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​Abstract: The primary goal of the present research is to study the effect of a neurofeedback training (NFT) period on balance problems associated with Parkinson’s disease. Sixteen patients were selected through purposive sampling and were randomly divided into experimental and control groups. The research procedure included eight sessions. Prior to and after training, pre-tests and post-tests of static and dynamic balance were administered using ‘‘limit of stability’’ for the Biodex as well as the Berg scale. The results revealed that, after neurofeedback training, a statistically significant improvement in both static and dynamic balance in the experimental group was achieved. The means of the Biodex and Berg scores in the experimental group increased from 18.87 to 42.87 and 17.62 to 46.37, respectively. The means of the Biodex and Berg scores in the control group in the pretest were 18.25 and 17.75 and increased to 20.00 and 20.50, respectively. The results suggest that NFT can improve static and dynamic balance in PD patients.

A study published in the American Academy of Neurology demonstrated the neurophysiological and biochemical value of repeated compression using blood pressure cuffs on ones arm and leg for 5 minutes. Brain blood flow was improved for over 24 hours beginning 6 hours after the compression treatments were conducted.
https://www.eurekalert.org/pub_releases/2019-05/aaon-crs052819.php

This struck me as a relative benign and cost effective method of treatment for people with neurodegenerative and neurodevelopmental conditions, e.g, dementia and autism. I recalled the gowing evidence for intermittent hypoxia and hypocaloric interventions enhancing mental and physical and immune system functioniong. I've been made aware of its use in physical fitness training and want to explore how it could be developed into a safe, low-cost, noninvasive and rather useful 'outside in' treatment for older adults where blood flow is constrained by various forms of cardiovascular disease and impaired functioning. 

Then I recalled Stan Grof's early work on what he termed basic perinatal matrices (Grof, 1976) where the fetus is compressed during the birth process and this confers important psychophysiological information that substnatively influences their future development. I saw a connection to Grof's insight about the challenges we experience in the birth process can carry forward into later life and manifesting as emotional and behavioral difficulties. Here we can see how the contraining of blood flow and then its sudden release repeats the experience of compression in the birth canal and subsequent release into progressively more independent, self-organizing and self-sustaining life. I then associated the paper's description of remote ischemic preconditioning to my use of Bioenergetic therapy as a psychophysiological way to enhance body-mind flexibility and self awareness.  

Quietmind's current treatment model focuses on using photobiomodulation to increase cortical microcapillary perfusion, regional cerebral blood flow, ATP and specific chaperone proteins while reducing beta amyloid buildup. This is combined with brainwave biofeedback training to repair the dysregulated neural connectivity and functional medicine that can address any underlying infectious or metabolic sources of impaired immune response and systems-oriented Bioenergetic Analysis to re-establish and support more grounded emotional and interpersonal functioning.  

Noninvasive non-drug treatment of dementia and other neurodegenerative disorders with photobiomodulation is getting more evidence of its effectiveness published in the traditional scientific literature. We are gratified and excited to see this approach gaining traction and hope this can lead to increased interest in Quietmind's integrated treatment model of photobiomodulation with infrared light and brainwave biofeedback training.  This study builds on the work done at MIT with animals and shows how the pulsed light can influence neurochemistry and cellular communication processes to mitigate neurodegenerative activity.

https://www.goodnewsnetwork.org/flickering-lights-can-slow-and-reverse-alzheimers-mit-study/

I found a paper https://www.ncbi.nlm.nih.gov/pubmed/21459521  
Med Hypotheses. 2011 Jun;76(6):769-73. doi: 10.1016/j.mehy.2011.01.020. Epub 2011 Apr 2.Tardive dysphoria: the role of long term antidepressant use in-inducing chronic depression.El-Mallakh RS1, Gao Y, Jeannie Roberts R.

This provoked me to inquire of my colleagues as to why there'd been no further exploration of this issue to be found in teh literature since 2011 and I got this reply from Robert Thatcher a neuroscientist and developer of the Neuroguide EEG analysis software that we use at Quietmind for our clnical and research activities. It is clear that the continued use of SSRI medications is now getting more critical attention now 30 years after the arrival of Prozac. Neurofeedback and other treatment methods are able to provide similar results without side effects and that last long after the training process has been completed. Here's Dr. Thatcher's reply:

This post concerns he science and publications showing negative effects after long term use of antidepressants.  The negative effect of the antidepresssants is called Tardive Dysphoria which is chronic depression induced by long term use of antidepressants.  There are several interesting studies on this topic if one does a simple Google search as well as a search of the National Library of Medicine database, e.g., https://www.ncbi.nlm.nih.gov/pubmed/30199999Tardive dysphoria: the role of long term antidepressant use in-inducing chronic depression
http://unthinkable.cc/long-term-evidence-we-cant-ignore-anymore-anti-depressant-outcomes/
http://behaviorismandmentalhealth.com/2014/04/08/antidepressants-make-things-worse-in-the-long-term/

A common hypothesis is that anti-depressants inhibit re-uptake that results in increased serotonin in the extracellular space however over time there are compensatory mechanisms that remove serotonin faster than the drug can block re-uptake or different re-uptake mechanisms develop that result in a worse and chronic outcome.

Ketamine has a different mode of action, e.g., midline thalamus de-coupling to the medial frontal lobes and hippocampus that appears to disrupt a cyclic dynamic and sort of refreshes the circuity for a while,e.g., Cortical-brainstem (nu. Raphe) regulatory control mechanisms.   A search of the National Library of Medicine database using the search terms "Depression Brain Network" results in 2,875 citations.  There is good agreement about the hubs of this network between different imaging modalities such as fMRI, PET and EEG/MEG.  Therefore, a reasonable idea is to measure the brain networks related to depression using QEEG and LORETA as a baseline assessment and then use NFB to reinforce increased stability and efficiency of the nodes and connections between the hubs of the depression network as well as to use QEEG to assess the relative effectiveness of non-SSRI treatment..   As Wes stated, exercise and good diet (Typtophan is a precursor of serotonin) and lifestyle changes and perhaps also Ketamine.  However, given the risk of doing harm based on the over use of anti-depressant drugs as published in the scientific literature points toward considering alternative treatments.  
Bob Thatcher, PhD  Applied Neuroscience Inc.

 

​brain_photobiomodulation-preliminary_results_from_.pdf

The above article supports the value of low-level infrared light stimulation using sophisticated blood oxygenation and imaging technology. We used similar though less advanced tools in our 2012 study 28 days of 6-minute, transcranial and intraocular 1065-1075nm photobiomodulation of subjects struggling with probable Alzheimer's disease.  The current study using the same device is now 56-days with more powerful lLED stimulation.