Audio-Visual Entrainment as a Treatment Modality for Post-Traumatic Stress Disorder (Part Two)

 

Audio-Visual Entrainment as a Treatment Modality for Post-Traumatic Stress Disorder (Part Two)

 

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.

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Electroencephalographic (EEG) Changes from Chronic Fear and Trauma

 

The increased norepinephrine and cortisol levels in those with PTSD have an effect on EEG activity. The bulk of Quantitative EEG (QEEG) studies involving PTSD, suggest that most often there is reduced alpha activity and increased beta activity, coincident with high arousal (Jokic’-Begic’ & Begic’, 2003), and alpha asymmetry with heightened right-frontal activity in those who have developed depression (Gordon, et al, 2010; Rabe, et al., 2008) and elevated beta and theta activity (Begic, et al., (2001).

 

Affective Disorders Stemming from Trauma

 

Many people, in the aftermath of trauma, also succumb to affective disorders. Affective disorders pertain to disorders of emotion, including depression, anxiety and mania. Depression is the most common psychiatric disorder by far. About 14% of the American population will experience clinical depression in their lifetime. Of these, an alarming 15% will unfortunately commit suicide (Rosenfeld, 1997). The helplessness of depression is not a quiet, passive state; rather it is an active, all-consuming dreadfulness! The reality of this situation in the military is exemplified in The New England Journal of Medicine; “Combat’s Toll on a Soldier’s Psyche,” by COL Charles Hoge’s, MD , Chief of Psychiatry and Behavioral Science, US Army (Hoge, 2004).

 

Shealy, et al, (1992) studied blood-serum levels of five neurochemicals (melatonin, norepinephrine, B-endorphin, serotonin, cholinesterase) in depressives. He found that 92% of depressives had abnormal levels in at least one of the five neurochemicals tested and 60% showed three or more abnormalities. In over half of the depressives, he found either elevated or low levels of norepinephrine/cholinesterase ratios. He also found magnesium deficiencies in 80% of depressed patients and 100% of those with depression were deficient in taurine, an amino acid found in meat and fish, which is used to help absorb fats and fat-soluble vitamins. His work supports the notion of dietary supplements for the treatment of depression.

 

The nucleus accumbens within the forebrain is the main reward and pleasure center and is particularly sensitive to dopamine, serotonin and endorphins (Ratey, 2002). Recent research has shown that those with suicide ideation are also low in serotonin, dopamine and norepinephrine along with hippocampal shrinkage as the result of chronic sympathetic and adrenal (cortisol) activation (Ezzel, 2003). Stimulant drugs such as amphetamines and cocaine produce a sense of pleasure by changing the concentration of dopamine in the nucleus accumbens.

Arango and Mann (Oquendo, et al., 2003) observed with positron emission tomography (PET) scans, a direct correlation between ventral pre-frontal hypofunction levels of serotonin, also in the pre-frontal cortex, and the severity of violence of the chosen suicide method. Slightly lower levels may produce death by an overdose of sleeping pills while extreme deficits will lead to the person jumping off of a cliff or blowing his/her brains out.

 

Serotonin depletion has been well implicated as a driving mechanism for suicide, where both genetic factors and a string of upsetting life events combine to trigger suicide (Ezzel, 2003). In sectioned brains of deceased suicide victims, it is clear that they have fewer than average neurons in the orbital-prefrontal cortex. A study by Chaouloff (2000) reinforced the hypothesis that the HPA axis, in reaction to stress, affects serotonin neurotransmission, partly through the actions of corticoids.

 

Violence and suicide are related. Aggression is aimed at others when there is a combination of low serotonin and high norepinephrine, whereas aggression is aimed inward (increased suicidal ideation) when there is a combination of low serotonin and low norepinephrine (Kotulak, 1997).

 

Antidepressants and Electroconvulsive Therapy in the Treatment of Depression

 

Several studies have examined cerebral blood flow (CBF) and metabolism using positron emission tomography (PET), single photon emission computerized tomography (SPECT) and functional magnetic resonance imaging (FMRI) analysis (Rubin, Sacheim, Nobler, & Moeller, 1994). Functional imaging studies are controversial as they have shown confounding (both high and low) irregularities in metabolism, primarily in the basal ganglia, prefrontal and limbic areas that tend to normalize in those who respond to medication. In some cases, sleep deprivation reduces depression and is tied to reductions in abnormally high CBF within the anterior cingulate gyrus (Wu, et al., 1992).

 

Antidepressant medication has been shown to affect capillary permeability and the brain-blood barrier (Preskorn, Raichle, & Hartman, 1982). With electroconvulsive therapy (ECT), the electrodes are placed for whole-brain or right-side shocks. ECT has been widely used to treat depression. CBF reductions follow shortly after exposure to ECT, even with people who already have hypo-perfusion of CBF. For depression, ECT is generally administered to the right side (Rubin, et al., 1994).

 

Right-side CFB reduction would help offset the alpha asymmetry, recognized in the QEEG (quantitative electroencephalography) field to be associated with depression and disturbed mood (Rosenfeld, 1997; Siever, 2003) by shutting down right frontal lobe function rather than boosting left frontal lobe function. This may explain why those on anti-depressants are troubled so much with foggy-headedness and cognitive impairments and one of the reasons why pilots and special duty personnel (i.e., Nuclear Surety Program) are medically suspended from duty while on antidepressants. Rubin concluded that both antidepressants and ECT (even with clinical improvements) might further affect regions in the direction of abnormality, not normalization.

Conclusion

 

The fear response involves the reduction of serotonin and activation of cerebral norepinephrine, and the adrenals as the threatened prepare for battle. However, severe traumas can cause a dysfunctional and never-ending activation of the fear response, which fatigues key neurotransmitters and the adrenals as it manifests into PTSD. The implications of PTSD include brain damage, a combination of family and societal violence, alcohol and drug abuse, loss of wages and increased suicide ideation. No adequate drug or medical treatment of PTSD exists today. Often, pharmaceutical agents and electroconvulsive therapy (ECT) may alleviate the depression, but usually drive the brain further into dysregulation, leaving the patient feeling emotionally numb and struggling with increased cognitive and social impairments. A new non-drug and non-ECT approach needs to be considered.

©Mind Alive Inc. (2012) Dave Siever