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Clinical and Research Reports
Published Online: 1 April 2012

Neurotherapy of Traumatic Brain Injury/Posttraumatic Stress Symptoms in OEF/OIF Veterans

Publication: The Journal of Neuropsychiatry and Clinical Neurosciences

Abstract

The Flexyx Neurotherapy System (FNS), a novel variant of EEG biofeedback, was adapted for intervention with seven treatment-refractory Afghanistan/Iraq war veterans, and brought about significant decreases in bothersome neurobehavioral and posttraumatic stress symptoms. FNS may help ameliorate mixed trauma spectrum syndromes.
An emerging legacy of the Afghanistan and Iraq Wars is a new generation of veterans with traumatic brain injury (TBI). Indeed, TBI, particularly due to blasts from improvised explosive devices, has been called the “signature injury” of those deployed to Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF).1 Prevalence estimates range as high as 22% of wounded soldiers with TBI in clinical reports.2,3 Although the more severely injured receive immediate care on the battlefield and are transferred to military hospitals, many return to duty after a brief period of light duty.4,5 Many significant mild head injuries (concussions) are likely to be overlooked during continued duty in conflict. Despite the trend for improvement over time that is frequently noted with mild TBI (mTBI), it is also apparent that, after discharge, many veterans continue to report significant postconcussive symptoms.4
The actual mechanism(s) of brain injury in these cases is uncertain, but diffuse axonal shearing, contusion, and subdural hemorrhage, similar in nature to other modes of closed head injury, may be reasons.6 Disruption of normal patterns of electrical power of the brain as well as disruptions of intra- and interhemispheric communication may be present and persist from the acute to the chronic stage in many patients.6
Also, there is high comorbidity of TBI and emotional disorders, particularly Posttraumatic Stress Disorder (PTSD). Even when PTSD is not formally diagnosable, a number of PTSD features may be present. Matters are further confounded by the overlap in symptoms characteristic of both TBI and PTSD, including concentration and recall problems, sleep disturbances, mood/emotional irregularities, and other difficulties. PTSD itself is associated with a wide range of psychiatric comorbidity, poor quality of life, and social dysfunction. Disentangling the effects of TBI and PTSD or less fully pronounced posttraumatic stress features can be extremely challenging. Also, both distinct and shared mechanisms may interact in producing features associated with TBI and PTSD.1,2,4,79
In any case, the nature of these injuries poses significant rehabilitation challenges.4,8 There is a critical need to develop more effective treatments. Recent developments in the bio-energy domain of complementary and alternative medicine have suggested the potential for electroencephalograph (EEG) biofeedback. EEG biofeedback is typically performed within an operant-conditioning framework, wherein subjects acquire the skills to change patterns of EEG activity, which involves considerable time and effort.10
Alternative procedures have also developed. One involves offsetting stimulation of brainwave activity by means of an external energy source. The Flexyx Neurotherapy System (FNS) involves conduction of electromagnetic energy (EM) stimulation via the connecting EEG cables.11 FNS has been further adapted by utilization of two-channel, rather than one-channel only, neurofeedback. This article reports on findings obtained in FNS treatment of a series of highly-symptomatic OEF/OIF veterans.

Methods

Seven OEF/OIF veterans with persistently bothersome symptoms of TBI and PTSD were referred for FNS treatment. All seven participants were not progressing on standard medication or comprehensive rehabilitation treatments. In order to be candidates for FNS treatment, they needed to be free of seizure disorder, sleep apnea, or ongoing substance abuse. Participants completed pre- and post-treatment questionnaires, including the Neurobehavioral Functioning Inventory (NFI)12 and the PTSD Symptom Scale (PSS).13 The NFI measures the frequency of neurobehavioral dysfunction, with separate scale scores for Depression, Somatic, Memory/Attention, Communication, Aggression, and Motor problems. The PSS contains 17 items designed to diagnose PTSD according to DSM criteria. The items are also grouped according to three PTSD symptom clusters of re-experiencing, avoidance, and increased arousal. A total severity and three subscale scores can be obtained. Also, at the beginning of each treatment session, participants rated their current levels of symptoms on separate 0–10 scales with appropriate anchors, including cognitive clarity (e.g., 0: fully clear; 10: worst imaginable cognitive problems), overall body pain, quality of sleep, fatigue, anxiety, depression, irritability/anger, and overall activity.
FNS equipment consists of a laptop computer and J&J Enterprises (Poulsbo, WA) I-300 Compact 2 (C-2) Channel EEG module with on-board feedback-generating power; it uses proprietary software to link the digital brainwave recording device (C-2 module) through the computer, which then sets the parameters for the C-2 module to emit pulsed EM stimulation.11 The system returns a signal to the participant via conduction from the C-2 module, varying as a function of the detectable peak EEG frequency (but offset from it), thereby permitting strategic distortion of the EEG. The amount of EM stimulation was standardized, with the feedback frequency being offset from the dominant EEG frequency at +20 Hz. Pulses of EM energy operated at a duty cycle of 1%; that is, of the maximum permissible on-time for each pulse, they were powered no more than 1% of the time (e.g., the maximum on-time at 1% for 1-Hz pulse was 0.01 sec). Testing revealed a power level of 100 pico watts through the sensor cable (Weber Innovations, Ann Arbor, MI).
Participants attended approximately 2–3 sessions per week. They sat comfortably with eyes closed and engaged in no specific activity. Electrodes were placed in a predeter-mined order over all areas of the cortex over the course of the sessions (range: 22–25). Each session included a total of 4 sec. of EM stimulation, spaced over 4 min. The stimulation was not immediately discernible, and adverse reactions (e.g., transient increases in typical symptoms after the first few sessions) were minimal. Participants were not asked to discuss past traumas as part of the process.
Data analyses included paired-sample t-tests for NFI and PSS scores. Curve-estimation linear-trend regression models were run for each of the current symptom ratings made over the course of 22 sessions. Given the exploratory nature of this study and desire to identify any significant patterns, no correction for multiple comparisons was made. However, effect sizes in terms of percentage of variance explained (r2) were calculated for each of the primary pre- to post-treatment comparisons.

Results

Five of the seven individuals fully completed the treatment protocol (22–25 sessions) and provided sufficient pre- and post-treatment outcome information. An additional two individuals discontinued treatment after experiencing substantial symptom-reduction to minimal levels in a shorter period of time (13 and 17 sessions). Descriptive information on these five participants: two women, three men; age range: 23–42; highest education level: two who completed high school, two with some college, and one with a B.S. degree; four served in the Army, one in the Marines; number of deployments ranged from 1 to 4; all with a history of at least mTBI, three with multiple episodes of loss of consciousness lasting up to 45 minutes; four involved in blast/explosive injuries (maximum of nine episodes in one case), and motor vehicle accidents; a variety of assorted physical injuries; all with PTSD; and three with history of psychiatric hospitalization for suicidal ideation.
Pre- to post-treatment comparisons for NFI and PSS scores are presented in Table 1. Results reveal significant decreases on four NFI dimensions and strong trends on the other two, and significant decreases in PSS Total scores as well as the re-experiencing and avoidance symptoms clusters and a strong trend in evidence for decrease in arousal symptoms. All pre- to post-treatment comparison effect sizes were large. Also, linear trends were all highly significant in terms of improvement for each of the current symptom ratings made at the beginning of each of the individual treatment sessions (for the five participants completing at least 22 sessions), including cognitive clouding (β = −0.23; R2=0.22; F[1, 108]=31.06; p<0.001), pain (β = −0.15; R2=0.12; F[1, 108]=14.76; p<0.001); sleep quality (β = −0.29; R2=0.49; F[1, 108]=103.69; p<0.001); fatigue (β = −0.23; R2=0.27; F[1, 108]=39.24; p<0.001); anxiety (β = −0.20; R2=0.29; F[1, 108]=43.99; p<0.001); depression (β = −0.15; R2=0.25; F[1, 108]=35.60; p<0.001); and irritability/anger (β = −0.11; R2=0.12, F[1, 108]=15.25; p<0.001); and for overall activity (β = −0.20; R2=0.33; F[1, 108]=52.61; p<0.001). All participants, if taking medication at the outset, substantially decreased their medication intake by posttreatment.
TABLE 1. Pre- to Post-Treatment Comparisons, mean (standard deviation)
Neurobehavioral Functioning Inventory (NFI)
 Pre-TreatmentPost-Treatmentt [df], pEffect Size
 Depression52.8 (9.0)39.2 (5.9)3.5 [4], 0.020.76
 Somatic54.4 (6.3)41.0 (4.1)8.9 [4], 0.0010.95
 Memory/Attention59.2 (13.0)41.4 (7.7)4.6 [4], 0.010.84
 Communication58.2 (14.7)42.8 (9.9)3.5 [4], 0.020.76
 Aggression49.6 (11.5)41.2 (3.0)1.8 [4], 0.140.45
 Motor56.4 (12.5)40.8 (6.9)2.6 [4], 0.060.63
PTSD Symptom Scale (PSS)
 Re-experiencing7.0 (4.7)2.2 (2.5)3.0 [4], 0.040.69
 Avoidance14.2 (6.4)3.4 (4.0)3.7 [4], 0.020.93
 Arousal9.4 (3.8)6.2 (4.0)2.6 [4], 0.060.62
  Total30.6 (13.0)11.8 (9.5)3.8 [4], 0.020.79
Medication Status, Participant #
 Pre-Treatment MedicationsPost-Treatment Medications
1aacetaminophen/oxycodone, lithium, promethazine, ropinirole, sertraline, tramadol, zolpidemlithium, sertraline
2bnonenone
3avalproic acidnone
4ahydroxyzine, nortriptylinenone
5ccitalopram, gabapentin, venlafaxinecitalopram
6aaripiprazole, clonazepam, sertraline, trazodone, zolpidemsertraline, zolpidem
7anonenone
a
Completed full course of (22–25) sessions; pre- and post-treatment measures available for comparison.
b
Discontinued treatment after 13 sessions after experiencing substantial symptom reduction to minimal levels; pre- but not post-treatment measures available for data analyses.
c
Discontinued treatment after 17 sessions after experiencing substantial symptom-reduction to minimal levels; pre- but not post-treatment measures available for data analyses.

Discussion

Findings from this small series of highly-symptomatic OEF/OIF veterans with mixed TBI/PTSD syndromes suggest that FNS treatment, a novel variant of EEG biofeedback, may be worth exploring more rigorously. This is encouraging because it is increasingly apparent that some of the most treatment-refractory cases are among those individuals who, in addition to sustaining TBI, manifest strong PTSD symptoms.2,8,9 FNS is one variant of minute-pulsed EM stimulation neurofeedback procedures, having evolved from a precursor photic stimulation paradigm known as EEG-Driven Stimulation14 and having been followed by another related low-intensity technology, the Low Energy Neurofeedback System.15 However, our experience with TBI/PTSD is only with FNS and the two-channel modification described herein. Future research is warranted to corroborate these preliminary results in a randomized, controlled trial and to explore the mechanisms that may underlie improvement, as we can only speculate at this stage that FNS may exert a positive effect on intra- and/or interhemispheric connectivity.

References

1.
Risdall JE, Menon DK: Traumatic brain injury. Philos Trans R Soc Lond B Biol Sci 2011; 366:241–250
2.
Polusny MA, Kehle SM, Nelson NW, et al.: Longitudinal effects of mild traumatic brain injury and posttraumatic stress disorder comorbidity on postdeployment outcomes in national guard soldiers deployed to Iraq. Arch Gen Psychiatry 2011; 68:79–89
3.
Terrio H, Brenner LA, Ivins BJ, et al.: Traumatic brain injury screening: preliminary findings in a US Army Brigade Combat Team. J Head Trauma Rehabil 2009; 24:14–23
4.
Okie S: Traumatic brain injury in the war zone. N Engl J Med 2005; 352:2043–2047
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Gondusky JS, Reiter MP: Protecting military convoys in Iraq: an examination of battle injuries sustained by a mechanized battalion during Operation Iraqi Freedom II. Mil Med 2005; 170:546–549
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Taber KH, Warden DL, Hurley RA: Blast-related traumatic brain injury: what is known? J Neuropsychiatry Clin Neurosci 2006; 18:141–145
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Bryant RA: Disentangling mild traumatic brain injury and stress reactions. N Engl J Med 2008; 358:525–527
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Hoge CW, Goldberg HM, Castro CA: Care of war veterans with mild traumatic brain injury—flawed perspectives. N Engl J Med 2009; 360:1588–1591
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Hoge CW, McGurk D, Thomas JL, et al.: Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med 2008; 358:453–463
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Duff J: The usefulness of quantitative EEG (QEEG) and neurotherapy in the assessment and treatment of post-concussion syndrome. Clin EEG Neurosci 2004; 35:198–209
11.
Ochs L: Flexyx Neurotherapy System Operating Manual for the J&J USE2 and the I-330 Compact 2C EEG. Walnut Creek, CA, Flexyx LLC, 1997–1998
12.
Kreutzer JS, Seel RT, Marwitz JH: Neurobehavioral Functioning Inventory Manual. San Antonio, TX, The Psychological Corporation, 1999
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Foa EB, Riggs DS, Dancu CV, et al.: Reliability and validity of a brief instrument for assessing post-traumatic stress disorder. J Trauma Stress 1993; 6:459–473
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Mueller HH, Donaldson CC, Nelson DV, et al.: Treatment of fibromyalgia incorporating EEG-Driven stimulation: a clinical outcomes study. J Clin Psychol 2001; 57:933–952
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Ochs L: The Low Energy Neurofeedback System (LENS): theory, background, and introduction. J Neurother 2006; 10:5–39

Information & Authors

Information

Published In

Go to The Journal of Neuropsychiatry and Clinical Neurosciences
Go to The Journal of Neuropsychiatry and Clinical Neurosciences
The Journal of Neuropsychiatry and Clinical Neurosciences
Pages: 237 - 240
PubMed: 22772672

History

Received: 14 February 2011
Revision received: 26 July 2011
Revision received: 8 September 2011
Accepted: 12 October 2011
Published online: 1 April 2012
Published in print: Spring 2012

Authors

Details

David V. Nelson, Ph.D.
From the Department of Psychology & Philosophy, Sam Houston State University, Huntsville, TX, and the Brain Wellness and Biofeedback Center of Washington, Bethesda, MD.
Mary Lee Esty, Ph.D.
From the Department of Psychology & Philosophy, Sam Houston State University, Huntsville, TX, and the Brain Wellness and Biofeedback Center of Washington, Bethesda, MD.

Notes

Address correspondence to David V. Nelson, Ph.D., Department of Psychology & Philosophy, Box 2447, Sam Houston State University, Huntsville, TX 77341; e-mail: [email protected]
Portions of this paper were previously presented at the 20th Annual Meeting of the American Neuropsychiatric Association, San Antonio, TX, February 18–22, 2009.

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