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Biofeedback �Association for Applied Psychophysiology & Biofeedback
Volume 41, Issue 4, pp. 158–173 www.aapb.org
DOI: 10.5298/1081-5937-41.4.07

SPECIAL ISSUESPECIAL ISSUE

Managing Traumatic Brain Injury: Appropriate
Assessment and a Rationale for Using Neurofeedback
and Biofeedback to Enhance Recovery in
Postconcussion Syndrome

Michael Thompson, MD,1 Lynda Thompson, PhD, CPsych, BCN,1 Andrea Reid-Chung, MA, CCC,
BCN,1 and James Thompson, PhD, BCN2

1ADD Centre/Biofeedback Institute of Toronto, Mississauga, Ontario, Canada; 2Evoke Neuroscience, Inc., New York, NY

Keywords: concussion, traumatic brain injury (TBI), electroencephalogram (EEG), neurofeedback, heart rate variability (HRV)

Impairments that may result from a mild traumatic brain

injury (TBI) or concussion can be both severe and long-

lasting. This article will list some of the common persisting

symptoms that may occur and give a brief description of

the neuropathological processes that can be triggered by

TBI, including diffuse axonal injury and its effects on the

mitochondrial Kreb’s cycle and the production of adenosine

triphosphate, the brain’s source of energy. This is followed

by a summary of a comprehensive assessment process that

includes quantitative electroencephalography, evoked po-

tentials, heart rate variability (HRV) measures, neuropsy-

chological testing, and blood and urine analysis. Details

concerning a neurophysiological approach to effective

treatment are given. These include conventional single-

channel neurofeedback (NFB), also called brain-computer

interface training, low-resolution electromagnetic tomog-

raphy z-score neurofeedback, HRV training, and counsel-

ing on diet, sleep, and exercise. The authors expand the

discussion on their treatment approach to include a

neuroanatomical explanation of why the practitioner

should consider combining the NFB training with HRV

training.

Introduction
This article provides an overview of how postconcussion

syndrome is assessed and, for the most part, successfully

treated even a number of years after injury. It provides a

clinical rather than a research perspective and is based

primarily on work carried out at the ADD Centre and

Biofeedback Institute of Toronto with clients who have

suffered traumatic brain injuries (TBI). Success is measured

in terms of patients having sufficient amelioration of

cognitive and emotional symptoms to be able to resume and

succeed in their social, academic, and/or employment

pursuits. To date, this has been achieved in all cases in

which the person did sufficient training (40 or more

sessions). Eventually, we will follow this descriptive article

with a case series detailing outcomes. (See also the initial

case study by Bhandari, Thompson, and Reid-Chung, 2013,

in this issue of Biofeedback). Here we summarize the most

common presenting symptoms and the assessment process,

including a rationale for the use of 19-channel quantitative

electroencephalogram (QEEG), evoked potentials (also

called event-related potentials [ERPs]), heart rate variability

(HRV) measures, biomedical analysis, and neuropsycho-

logical testing. Also included is a short description of the

treatment approach. Interventions may include single-

channel neurofeedback, low-resolution electromagnetic

tomography (LORETA) z-score neurofeedback,1 HRV

training, and metacognitive strategies, plus counseling

regarding diet and supplements, sleep hygiene, and

exercise.

Symptoms
There is nothing mild about the impairments that may

result from a mild TBI, which is commonly called a

concussion. A lack of objective pathognomonic signs of

concussion means that a physician’s diagnosis often rests,

for the most part, on the patient’s report of subjective

symptoms, such as headache or ‘‘seeing stars.’’ In 95% of

cases in athletes, concussion does not involve loss of

1LORETA is a widely used statistical technique to analyze surface EEG
signals and determine which sites deeper in the cortex are the sources of
the surface electrical activity. Today’s LORETA software produces
instantaneous displays of cortical processes, usable for neurofeedback
training. LORETA z-score training involves training cortical processes
toward normalcy, based on a comparison to a normative database.

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consciousness (McCrory et al., 2013). Common presenting

symptoms shortly after a concussion include dizziness,

nausea, headaches, balance deficits, and blurred vision. The

diagnosis of concussion should be made by a physician in

the period immediately following the trauma, preferably

within a few hours of the injury. A designated health care

professional with appropriate training may make the

diagnosis in remote areas where there is no physician

available (Tator, 2013).

The longer-term problems are referred to as postcon-

cussion syndrome when symptoms persist for weeks or

months, and this is more common after repeated brain

injuries. Symptoms include fatigue, sleep disturbance,

slowed reaction time, plus cognitive and emotional changes

that produce difficulties in everyday life. The cognitive

problems include slowed processing speed, poor sustained

attention, poor concentration, impaired short-term and

long-term memory, and learning problems. Language

problems, including word-finding difficulties as well as

poor comprehension, are also frequently observed among

patients with TBI. Emotional changes may include depres-

sion, anxiety, labile mood, irritability, and anger (‘‘a short

fuse’’). Unfortunately, in some cases, family and friends

notice a major personality change to which the patient may

be oblivious because self-perception can also be affected. It

is not at all uncommon for someone to present years after

the injury with all of these difficulties present to varying

degrees.

Pathology of a TBI
A variety of neuropathological processes can be triggered

by damage caused when brain matter collides with the

rough, ridged inside edges of the skull or the tough falx

cerebri, which is an infolding of dura mater between the

hemispheres. With rapid deceleration, as in an automobile

crash or when a football player is running at full speed and

is tackled, there is a coup injury, where the brain first hits

the skull, and a contrecoup injury, as it rebounds and hits

against the opposite wall of the skull (see Figure 1). The

results of this type of injury are usually assessed in the

hospital with the more commonly used imaging techniques.

These techniques may include positron emission tomogra-

phy (PET), single-photon emission computed tomography

(SPECT), magnetic resonance imaging (MRI), and func-

tional MRI (fMRI). A PET scan measures glucose

metabolism, and PET images provide a visual display of

brain activity by detecting where a radioactive form of

glucose goes while the brain performs a given task. SPECT

scans, which track perfusion (blood flow), are significantly

less expensive than PET scans, in part because they are able

to use longer-lived and more easily obtained radioisotopes

than PET. Both of these measures are invasive in the sense

that radioactive isotopes must be used. MRI and fMRI have

the advantage of not requiring any injection or ingestion of

radioactive material, but they involve a noisy environment,

and they do require the patient to lie very still in the tube

while the magnetic imaging is being done. Charles Tator, a

neurosurgeon and concussion expert in Toronto, in a

review article states that routine computed tomography and

MRI scans almost always appear normal in concussion

(Tator, 2013). Even PET, which indicates tissue metabolic

activity by virtue of the regional glucose uptake; SPECT,

which measures blood flow in the brain; and fMRI, which

measures the blood-oxygen level–dependent response that

will vary with oxygen uptake, may fail to detect a common

type of injury associated with TBI called diffuse axonal

injury (DAI; Thatcher, 2012; Thatcher, Walker, Gerson, &

Geisler, 1989).

Diffuse Axonal Injury
DAI is a primary pathologic feature of brain injury in

concussions at all levels of severity (Kushner, 2001;

Thompson & Hagedorn, 2012). DAI occurs both with

hitting the head and also when there is rapid acceleration/

deceleration and/or quick rotation of the brain such as may

occur with a whiplash or a blast injury. DAI is caused by the

twisting and stretching of axons or, in severe head injuries,

the tearing or shearing of axons (see Figure 2). An axon is a

nerve connection that goes from the cell body of one

neuron to the dendrite or cell body of another neuron. It

connects to the next neuron at a chemical junction called a

synapse. When a neuron fires, the electrical impulse travels

down the axon, at times a long distance, to the end of the

axon, where it causes the release of a chemical called a

neurotransmitter. This neurotransmitter enters the synap-

tic space between the end of the axon and the receptor sites

on the dendrite of the neuron that is receiving the

‘‘message.’’ One such neurotransmitter is glutamate, which

is important in this discussion and is shown in Figure 3.

Clearly, damage to an axon will interfere with the

transmission of messages from one neuron to another.

Although the biochemical and structural changes caused by

DAI may not be detectable by MRI, EEG is able to detect

the electrophysiological results of the disruption in

communication between neurons.

The rotational forces affecting the brain that result in

DAI also set off a metabolic cascade that includes a flood of

neurotransmitter release, including glutamate. Glutamate

excess will stimulate neurons to fire incessantly. This

results in an increase in neuronal permeability with an

Thompson et al.

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influx of sodium and calcium and a release of potassium.

Both sodium (Naþ) and calcium (Ca2þ) excess can interfere

with mitochondrial function. With normal blood flow and

nutrition, the mitochondria can produce energy in the form

of adenosine triphosphate (ATP) by means of the citric acid

cycle (Krebs cycle). Energy is essential to life, and it is

required in the cell membrane for the transport of ions

against a concentration or electrical gradient. Without this

Figure 1. Example of sites of injury in traumatic brain injury. Drawing by Maya Berenkey from The Companion to the Neurofeedback Book (in press) using figures by
Amanda Reeves in The Neurofeedback Book.

Figure 2. Structure of a neuron drawn by Maya Berenkey. The terminal button is the presynaptic link to the dendrite of the next neuron. This synaptic transmission
is disrupted when there is diffuse axonal injury. (Note that this figure shows a pyramidal cell. Only pyramidal cells produce the extracellular currents that summate
to produce the electroencephalogram.) Figure from The Companion to the Neurofeedback Book (in press).

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energy source, the cell cannot depolarize and repolarize

normally. Cell death is the eventual result. With a shut

down of the mitochondrial production of ATP, there is a

reduction of energy production and a resulting energy crisis

because, to keep firing, the neurons demand extra energy.

In addition to the direct interference with ATP formation

in the mitochondria due to the influx of sodium and

calcium, there is also an additional problem due to the

vasoconstriction caused by the excess release of potassium.

Potassium constricts the blood vessels and decreases blood

flow to the compromised area in the brain. The mitochon-

drial Krebs cycle requires fuel to keep running. In simple

terms, this fuel includes glucose, fats, amino acids for

coenzymes, and vitamins for the enzymatic processes.

However, the constriction of the blood vessels caused by the

excessive release of potassium limits the supply of these

necessary nutrients and oxygen to the cell.

The high-energy demand, restricted blood flow, and

oxygen debt together create the aforementioned energy

crisis that exhausts the neurons (see Figure 4). This will

inevitably lead to symptoms such as mental confusion and

failed memory, symptoms commonly seen in people who

have had a concussion. The brain will take varying amounts

of time to recover. The time to restore the chemical balance

will vary between people and will depend on many variables

including age, general health, and many other factors, such

as nutrition. Children and females, for example, are more

vulnerable to the effects of concussion, as mentioned by

Tator (2013). Long-term potentiation is decreased, and

long-term depression is increased. The membrane excit-

ability is reduced.

The diagram in Figure 5, adapted after a figure from the

UCLA Brain Research Centre, implies that within about 1

week, one may observe neurochemical recovery. However,

time lines predicted by different authors do show a wide

range. Because of changes and subsequent derangements in

cerebral glucose metabolism, persons suffering from even

minimal TBI may remain vulnerable to second-impact

injury for periods of up to a few months (Giza & Hovda,

2001). Other authors note that hypermetabolism and an

Figure 3. Schematic diagram of a synaptic junction. The figure shows, at the top, the presynaptic ending of the axon (called a ‘‘button’’ in Figure 2) and the
postsynaptic receptor sites for glutamate: the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA), which is a glutamate receptor site, and the
N-methyl-D-aspartate (NMDA) receptor site, which is initially blocked by magnesium ions. This figure is often used to explain long-term potentiation. It is illustrated
here to show the synapse. Thanks are extended to Wikipedia Images; Bruno Dubuc, Website of Canadian Institutes of Health Research; Institute of Neurosciences;
Mental Health and Addiction (NMHA); and to Copyleft; The content of the site The Brain from Top to Bottom is under copyleft. � is also from Nature Reviews,
Neuroscience, Nature Publishing, 2005.

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energy crisis lead to a secondary reaction with increased

regional cerebral blood flow (rCBF; occurs after about 1

minute) to meet increased energy demands needed to

restore ionic membrane balances (DeWitt et al., 1986;

Meyer, Kondo, Szewczykowski, Nomura, & Teraura, 1970;

Nilsson & Nordström, 1977). Shaw (2002) notes that this

initial increase in rCBF is followed by a subsequent decrease

of up to 50% in rCBF for 2 to 4 weeks depending on the

severity of injury. Because of factors that include the

gradual death of some neurons after DAI and the long-term

decrease in CBF that means the energy crisis in cells cannot

be resolved, it is possible for symptoms to worsen a few

weeks after the concussion so that they are more serious

than symptoms seen after initial neurochemical recovery

during the first week. This may be a factor contributing to

the susceptibility of athletes who have experienced one head

injury to experience a second concussion in the period after

an initial head injury. The results of subsequent head

injuries can be more profound, even when the severity is

less, and resolution of symptoms will take longer. Second-

impact syndrome is a term used when the second injury

occurs before there has been recovery from the first TBI,

and it is a serious condition that involves cerebral swelling

that results in death or major neurological deficits. This is

why doctors have to be careful when making return-to-play

decisions in athletes.

Assessment

General Considerations
Conventional imaging techniques may miss DAI in mild-

to-moderate TBI. Further, conventional neuropsychological

testing and symptom checklists, such as those traditionally

used with injured athletes, have been found to normalize

within a few days to a few weeks. For this reason, a more

advanced paradigm is needed to detect this type of injury.

Figure 4. Steps contributing to neuronal cell death. National Institutes of Health (NIH) government document in public domain. Although originally used by the NIH
to illustrate changes after a stroke, this diagram applies equally well to the energy crisis that ensues after traumatic brain injury. The next figure summarizes some
of the factors that contribute to this energy crisis.

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In a half dozen points, the authors summarize research

done with athletes who suffered a mild TBI. This research

used comparisons of multiple testing domains and involved

development of a new metric for assessing the sequelae of

concussion and measurement of recovery (Thompson,

Sebastianelli, & Slobounov, 2005):

1. SR (self-report) is sensitive within 24 hours.

2. NP (neuropsych) testing typically normalizes within 1

week.

3. Postural testing typically normalizes within 7 to 10

days.

4. EEG measures, when combined with postural tasks, are

sensitive beyond the 10-day period.

5. Combining modalities is more sensitive and reliable

than any single method.

6. LORETA is effective to localize cortical areas affected by

the head injury.

Thompson found that no one test was sufficient, and he

recommended the use of a testing paradigm that combines

the most sensitive tests from each modality. Based on this

research, and that of others in this field, a multimodal

assessment method for the comprehensive measurement of

brain functioning was developed. The primary tool for data

collection is the Brain Injury Assessment Tool (BIAT), and

this is used along with computerized neuropsychological

testing and biochemical analysis (www.Evokeneuroscience.

com). The BIAT instrument rapidly, with 20 minutes of

data collection, measures 19-channel EEG, QEEG, ERPs,

and HRV. The assessment employs a simultaneous

continuous performance test during which ERPs are

measured and also uses a standardized questionnaire. An

additional balance assessment using a force plate is also

available and can be integrated into this assessment.

Biochemical testing of blood and urine can be added as

deemed necessary. This is the methodology now used at the

ADD Centre/Biofeedback Institute in Toronto. This testing

is uniformly revealing abnormalities in our clients, even

years after the primary injury.

Role of QEEG in Assessment

The principle findings in a QEEG, regardless of the time

elapsed since the concussion, can include EEG slowing,

decreased power, episodic discharges, and changes in

Figure 5. Chemical and metabolic changes after traumatic brain injury. Adapted from David A. Hovda, PhD, UCLA Brain Injury Research Center, and from a drawing
in Giza and Hovda (2001).

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coherence. A slowed peak frequency, also referred to as the

dominant frequency, is a common finding after a TBI

(Angelakis, Lubar, Stathopoulou, & Kounios, 2004).

Normal adult peak frequency, measured in the occipital

region with eyes closed, is about 10 Hz. After a concussion,

it may drop into the low alpha range, perhaps 8 Hz, or even

fall into the theta range. A dominant frequency less than 8

Hz in an adult is considered abnormal. Another common

finding is reduced overall power. The most consistent

power findings after a concussion are reduced power in the

higher-frequency bands (8–40 Hz) and increased slow

waves (1–4 Hz; Slobounov, Sebastianelli, & Simon, 2002;

Thatcher, 2009). There are long-term changes in the 1- to

4-Hz/8- to 12-Hz ratio (Korn, Golan, Melamed, Pascual-

Marqui, & Friedman, 2005; Slobounov, Cao, & Sebastia-

nelli, 2009). A change (increase) in this 1- to 4-Hz/8- to 12-

Hz ratio activity is negatively correlated with patient

outcome 6 months after injury (Leon-Carrion, Martin-

Rodriguez, Damas-Lopez, Barroso y Martin, & Domi-

nguez-Morales, 2009). Thatcher has suggested that power

changes in the EEG following concussion result from

dysfunctional ionic channels of neuronal membranes (e.g.,

Naþ, Kþ, Caþþ) and reduced average current flux (Thatcher
et al., 2001). Decreased and/or increased coherence is a

common finding. Coherence reflects communication be-

tween different sites in the brain and represents the amount

of phase-locked activity in a particular frequency band. TBI

will disrupt coherence. The most common finding is a

decrease in coherence that is colloquially called a ‘‘discon-

nect.’’ A less frequent but important finding may be

episodic discharges. A dramatic example reported by M.

Barry Sterman (personal communication, March 2012) was

that one of his patients dropped his 6-month-old infant and

was accused of abuse. Sterman determined that the probable

cause of the accident in this very conscientious parent was a

sudden episodic discharge with momentary loss of muscle

tone and consciousness.

Addition of ERPs to Assessment Measures
Information from evoked potentials, also called event-

related potentials (ERPs) because they are time locked to a

specific event (sight or sound or even touch), can be used

following concussion to determine the intactness of cortical

pathways and speed of processing within these pathways

(De Beaument et al., 2009; Dupuis, Johnston, Lavoie,

Lepore, & Lassonde, 2000). ERPs reflect the neural activities

associated with cognitive/behavioral demands and thus

provide access to an improved understanding of brain

functioning that goes beyond either neuropsychological

testing or motor testing (Gosselin et al., 2010). ERPs have

been shown to be resistant to practice effects and are

therefore a hearty diagnostic assessment tool (Mendez,

Hurley, Lassonde, Zhang, & Taber, 2005) that can be

repeated as often as necessary. The population of people

who have suffered a TBI demonstrate reduced amplitudes

for the P3 components (P3a and P3b) of their ERPs. (For a

detailed explication of P3a, P3b, and other ERP components,

see Polich, 2007). When describing ERPs, ‘‘P’’ refers to

positive-going waves and ‘‘N’’ to negative-going waves.

The number, such as 300 (sometimes shortened to just 3),

refers to the number of milliseconds after the stimulus

when you expect the response to occur. This reduced

amplitude can indicate diminished attention because the

amplitude of the P3 has been shown to be related to the

amount of attention allocated to information processing

(Bernstein, 2002; Duncan, Kosmidis, & Mirsky, 2005). In

addition to lower amplitude, the latency of the P3 response

has been found to be greater, and this delay in conscious

processing of information is called a slowed P3. This

increased latency in the P3 response correlates with slowed

cognitive processing (Lavoie, Dupuis, Johnston, Leclerc, &

Lassonde, 2004). Earlier ERP responses are observed at less

than 250 milliseconds, which is before there is conscious

awareness of the stimulus. They reflect early brain sensory

processing. In our experience, patients with TBI generally

have sensory components (P1 and N2) that are longer

latency and lower amplitude compared with non-TBI

patients. P3 also tends to be longer latency and of lower

amplitude (see Figure 6). P3a is an attention-orienting

frontal component, whereas P3b reflects sustained attention

and is more central-parietal, with the largest amplitude

being observed at Pz. These observations of longer latencies

with the P300 ERPs may help us understand why there are

persistent problems with attention and concentration after

concussion.

Addition of HRV to Assessment Measures
The observation that TBI impairs cardiac function has

become increasingly apparent through work done with

relatively young athletes and with clients who have had

vehicular accidents (car, motorcycle, bicycle).

Figure 7 contrasts HRV in a healthy adult with that of an

athlete who has suffered a concussion. It demonstrates that,

after a concussion, even a healthy athlete can show

significant HRV changes. The top electrocardiogram shows

a 3-second sample, and below it is a tracing of variations in

heart rate over a 300-second time period, both from the

same healthy 36-year-old male. These demonstrate what

one would expect in a healthy person: heart rate variations

are even with high amplitude and steady rhythmicity. The

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Figure 6. Pre (black) and post (gray) P300 event-related potential (ERP) recordings from the same subject comparing a baseline measurement and a postinjury
measure. Latency of the P3 wave is delayed in the postconcussion test, and amplitude of the P3 wave is reduced following injury. (‘‘Big Circle’’ refers to the target
stimulus in this ERP test that is in the program from Evoke Neuroscience.) Figure from Thompson & Hagedorn in The Companion to the Neurofeedback Book (in
press).

Figure 7. Heart rate variability profile from a healthy adult and from a concussed athlete. From Thompson and Hagedorn (2012).

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figure below it shows data from a highly trained male

athlete 2 weeks postconcussion. It demonstrates low

amplitude and poor rhythmicity of heart rate variations.

The amplitude of the variations in heart rate and the

standard deviations of the heart rate variations after

artifacts have been removed (SDNN) were also both lower

than would be expected in a young athlete. These data

provide an illustration of how brain injury affects not just

the brain but also the heart, specifically that concussion has

a negative effect on HRV. Similar observations are found

postconcussion in clients at the ADD Centre and also have

been published by researchers. One example is a study by

Baguley, Heriseanu, Felmingham, and Cameron (2006).

They compared HRV data on 16 TBI age-matched subjects

with and without dysautonomia with that of 16 noninjured

controls. The mean SDNN (milliseconds) for the control

group was 60.2 with a standard deviation (SD) of 26.9,

whereas the mean SDNN (milliseconds) for the TBI group

was 40.6 with an SD of 16.4. The total power (ms2/Hz) of

the controls was 4065 (SD ¼ 4,082) and in the TBI group
only 1656 (SD ¼ 1,237). The LF power (ms2/Hz) of the
control group was 1,304 (SD¼1,484) and in the TBI group
only 189 (SD ¼ 152). They demonstrated that the TBI
group revealed significant differences in HRV parameters

compared with controls.

Neuropsychological Testing
In a clinical as contrasted to a research setting, testing must

be confined to that which can be useful to assist in diagnosis

and, more importantly, to design an appropriate treatment

program and track the patient’s progress during rehabili-

tation. The Weschler Intelligence Scale may be used to

obtain a profile of intellectual strengths and deficits with

other testing carried out as appropriate for a particular

patient. Problems with memory and concentration are

among the common cognitive sequelae of TBI. In adoles-

cents and adults with a TBI presentation, a computerized

neuropsychological test battery is used at the ADD Centre.

In the interest of brevity, an example from the first page of

the report is given in Figure 8. Completion of this test

battery takes the patient approximately 45 minutes to 1

hour, and the full report is delivered by computer within 1

hour after the testing is competed. The objective testing of

aspects of response time and memory involves tests that can

be quite difficult, and results, for the most part, do pinpoint

the difficulties the patient is experiencing. This computer-

ized methodology is simple to administer and can be

repeated so the results can be used, in a clinical setting, to

follow progress during treatment. The objective test

procedures in this computerized neuropsychological test

are complemented by subjective self-report questionnaires

and validated neuropsychological behavioral and cognitive

testing tasks. Questionnaires include an Alertness Rating

Scale, the Zung Anxiety and Depression Self-Report Scales,

an Adult ADHD Self-Report Scale, a Neuropsych Ques-

tionnaire Short Form (a series of questions about the

patient’s clinical state including mood, attention, sleep,

fatigue, aggressiveness, and so on), and a 16-item Medical

Outcomes Survey.

This computerized neuropsychological test battery is a

cost-effective way to obtain objective and subjective

information about the patient and track changes during

training. It may be a particularly useful tool for clinicians

who do biofeedback but who are not trained in the

administration of psychological tests. It is also very helpful

in the assessment of patients who could not afford

individual testing done by a psychologist.

Vestibular/Balance Assessment
At the ADD Centre, we are considering adding an

assessment tool that uses a force plate to quantify a

person’s balance, coordination, and vestibular system

following a brain injury. This can be a very sensitive tool

that, especially when combined with simultaneous EEG

measurements, will pick up functional deficits well after the

time that conventional instruments, such as self-report

questionnaires and psychometric tesing, have returned to

the normal range. The subject has his or her balance tested

in various modes (both feet, one foot, eyes open and closed)

while standing on a small rectangular force board that sends

signals to the computer that evaluates subtle movements.

A Neurophysiological Approach to Effective
Treatment
In the acute phase, rest from both physical and cognitive

activities is the only treatment that is agreed upon for

concussion (McCrory et al., 2013). Basic rehabilitation

procedures, as are carried out in hospital settings and in

rehabilitation centers, should be adhered to as well. These

interventions are necessary but often not sufficient for full

cognitive recovery. For later stages of treatment, both

neurofeedback/biofeedback practitioners and nutritionists

have important complementary techniques to apply. These

are now being demonstrated to achieve further results that

may be significant and, indeed, often life changing.

Normalizing the EEG deviations is a first step. This

intervention must be designed while keeping in mind that

not all deviations from a normative database will corre-

spond to symptoms. Indeed, we have seen examples of

genius correlating with significant deviations from a normal

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Figure 8. The ADD Centre logs in to CNS Vital Signs (www.cnsvs.com) to run a computerized Neuropsychological Test Report (administered through Evoke
Neuroscience). This 38-year-old client presented 15 months after experiencing a brief loss of consciousness in a fall. This very bright and capable individual has a
doctoral degree, yet she was plagued by memory problems and even forgot appointment times, despite e-mail reminders the day before. Given past academic and
work history, one would expect consistently above-average scores, but testing corroborated self-report of memory problems continuing more than 1 year after the
head injury.

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database. The person with deviations in the auditory cortex

who has perfect pitch, for example, does not have the goal

of normalizing that aspect of his auditory processing. Thus,

the cautious practitioner will include only Brodmann areas

with z-score deviations that correlate with a particular

patient’s symptoms of concern and will carefully assess

during each session whether the patient’s changes, when

meeting the feedback criteria, correlate with symptom

relief. Normalization should not induce any decrement in

cognitive functioning. Training that addresses shifting

brain functioning toward what is expected for the person’s

age is often done using LORETA z-score neurofeedback

(LNFB). Nevertheless, we must note that we have had

excellent results using single-channel neurofeedback train-

ing with clients who had suffered a TBI in past years. In

some cases, we are doing one session of LNFB and one of

regular, single-channel neurofeedback each week. LNFB is a

logical choice of intervention when working with patients

who have had concussions and show multiple deviations

involving areas deep in the cortex. Single-channel training

can affect these due to network properties in the brain’s

cortical-subcortical loops, but the LORETA training is

hypothesized to have a more direct influence on these

structures. The initial assessment in the majority of patients

who have suffered a TBI typically shows both positive and

negative deviations in amplitude (.2 SD) at multiple sites,

often in central midline areas, accompanied by both

coherence and phase differences as compared with database

norms. LNFB allows the practitioner to address up to 24

parameters, correcting the activity at various sites at the

same time for amplitude and/or coherence and/or phase

according to the Neuroguide database. An example of a

summary graph of LORETA neurofeedback training is

shown in Figure 9.

The graph of the learning curve across 17 sessions of

LORETA neurofeedback training in Figure 9 shows a

sudden increase at Session 7. This was because the client

had to leave the country for several months after six

sessions of training. When he came back to Canada, some of

his symptoms had returned, so he came back to complete

his training and achieved good results.

Neurofeedback training is nearly always combined with

HRV training and with monitoring of diet, sleep, and

exercise. Exercise needs to be appropriate and not jarring to

the spine and brain. In the immediate postinjury period,

even before nutritional assessment is carried out, an

increase in supplementation of omega-3 essential fatty

acids (i.e., fish oil) to several grams per day is usually

appropriate.

Figure 9. Neuroguide Program diagram of progress across 17 LORETA z-score neurofeedback training sessions. At 17 sessions, this client’s z-scores had moved
from .4–6 standard deviations (SD) to ,2 SD at all the Brodmann Area sites that were chosen to be trained. The cursor has been placed on the highest SD site for
the 7th session and the message that pops up is shown in the figure. This message indicates that this site represents the SD of amplitude (AP) for Brodmann Area
13 (the insula) on the right side (R) for Beta 2 (15–18 Hz in this program). The right insula will have major effects on heart rate variability. It is also involved in affect
and executive networks. Figure from The Companion to the Neurofeedback Book (in press).

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At the ADD Centre, HRV training is carried out

simultaneously with the neurofeedback. As reported in

the literature (Thompson & Hagdorn, 2012) and in our

clinical experience, even healthy athletes can show major

cardiac changes postconcussion. Instead of heart rate

variations that are even, with high amplitude, and steady

rhythmicity, the picture becomes one of low amplitude and

poor rhythmicity, as illustrated earlier in Figure 7. The

standard deviation of RR intervals with artifacts removed

(SDNN) has been observed to be unexpectedly low (usually

,50 milliseconds) in concussed athletes before HRV

training is done. In one controlled study concerning HRV

after a TBI, the TBI group revealed significant differences in

HRV parameters compared with controls (Baguley et al.,

2006). At the ADD Centre, it is frequently observed that

the insulae (right insular cortex as well as left insular

cortex) show values that are outside the database norms

when analyzed using QEEG and LORETA. The insulae are

important regulators of autonomic balance, with the right

insula affecting the sympathetic and the left the parasym-

pathetic nervous system, in part through connections to the

nucleus accumbens, which has a role in balancing the

sympathetic and parasympathetic systems (Nagai, Hoshide,

& Kario, 2010). There are reciprocal connections between

the insula and the anterior cingulate gyrus, amygdala,

entorhinal cortex, medialfrontal and orbitofrontal cortex,

and the hippocampus. There are reciprocal connections with

subcortical autonomic structures, including the lateral

hypothalamic area, nucleus tractus solitarius, and the

parabrachial nucleus. These areas are also reciprocally

connected to each other. The medial prefrontal cortex

(MPFC) normally gives a tonic inhibition of the amygdala

(Thayer, Åhs, Fredrikson, Sollers, & Wager, 2012).

Dysfunction of the ventral MPFC that results in hypo-

Figure 10. Figure by Maya Berenkey after drawings by Amanda Reeves from The Companion to the Neurofeedback Book (in press). Midsagittal representation of
selected central midline cortical and subcortical structures (plus the insula, which in reality is not midline but more lateral).

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activation can result in amygdala excitation of the

sympathetic system and results in changes in HRV. Figures

10 and 11 illustrate, in a summary format, influences of

cortical and subcortical areas that can affect both the

patient’s responses to stress and to neurofeedback combined

with HRV training.

With HRV training, the feedback from the baroreceptors

goes directly to the nucleus tractus solitarius. We postulate

that it is quite probable that, through these connections,

HRV training may directly affect all of the aforementioned

cortical and subcortical structures and thus have some

influence on affect, stress, and executive networks in the

brain. In a clinical setting, it is our responsibility to do all

the interventions that may reasonably be expected to help

our patients. We therefore combine the HRV training with

neurofeedback. For a single-channel feedback session, one

sample screen is shown in Figure 12.

Figure 12 shows conventional single-channel neurofeed-

back at FCz2 combined with HRV training. This screen is

often used as an example in teaching because it is a client

favorite. It induces a sense of competition between the boats

with the client attempting to have a green boat win. To do

this they must focus, eliminate all unnecessary thoughts

and ruminations, relax, and concentrate. In addition, clients

are asked to maintain synchrony between the variations in

heart rate (red line) and their breathing (inspiration and

expiration shown by the blue line). Their SDNN and HRV

amplitudes can be immediately calculated for them at the

end of the session using the CardioPro program from

Thought Technology. When LORETA neurofeedback is

being done, the client may do the HRV training as the 19-

channel cap is being put on. Clients can also do it during the

session by using a second computer with the biofeedback

sensors attached to another instrument such as the Infiniti

from Thought Technology, as is being used in the foregoing

example. From a subjective point of view, our patients have

been unanimous in their opinion that one of the most

important aspects of their training program has been HRV

training followed by using their effortless diaphragmatic

breathing when under stress in their everyday life.

At the ADD Centre, we also address nutrition. Given

that nutrition is a complex area requiring an extensive

background in biochemistry and physiology, how can the

neurofeedback practitioner be of practical assistance to the

patient? The simplest route is to have the blood and urine

work ordered by their family practitioner and the results

forwarded to a nutrition specialist. At the Biofeedback

Institute, we usually do one of the following.

Figure 11. Schematic representation of structures to highlight the synergistic influences of neurofeedback and biofeedback–heart rate variability.

2The International 10–20 system defines scalp sites for EEG placements,
in a grid organized around two axes. FCz is a midline location half way
between Cz (the center or vertex of the scalp) and Fz (the next more
frontal midline location).

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1. For regular clients (for example, with attention-deficit/

hyperactivity disorder), we recommend OHIP (provin-

cial health insurance)–covered blood and urine work as

recommended by a PhD nutritionist/dietitian. This is

ordered by the family practitioner, and the results are

forwarded to the nutrition specialist.

2. For complex clients (depression, posttraumatic stress

disorder, TBI), we recommend the TRIAD Profile from

Metametrix in the United States, which is then

interpreted for us by licensed specialists at EvokeNeur-

oscience. This analysis can go in progressively more

advanced stages. It will look at markers for all the

relevant nutrients plus toxins and will identify all major

imbalances. There is a cost involved for the patient.

Conclusion
In our experiene, postconcussion symptoms may be

sufficiently severe and long-lasting as to completely disrupt

the academic pursuits or employment of the affected

individual. This puts considerable strain on the patient’s

social and family life. The emotional and personality

changes after a minor traumatic head injury, especially if

it is not the first such injury, can be very severe. At the

tragic end of the continuum are deaths from accidental

overdose, second-impact syndrome in athletes, accidents, or

even suicide. Traditional assessment procedures do not fully

detect the problems, especially not DAI. Traditional

rehabilitation can be helpful but may not fully ameliorate

the patient’s cognitive and emotional difficulties. Currently,

we are able to report that all postconcussion patients who

completed a neurofeedback plus biofeedback program at the

ADD Centre have been able to return to work and have

been successful in the amelioration of most cognition and

affect symptoms. Clients have included an author who

could barely compose a paragraph when first seen 2 years

postinjury who subsequently authored three books, a

student who had to take a greatly reduced course load all

through his undergraduate years after suffering a head

injury in first year of university who completed a

demanding graduate program in actuarial science with

absolutely no accommodations while concurrently doing

neurofeedback, and a PhD candidate who had been stalled in

his thesis work and unable to teach for 2 years after a

whiplash injury who returned to his studies and subse-

quently completed his doctoral work on artificial intelli-

Figure 12. Screen from Thought Technology instruments and programs using the Thompson suite, Setting up for Clinical Success (www.BFE.org) for simultaneous
neurofeedback and biofeedback training.

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gence, sending us a copy of his graduation certificate along

with a note crediting his recovery to the neurofeedback

intervention. These are three examples of what is meant

when we say that training can be life changing. A case

study of another long-term patient, who had been in a coma

and was deemed by insurance to have suffered a

catastrophic injury, is described in an accompanying article.

The combination of neurofeedback with HRV training

and nutritional interventions offers hope for better

outcomes because it can result in significant improvements

for patients who have suffered a TBI. As was stated at the

outset, there is nothing ‘‘mild’’ about the impairments that

result from a mild TBI, and individuals who suffer these

injuries deserve the opportunity to receive modern

treatment methodologies that have the potential to ensure

positive outcomes.

Acknowledgments
Thanks are extended to Tanushree Bhandari for assisting

with references and Maya Berenkey for illustrations.

Competing Interests
James Thompson is the Chief Science Officer at Evoke

Neuroscience Inc. Michael Thompson and Lynda Thomp-

son are the authors of the Setting up for Clinical Success

Suite available from the Biofeedback Federation of Europe.

References

Angelakis, E., Lubar, J. F., Stathopoulou, S., & Kounios, J. (2004).
Peak alpha frequency: An electroencephalographic measure of
cognitive preparedness. Clinical Neurophysiology, 115, 887–897.

Baguley, I. J., Heriseanu, R. E., Felmingham, K. L., & Cameron, I.
D. (2006). Dysautonomia and heart rate variability following
severe traumatic brain injury. Brain Injury, 20, 437–444.

Bernstein, D. M. (2002). Information processing difficulty long
after self-reported concussion. Journal of the International
Neuropsychological Society, 8, 673–682.

Bhandari, T., Thompson, L., & Reid-Chung, A. (2013). Treating
post-concussion syndrome using neurofeedback: A case study.
Biofeedback, 41(4).

De Beaumont, L., Theoret, H., Mongeon, D., Messier, J., Leclerc,
S., Tremblay, S., & Lassonde, M. (2009). Brain function decline
in healthy retired athletes who sustained their last sports
concussion in early adulthood. Brain, 132(Pt 3), 695–708.

DeWitt, D. S., Jenkins, L. W., Wei, E. P., Lutz, H., Becker, D. P., &
Kontos, H. A. (1986). Effects of fluid-percussion brain injury
on regional cerebral blood flow and pial arteriolar diameter.
Journal of Neurosurgery, 64, 787–794.

Duncan, C. C., Kosmidis, M. H., & Mirsky, A. F. (2005). Closed
head injury-related information processing deficits: An event-
related potential analysis. International Journal of Psycho-
physiology, 58, 133–157.

Dupuis, F., Johnston, K. M., Lavoie, M., Lepore, F., & Lassonde, M.
(2000). Concussions in athletes produce brain dysfunction as
revealed byevent-relatedpotentials. Neuroreport,11,4087–4092.

Giza, C. C., & Hovda, D. A. (2001). The neurometabolic cascade of
concussion. Journal of Athletic Training, 36, 228–235.

Gosselin, N., Saluja, R. S., Chen, J. K., Bottari, C., Johnston, K., &
Ptito, A. (2010). Brain functions after sports-related concus-
sion: Insights from event-related potentials and functional
MRI. Physician and Sports Medicine, 38(3), 27–37.

Korn, A., Golan, H., Melamed, I., Pascual-Marqui, R., &
Friedman, A. (2005). Focal cortical dysfunction and blood-
brain barrier disruption in patients with Postconcussion
syndrome. Journal of Clinical Neurophysiology, 22(1), 1–9.

Kushner, D. S. (2001) Concussion in sports: Minimizing the risk
for complications. American Family Physician, 64, 1007–1014.

Lavoie, M. E., Dupuis, F., Johnston, K. M., Leclerc, S., & Lassonde,
M. (2004). Visual p300 effects beyond symptoms in concussed
college athletes. Journal of Clinical and Experimental Neuro-
psychology, 26(1), 55–73.

Leon-Carrion, J., Martin-Rodriguez, J. F., Damas-Lopez, J.,
Martin, J. M., & Dominguez-Morales, M. R. (2009). Delta–
alpha ratio correlates with level of recovery after neuro-
rehabilitation in patients with acquired brain injury. Clinical
Neurophysiology, 120, 1039–1045.

McCrory, P., Meeuwisse, W. H., Auby, M., Cantu, B., Dvořák, J.,
Echemendia, R. J., Engebretsen, L., et al. (2013). Consensus
statement on concussion in sport: The 4th International
Conference on Concussion in Sport held in Zurich, November
2012. British Journal of Sports Medicine, 47, 250–258.

Mendez, C. V., Hurley, R. A., Lassonde, M., Zhang, L., & Taber,
K. H. (2005). Mild traumatic brain injury: Neuroimaging of
sports-related concussion. Journal of Neuropsychiatry and
Clinical Neurosciences, 17, 297–303.

Meyer, J. S., Kondo, A., Szewczykowski, J., Nomura, F., &
Teraura, T. (1970). The effects of a new drug (Hexobendine) on
cerebral hemodynamics and oxygen consumption. Journal of
the Neurological Sciences, 11, 137–145.

Nagai, M., Hoshide, S., & Kario, K. (2010). The insular cortex and
cardiovascular system: A new insight into the brain-heart axis.
Journal of the American Society of Hypertension, 4, 174–182.

Nilsson, B., & Nordström, C. H. (1977). Experimental head injury
in the rat: Part 3: Cerebral blood flow and oxygen consumption
after concussive impact acceleration. Journal of Neurosurgery,
47, 262–273.

Polich, J. (2007). Updating P300: An integrative theory of P3a and
P3b. Clinical Neurophysiology, 118, 2128–2148.

Shaw, N. (2002). The neurophysiology of concussion. Progress in
Neurobiology, 67, 281–344.

Slobounov, S., Cao, C., & Sebastianelli, W. (2009). Differential
effect of first versus second concussive episodes on wavelet
information quality of EEG. Clinical Neurophysiology, 120,
862–867.

Slobounov, S., Sebastianelli, W., & Simon, R. (2002). Neuro-
physiological and behavioral concomitants of mild brain
injury in collegiate athletes. Clinical Neurophysiology, 113,
185–193.

Using Neurofeedback and Biofeedback in Postconcussion Syndrome

172

W
in
te
r
2
0
1
3

|
B
io
fe
e
d
b
a
c
k



Tator, C. H. (2013). Concussions and their consequences: Current
diagnosis, management and prevention. Canadian Medical
Association Journal, 185, 975–979.

Thatcher, R. W. (2009). EEG evaluation of traumatic brain injury
and EEG biofeedback treatment. New York: Elsevier.

Thatcher, R. W. (2012). Handbook of quantitative electroenceph-
alography and EEG biofeedback. St. Petersburg, FL: Author.

Thatcher, R. W., Biver, C., Gomez, J. F., North, D., Curtin, R.,
Walker, R. A., & Salazar, A. (2001). Estimation of the EEG
power spectrum using MRI T2 relaxation time in traumatic
brain injury. Clinical Neurophysiology, 112, 1729–1745.

Thatcher, R. W., Walker, R. A., Gerson, I., & Geisler, F. H. (1989).
EEG discriminant analyses of mild head trauma. Electroen-
cephalography and Clinical Neurophysiology, 73, 94–106.

Thayer, J. F., Åhs, F., Fredrikson, M., Sollers, J. J., III, & Wager, T.
D. (2012). A meta-analysis of heart rate variability and
neuroimaging studies: Implications for heart rate variability
as a marker of stress and health. Neuroscience & Biobehavioral
Reviews, 36, 747–756.

Thompson, J., & Hagedorn, D. (2012). Multimodal analysis: New
approaches to the concussion conundrum. Journal of Clinical
Sport Psychology, 6, 22–46.

Thompson, J., Sebastianelli, W., & Slobounov, S. (2005). EEG and
postural correlates of mild traumatic brain injury in athletes.
Neuroscience Letters, 3, 158–163.

Michael Thompson Lynda Thompson

Andrea Reid-Chung James Thompson

Correspondence: Lynda Thompson, PhD, CPsych, BCN, ADD
Centre, 50 Village Centre Place, Mississauga, Ontario, Canada,
L4Z 1V9, e-mail: landmthompson@gmail.com.

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