example, among soldiers and Marines who had been deployed to Iraq, the prevalence of PTSD increased in a linear manner with the number of firefights during deployment: 4.5% for no firefights, 9.3% for one to two firefights, 12.7% for three to five firefights, and 19.3% for more than five firefights. Rates for those who had been deployed to Afghanistan were 4.5%, 8.2%, 8.3%, and 18.9%, respectively (Hoge, et al., 2004).

Other major contributing factors related to PTSD are combat casualties, such as those related to a permanent disability such as amputation. These soldiers not only experience the immediate trauma from the event and struggle to dissociate from its significance, but also must deal with a physical, irreversible change in their life, where psychological therapy is required for adaptation. The effects of PTSD are not one-sided. It also affects the spousal and family relationship, and puts as much or more stress on the spouse and children with the burden and apprehension of deployment and feelings of abandonment. Upon returning home, the dysfunction of PTSD has an immediate effect on the relationship of the veteran, spouse and family. If not diagnosed and treated promptly, PTSD quickly manifests itself into a socio-economic burden on society. To exemplify the far-reaching aspects of PTSD, it has been reported that more veterans have died in motorcycle accidents at home in the USA from thrill seeking (350 deaths) as compared with 259 deaths Afghanistan (Edmonton Journal, 2006).

With the exceeding numbers of civilian and military Americans that suffer from PTSD, research to develop a non-drug treatment/method of therapy for treating PTSD, and without adverse side effects, would be an asset to both the inflicted as well as society.

About the Zone

Socialized mammals, and particularly humans, have two performance zones (Figure 1). There is one zone requiring higher arousal for simple tasks and the other requiring lower arousal for complex tasks. So what would be a simple task? Running fast, climbing a tree, spearing some food, punching an attacking animal or tribal enemy in the nose are examples of where we show peak-performance under high arousal, in other words, fight-or-flight activity. This is generally accompanied by excitement and often anxiety. A highly aroused state of body/mind involves the suppression of serotonin and increased production of norepinephrine, the brain’s adrenalin (Bremner, 2002). This is why athletes who perform highly physical activities do better under the influence of caffeine, as caffeine has been shown to increase norepinephrine. 

Complex tasks, on the other hand, typically involve the cognitive mind on a much grander level than simple tasks. Complex tasks involve calculating a math formula, learning new concepts, and driving a car in busy traffic, but the most important aspect of calm-arousal is socialization.

Those with PTSD have lost their ability to learn new skills or occupations, reason and socialize (Bremner, 2002). The responsibility of making an income, pride in having a steady job and the toll on relationships with family and friends exacts a heavy price.

Physiology of the Fear Response

The survival response rapidly activates via the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is a “triangle” in which the hypothalamus and pituitary glands in the brain communicate with the adrenals. In response to stress, the hypothalamus releases corticotrophin-releasing factor (CRF), which causes the anterior pituitary gland to make adrenocorticotrophic hormone (ACTH). This in turn causes the adrenals to produce glucocorticoids such as cortisol and adrenalin which stimulates the spleen to increase red blood cells to send more oxygen to the muscles, dilates the pupils of the eyes for better vision, and releases endorphins to dull the sense of pain (Bremner, 2002). Cortisol also raises blood sugar concentrations, increases energy to the periphery and inhibits the immune system.

The Role of Serotonin in Behavior

Serotonin acts as the brain’s brakes, keeping basic emotions (such as sex, mood, appetite, sleep, arousal, pain, aggression, and suicide ideation) in check. Serotonin also influences dominance and has been shown to be high in salesmen with outstanding sales performance. These salesmen averaged 180 ng/ml levels of whole blood serotonin (WBS), whereas poor performers had average WBS levels of 140 ng/ml of blood volume (Walton, et al., 1992). A study by Raleigh (Kotulak, 1997) found that when subordinate monkeys were given a serotonin reuptake inhibitor like Prozac, they became dominant through friendship and alliances with the females. Dominant monkeys deficient in serotonin ruled with aggression. Females have 20% to 30% more serotonin than men, which contributes to their reduced aggression (Kotulak, 1997). Like the “Prozac” monkeys and salesmen, college students with the most friends had serotonin levels 20% to 40% above the norm. Those with high levels of serotonin, connect better socially with improved ability to read facial, verbal and body expressions (Harmer, et al., 2003).

In a serotonin experiment by Young and Pihl, (1988), pairs of normal, young males were given the task to be the first person to push a button when a light flashed. The winner had the option of also giving his opponent an electric shock in the range from 1 (mild) to 8 (strong). Normally, the shocks given were mild and relatively “tit-for-tat.” However, when one of the pair was given a serotonin antagonist, that person would frequently deliver more severe shocks (above “4”) even if they received mild shocks. On the other hand, if one of the pair was given tryptophan, a pre-cursor to serotonin, that person tended to deliver milder shocks to his partner, even if he previously received stronger shocks.

Low levels of serotonin are tied to loss of control and helplessness, which manifests as temper and rage (Sapolsky, 2003). Many of my clients report increased anxiety from traffic congestion, tight scheduling, computer problems, terrible customer service with many businesses, and other frustrations that have come with the “modern” age. All of these “highlighters of helplessness” contribute to highly increased frustration and aggression, much like studies with mice that are given random electrical shocks beyond their control (Sapolsky, 2003). So it’s no wonder that even though the population of the USA has only increased by 40% from 1960 through 1991, aggravated assaults have increased by 600%, violent crime by 560%, rapes increased by 520%, and murders by 170%, according to FBI statistics (Kotulak, 1997).

People low in serotonin and 5HTP have an increased risk of sexual deviance, alcoholism, fire-setting, obesity, and other impulse-control disorders (Kotulak, 1997). Conditions such as anxiety, depression and tendencies toward alcohol and drug abuse have been shown to run in families (Virkkunen, 1989). A study of 114 male alcoholic and violent offenders and fire-setters showed that low levels of cerebral spinal fluid, 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid were strongly associated with a family history of paternal violence and alcoholism. A study by Linnoila (1983) of prisoners who were in jail for manslaughter, used serotonin levels as a basis in predicting with 84% accuracy those who would recommit manslaughter following their release from prison.

The Role of Norepinephrine in Behavior

Noradrenalin or norepinephrine (NE), a close relative of adrenaline is also a player in vigilance (Bremner, 2002). Low levels of noradrenalin are associated with under-arousal including lethargy and mental fuzziness (Amen, 1998). Above average levels are related to peak performance, while abnormally high levels correlate to impulsive “hot-headed” violence (Kotulak, 1997).

Norepinephrine is manufactured in the locus coeruleus (dorsal pons), a site in the brainstem. Long neurons project to multiple sites throughout the brain for direct and immediate release. NE activates in response to both internal stressors such as a drop in blood pressure due to a lack of blood and external stressors such as threats (Aston-Jones, Chiang & Alexinsky, 1991). During rest, feeding and grooming in primates, the NE system is quiet. However, NE activates rapidly with the perception of a threat; increasing heart rate and blood pressure and behaviors of aggression (Aston-Jones, Chiang & Alexinsky, 1991). NE activates on an as-needed basis. Monkeys taught to play a video game showed increased NE activation along with alertness and vigilance as the game increased in challenge. However, a threshold exists where past a certain point of challenge, the monkeys became more anxious and distracted and performance began to decline (Aston-Jones, Chiang & Alexinsky, 1991). Animal studies have shown that animals exposed to repeated stress and cannot escape, leads to the emotion of learned helplessness, which correlates with the depletion of norepinephrine.

The Sympathetic Loop

The aftermath of trauma results in a double-edged sword. First, with the experience of trauma comes a fall in serotonin and increased norepinephrine, as the mind prepares to protect itself from further assault by “keeping its guard up.” However, these neurotransmitter changes also lowers the threshold whereby a person perceives events in his environment as threats; a mere wrong look or sense of rejection from anyone encountered in the acute/posttraumatic stress disordered person’s travels (including family members,) could constitute a perceived threat and launch the PTSD survivor into aggression against “threats” that were never previously perceived to be as such, thus maintaining a trauma-generating mindset to typical daily events. The PTSD survivor could blow up into rage from a baby crying, at the supermarket or into road-rage while driving. Therefore, trauma poses a socio-economic toll, producing aggression and violence, family breakup, and lost productivity in the workplace, as well as hundreds of millions spent annually on recreational and prescription drugs.

Unfortunately, the limbic system never evolved beyond the reptilian stage, and given that humans are primarily pack (social) animals, very basic socio-emotional perceptions such as a mere wrong look or sense of rejection from anyone encountered in the acute/posttraumatic stress disordered person’s travels (including family members or rejection from the individual him/herself) could constitute a threat and launch the PTSD survivor into aggression.

Survivors of trauma, once crossing the serotonin/norepinephrine threshold, get locked into the sympathetic loop. Assuming that the original traumatic event has come and gone, the loop is maintained from persistent thoughts, reminders of, and imagination of past threats (and/or new threats with the now reduced fear threshold). This continues to suppress serotonin and increased norepinephrine, and in turn maintains increased aggression and endless rumination or “racy head,” which keeps the self-imagined fear going. (In part, this is caused by outgoing fibers feeding into the frontal cortex causing one to believe he/she is threatened, which in turn reinforces activation of the amygdala). This triggers the production of CRF, which, in turn, triggers ACTH, which then stimulates the adrenals as the body of the threatened individual prepares for battle.

Somatic (Body) Damage from Chronic Fear and Trauma

Continuous bouts of activation of the hypothalamic-pituitary-adrenal-axis (HPA) exact a personal toll on the body. This results in irritable bowel syndrome, tension and migraine headache, neck and spine problems, temporo-mandibular dysfunction, heart disease, skin rashes, slow recovery from viral and bacterial infections, insomnia, alcoholism and drug abuse (Everly, 2002) and ulcers, diabetes and osteoporosis (Bremner, 2002). The eventual adrenal fatigue leads to low blood pressure, chronic fatigue, and fibromyalgia, frequent respiratory infections and difficulty recovering from them (Wilson, 2001). Behavioral components are extreme fatigue in the morning – leading to consumption of caffeine, and an energy surge in the late evening – leading to consumption of alcohol and drugs for sleep (Wilson, 2001).

Cognitive Damage from Chronic Fear and Trauma

While acute (mild) stress enhances mental function, chronic (severe) stress impairs hippocampal function (Gurvits, 1996), and correlated with impaired memory, (Bremner, Randall, Scott, et al., 1995). PTSD may also lead to increased risk of multiple sclerosis, anxiety, depression, schizophrenia and Alzheimer’s disease (Esch, et al., 2002).

Anxiety and fear increases cortisol in the brain. Cortisol counteracts a brain-nourishing hormone called brain-derived neurotrophic factor or BDNF (Bremner, 2002). Loss of BDNF leads to neuronal cell death in various regions of the brain. The most common structural changes from PTSD are reduced hippocampal volume, amygdala (emotional) activation, decreased Broca’s area activity, and decreased pre-frontal lobe activity.

Brain Structural Damage from Trauma

People who were physically or sexually abused as children had smaller hippocampal volume and the same pattern of memory deficits as veterans (Bremner, Randall, Capelli, et al., 1995). Of particular interest is that depression was associated with an average 19% smaller left hippocampal volume (Bremner, Narayan, et al., 2000).

The effects of increased cortisol also strips GABA within the amygdala, impairing the ability to relax, thus increasing tics, twitches and incidence of temporal-lobe seizures (Teicher, 2002). Decreased activity in Broca’s area causes impaired verbal expression, (Hull, 2002).

Those living in fear have further impairments in their memory and self-reliance in remembering, as they become seniors (Levy, 1996). The military would benefit from assessing new recruits with brain Magnetic Resonance Imaging (MRI), as those going into combat with pre-existing smaller hippocampal volumes are predisposed to developing PTSD (Gilbertson, et al., 2002).

Hippocampal loss also plays a major role in the early onset of dementia of the Alzheimer’s type, where the ability to form memories later in life is impaired.

Impact On Socialization

Socialization has brought about a rich wonderment of expressiveness. We have roughly 4000 facial expressions (Ekman, 2007 & 2009), over a thousand body-language positions and movements, and all kinds of verbal expressions and intonations (Navarro, 2008). Those with PTSD cannot perceive typical facial, verbal and body expressions – only the extreme ones. In a sense, they become perceptually Attention Deficit Disorder (ADD). They struggle to read social and emotional expression; they generally overreact in an impulsive and aggressive way; and often don’t realize the hurt they inflict on their victims (Bremner, 2002).

And as the PTSD survivor alienates and loses his/her support network of family and friends, he/she feels more isolated and rejected. This perceived barrage of threats to the livelihood of those with PTSD keeps serotonin low, cortisol flowing, norepinephrine (and anger) high and the continual stripping of amygdala GABA receptors, resulting in the inflicted being no longer able to idle, and keeps them in a revving state, constantly on guard. Eventually, the endocrine system burns out, in a condition known as hypoadrenia or adrenal fatigue (Wilson, 2001). As the adrenals fatigue, so does the locus coeruleus resulting in reduced NE levels in the brain and increased suicide ideation.

Both Vietnam War veterans and women with abuse-related PTSD have reduced blood flow in the hippocampus and medial prefrontal cortex (Bremner, et al, 1999). The medial aspects of the pre-frontal cortex are instrumental in extinguishing fear responses to conditioned stimuli (Ledoux, 1996). People with PTSD do not have normal activation of the prefrontal medial cortex and are not able to extinguish their own fear responses while watching a movie involving violence (Bremner, et al., 1997). Whereas people without PTSD are able to rationalize that they are only watching a movie and do not show a trauma response to the movie. This means that people with PTSD have crossed the threshold of being able to return to a relaxed homeostasis, and therefore live in an irrational and constant state of fear. The U.S. Army is researching the use of Virtual Realty (VR) Exposure Therapy with biofeedback for Iraqi veterans diagnosed with PTSD (Rizzo, 2005).

This continued state of fear also inflicts damage to the frontal and temporal regions, known as frontotemporal dementia (Bremner, 2002). Frontotemporal damage further impairs a person’s ability to control fear and the ability to reason and understand the significance of events in his/her life (Bremner, 2002), leaving the inflicted in a generalized state of anxiety, fear and confusion.

Unfortunately, PTSD inflicted dementia can affect persons as young as teenagers (Bremner, 2002). Dementia is a problem, particularly for war veterans and is the reason why it is difficult to succeed in career retraining for civilian life (Bremner, 2002). T

End of Part One

©Mind Alive Inc. (2012) Dave Siever. Posted with permission.