View Full Version : Article: Neurofeedback with anxiery and affective disorders (Depression, OCD, PTSD)


DominoPhreak
01-07-08, 11:17 AM
From Child And Adolescent Psychiatric Clinics of North America, 14 (2005) 105– 123

"Neurofeedback with anxiety and affective disorders" (http://www.bf-israel.org/neurofeedback/Hammond%202005.pdf)

Intro:
Compelling evidence exists for a neurophysiologic basis for obsessive-compulsive disorder (OCD). A large number of positron emission tomographic and single photon emission computed tomographic studies have found increased blood flow and metabolism in the mediofrontal, anterior cingulate, right frontal, or orbitofrontal areas [1–14], which implicates a cortico-striato-thalamocortical network. Functional abnormalities also have been documented in a large number of quantitative EEG (qEEG) studies [15–22] and evoked potential studies [23–27]. OCD seems to be somewhat heterogeneous, however, with at least two qEEG subtypes that have been found [17–21]. Prichep et al [20] and Kuskowski et al [15] found a group with excess alpha brain waves throughout most of the head, with frontal excess beta, whereas another subgroup has an excess of theta activity, particularly in frontal and posterior temporal areas. Clinical experience in conducting qEEG assessment with patients with OCD also has shown that excess beta activity is often found along the midline, in cortical areas approximately over the anterior cingulate.

Strong research evidence also indicates that there are functional brain abnormalities associated with anxiety and panic disorder [28–30] and posttraumatic stress disorder (PTSD) [31]. A particularly robust body of research, summarized by Davidson [32], has documented that depression is associated with an activation difference between the right and left prefrontal cortex. A large number of EEG studies, reviewed in earlier papers by Davidson [32–34], have established that the left frontal area is associated with more positive affect and memories, whereas the right hemisphere is more involved in negative emotion. A biologic predisposition to depression exists when there is a frontal asymmetry in brain wave activity, with more left frontal alpha activity. This imbalance with more left frontal alpha means that the left frontal area is less activated. Such persons may be anticipated to be less aware of positive emotions while at the same time being more in touch with the negative emotions that are associated with the right hemisphere. This asymmetry in EEG activity is best seen when the EEG is examined with an average reference or a reference on the vertex at Cz [32,35,36].

Researchers have observed for decades that individuals who are depressed are also typically withdrawn. We know that there is a neurophysiologic basis for such withdrawal. Henriques and Davidson [37] found that the frontal area in the left hemisphere is associated with approach motivation and behavior, whereas the right frontal area is involved in avoidance motivation and withdrawal behavior. Researchers found that when the left hemisphere is basically ‘‘stuck’’ in an alpha idling rhythm, there is not only a deficit in positive affect but also more withdrawal behavior. This biologic predisposition to depression is also firmly documented in research findings that have shown that infants of depressed mothers display this same reduced left frontal EEG activation [38,39], even as young as 3 to 6 months [40] and 1 month of age [41].

The belief has been expressed (J.H. Askew, unpublished data) [35] that this frontal alpha asymmetry may represent a state marker of depression, as well as reflecting a biological or trait marker of a vulnerability [37,42] to depression. This has been supported in a study (J.H. Askew, unpublished data) that found a strong correlation between alpha asymmetry scores and the Beck depression Inventory (P b 0.0001) and the Minnesota Multiphasic Personality Inventory (MMPI-II) depression scale (P b 0.0001).

Davidson [43], who has contributed more research in this area than any other individual, has expressed his belief that this asymmetry is not necessary or sufficient for the production of a specific type of affective style or psychopathology but that differences in prefrontal asymmetry are perhaps most appropriately perceived as diatheses that bias a person’s affective style and then modulate someone’s vulnerability to developing depression. He does not subscribe to a purely biologic model of depression, but he believes that the frontal alpha asymmetry does predict a vulnerability to depression so that when negative life events occur over a prolonged period of time to such an individual, there is an increased probability that he or she will become depressed. Based on his research, Davidson [43] believes that not everyone with this asymmetry will be depressed, despite being more vulnerable to becoming so, and someone can experience negative life events and still become depressed in the absence of this asymmetry.
Article goes on to review multiple studies of using Neurofeedback. Outlines how Neurofeedback is shown to change the brain patterns listed above, and removing/reducing symptoms of Anxiety/PTSD/OCD/Depression.

Also shows a comparison of how medication treatment doesn't change the brain patterns long term, where as people who completed Neurofeedback seemed to continue to improve in various follow-up studies averaging around 1 year post-treatment.