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The Usefulness of Quantitative EEG (QEEG) and Neurotherapy in the Assessment and Treatment of Post-Concussion Syndrome

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Abstract

Evidence for a role for drugs of abuse in the development of chronic psychotic syndromes is scattered throughout 40 years of literature. Electrophysiological studies examining groups believed to have chronic drug-induced psychotic symptoms yielded interesting findings. To our knowledge, no studies directly compared schizophrenia patients whose drug use preceded and those whose drug use followed the onset of psychotic symptoms. Twenty-six schizophrenia patients and 10 healthy control subjects were recruited for the study. Based on the SCID interview, schizophrenia subjects were classified into a Psychosis First (Psy 1st) group (N=11), Drugs First (Drugs 1st; N=8), and No Drug Use (No Drugs; N=7). Schizophrenia subjects were administered the Positive and Negative Symptoms Scale (PANSS). The P300 evoked response and sensory gating were measured for all subjects. Despite the small sample sizes significant differences were found between the groups. Most significantly, the P300 amplitude was smallest in the Drugs 1st as compared to the No Drugs groups, while sensory gating deficit was worst in the Psy 1st group. The data suggest that significant clinical and electrophysiological differences between these groups can be identified. Further research to better define these differences seems warranted.
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Key Words
Database
Electroencephalography
Neurotherapy
Post-concussion Syndrome
QEEG
Traumatic Brain Injury
ABSTRACT
Mild traumatic brain injury (TBI) is associated with dam-
age to frontal, temporal and parietal lobes. Post-concus-
sion syndrome has been used to describe a range of resid-
ual symptoms that persist 12 months or more after the
injury, often despite a lack of evidence of brain abnormali-
ties on MRI and CT scans. The core deficits of post-con-
cussion syndrome are similar to those of ADHD and mood
disorders, and sufferers often report memory, socialization
problems and frequent headaches. While cognitive reha-
bilitation and psychological support are widely used, nei-
ther has been shown to be effective in redressing the core
deficits of post-concussion syndrome. On the other hand,
quantitative EEG has been shown to be highly sensitive
(96%) in identifying post-concussion syndrome, and neu-
rotherapy has been shown in a number of studies to be
effective in significantly improving or redressing the symp-
toms of post-concussion syndrome, as well as improving
similar symptoms in non-TBI patients.
INTRODUCTION
The differential movement between the brain and the
skull when the head is dealt a sharp blow produces percus-
sive, centripetal and shearing forces resulting in traumatic
brain injuries (TBI). Although maximum injury is suffered at
the point of impact, the frontal and temporal regions adja-
cent to the sphenoidal ridges have been shown to be con-
sistently vulnerable to contusions regardless of the direction
or the point of impact.
1
A “contre coup” due to a percussion
wave traveling through the brain matter and impacting the
skull diagonally opposite can cause further contusion, and
shear forces at the boundary between white and grey mat-
ter can result in axonal shearing.
1
Mild TBIs, characterized by high score (>12) on the
Glasgow Coma Scale (GCS), short or no period of loss of
consciousness (LOC), short post-traumatic amnesia (PTA)
duration, brief or no hospital stay, are generally considered
benign. Yet, a significant number of patients report persist-
ent symptomatology for weeks or months
2
and some for
years after injury.
3-17
The cluster of symptoms reported by
these patients is referred to as the post-concussion syn-
drome.
4
Amongst the reported symptoms of post-concus-
sion syndrome are: (a) attention deficits and difficulty sus-
taining mental effort, (b) fatigue and tiredness, (c) impulsiv-
ity, irritability, temper outbursts and changes in affect, (d)
learning and memory problems, (e) impaired planning and
problem solving, (f) inflexibility, concrete thinking and lack of
initiative, (g) dissociation between thought and action, (h)
communication difficulties, (i) socially inappropriate behav-
iors, (j) self-centeredness, lack of insight and poor self-
awareness, (k) impaired balance and (l) headaches
6,15,18,19
and personality changes.
20,21
The subjective nature of these complaints are at odds
with negative medical findings and have often generated
controversy as to whether post-concussion syndrome has
an organic or psychological etiology.
4
However, over the
past 30 years evidence for an organic etiology of post-con-
cussion syndrome has accumulated through studies of
cerebral blood flow, neuropsychological deficits, evoked
potential recordings, PET, SPECT, MRI and quantitative
EEG (QEEG).
22-30
The nature of concussive head injury has
been extensively discussed and theoretical concepts have
been formulated, which are supported by electrophysiolog-
ical evidence.
31,32
QEEG is particularly suitable for the eval-
uation of post-concussion syndrome, as it is empirical,
objective, nonintrusive and has been shown to be highly
accurate in identifying and discriminating various neuro-
physiological patterns of brain dysfunction.
33
Neurotherapy (EEG biofeedback), is an operant condi-
tioning paradigm whereby patients are given contingent
audio/visual rewards for producing specific patterns of
brainwave activity. Since the 1960s, studies have shown
that, through neurotherapy, patients can be taught to pro-
mote normal functioning in the brain by normalizing dys-
functional brainwave patterns characterized by excessive
The Usefulness of Quantitative EEG (QEEG)
and Neurotherapy in the Assessment and
Treatment of Post-Concussion Syndrome
Jacques Duff
Jacques Duff, MAPS, AMACNEM, MAAAPB Psychologist, is from the
Swinburne University of Technology, Brain Sciences Institute, 400 Burwood
Rd, Hawthorn 3122, Australia. Email: jacquesduff@optusnet.com.au
slow wave activity.
34-37
A more recent improvement in neu-
rotherapy is in the use of QEEG to identify the specific
brainwave patterns that need to be redressed.
38-40
This paper examines research findings that provide
evidence for the effectiveness of QEEG in the assessment
of the underlying neurophysiology of post-concussion syn-
drome, and its use in the determination of appropriate neu-
rotherapy protocols. Furthermore, this paper reports on
findings that indicate that neurotherapy is effective in the
treatment of post-concussion syndrome and disorders
whose symptoms overlap with post-concussion syndrome.
QEEG IN THE ASSESSMENT OF
POST-CONCUSSION SYNDROME
A search of the literature from the National Library of
Medicine reveals that although the key word EEG returned
in excess of 34,000 citations since 1990, most of these are
concerned with QEEG methodology, and few involve only
visual analysis of the EEG. The use of QEEG in clinical
practice for the evaluation of a wide range of mental disor-
ders including mild TBI has been extensively researched,
evaluated and reviewed.
33,41-53
The QEEG can provide clini-
cians with better, more targeted treatment options by pro-
viding functional information on the underlying neurophys-
iology associated with symptoms of post-concussion syn-
drome.
1,33,39,53,54
Furthermore, in medico/legal disputes,
QEEG can provide important empirical evidence of func-
tional abnormalities that correlate with symptoms of post-
concussion syndrome following traumatic brain injury.
The U.S. Supreme Court’s 1993
Daubert criteria of the
scientific method replaced the 70-year-old
Frye standards
of “general acceptance” for admissibility of evidence in the
U.S. Federal Court. Subsequently, Thatcher showed that
QEEG met the four factors of the
Daubert criteria: (a)
hypothesis testing, (b) estimates of error rates, (c) peer
reviewed publication and (d) general acceptance
(Daubert
v. Merrell Dow Pharmaceuticals, 61 U.S.L.W 4805 (U.S.
June 29, 1993)).
30
Thatcher also argued that the technical
aspects of QEEG in measuring the effects of neurological
and psychiatric dysfunction match the Supreme Court
standards of “technical” and “other specialized” knowledge
(
General Electric Co v. Joiner, 1997; Kumho Tire Company,
Ltd. v. Carmichael, 1999).
QEEG “scientific,” “technical”
and “other specialized” knowledge meet the standards of
the Supreme Court rulings, thereby supporting QEEG as
an admissible and clinically valid method in the evaluation
of the nature and severity of neuropsychiatric disorders.
55
Fenton
4
reviewed two prospective studies from the
United Kingdom that looked at the evolution and course of
post-concussion syndrome using psychosocial, neuropsy-
chiatric, QEEG and brainstem auditory evoked potential
measures. Findings indicated that increases in theta power
occurred immediately following injury, with resolution with-
in 10 days in most cases. However, chronic symptoms of
post-concussion syndrome were noted in 13% of patients
and were associated with a high prevalence of brainstem
dysfunction and residual slow wave activity in the QEEG,
which appeared related to the intensity of early symptoms.
In an earlier study, identifiable QEEG changes were found
to persist for years following moderate to severe closed
head injury, with these changes related to residual cogni-
tive deficits.
56
Wirsen and colleagues
57
confirmed with QEEG the
pathological findings detected by conventional visual EEG
inspection. However, they found that QEEG topographic
mapping was superior at detecting some regional abnor-
malities. The QEEG showed that regional excess slow
wave activity corresponded well with morphological lesions
in most patients. Low modal frequency of QEEG correlat-
ed both with lesion volume and injury severity and with the
behavioral outcome variables.
Standard or conventional visually read EEG and con-
ventional magnetic resonance imaging (MRI) are not con-
sidered sensitive enough or reliable enough in their detec-
tion of differences between mild and moderate TBI, nor do
they predict outcome and gradations of severity of trau-
matic injury very well.
1
In contrast, recent studies have
shown that QEEG evaluations in the post-trauma period
ranging from months to several years can predict the
severity of the injury and, in some cases, long-term prog-
nosis, even if the initial GCS, LOC, and PTA information
are not available.
58
Studies by Trudeau and colleagues
59
have demonstrated the high accuracy of QEEG in identify-
ing patients with blast concussions years after the event,
and studies by Hoffman and colleagues
60
have shown sim-
ilar accuracy in the detection of TBI using QEEG methods
in outpatients.
QEEG, conventional EEG examination and neuroimag-
ing were performed on 100 patients by Jerrett and
Corsak.
61
QEEG topographic maps were abnormal in 78%
of patients with stroke, 50% with TBI and 100% of those
with space occupying lesions. Of patients with abnormal
EEG maps 30% had either better or sole insult localization
with QEEG than routine EEG or neuroimaging procedures.
EEG mapping had no false positives in localizing abnor-
malities. The authors concluded that QEEG mapping pro-
vided better detection of low amplitude slow wave activity
than routine EEG, and faithful correspondence with neu-
roimaging procedures in localization of lesions. In fact,
QEEG at times distinguished abnormalities not immediate-
ly definable by CT/MRI.
In a retrospective clinical study Henry and colleagues
62
investigated the neuropsychological, physiological, and
behavioral functioning of 32 adult outpatients up to 65
months following non-impact (whiplash) brain injury. They
found that despite significant and persistent age-adjusted
cognitive deficits, mostly in executive functioning and fre-
quent complaints of problems with attention, behavioral
control, sleep and sexuality, structural neuroimaging was
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
199
not sensitive in detecting brain pathology. However,
QEEG was abnormal in all the participants evaluated, with
evidence of frontocentral slowing and increased spike
wave activity.
Thornton
63
used QEEG variables at 19 scalp locations
and five frequency bands up to 64 Hz, recorded under eyes
closed condition on 91 subjects. These consisted of 32
mild TBI (MTBI) with no LOC > 20 minutes, 7 with LOC> 20
minutes and 52 normals all over the age of 14. A high fre-
quency (64Hz) discriminant function effectively identified
87% of the minimal LOC MTBI subjects across all time
periods and 100% of subjects within 1 year of accident.
The combination of the multiple discriminants resulted in
100% accuracy rate for the 39 brain injured subjects.
Thornton
64
later examined the QEEG variables of 85
MTBI and 56 normal subjects during three auditory memo-
ry tasks. The MTBI subjects exhibited consistent patterns
of phase and coherences anomalies and increased relative
power in the beta band, which were correlated with the dif-
ferences in memory recall. Memory functioning was found
to be positively correlated with phase and coherence
(measures of brain connectivity) and negatively correlated
with increased beta activity at specific locations. It is inter-
esting to note that Thatcher et al found similar patterns of
phase, coherence and beta power anomalies when com-
paring TBI patients with normal database controls.
58,65
In order to examine the accuracy of QEEG discriminant
functions, Thatcher and colleagues
65
obtained measures of
QEEG from 608 mild TBI patients and 108 normal subjects
matched for age. A discriminant function developed from
264 mild TBI patients and 83 age-matched controls yielded
a discriminant classification accuracy of 94.8%. An inde-
pendent cross-validation of the discriminant function using
130 mild TBI patients and 21 controls yielded a discrimi-
nant accuracy of 96.2% for the TBI patients and 90.5% for
normals. A second independent cross-validation of the dis-
criminant function was carried out using 51 patients, and
measures of test-retest reliability were carried out using 93
patients. Results yielded classification accuracies between
77.8% and 92.3%. A third independent cross-validation
using 70 mild TBI patients from a different location and with
different QEEG recording equipment yielded a discriminant
accuracy of 92.8%.
In order to determine the prognostic strength of QEEG
discriminant functions on outcome 1 year after injury,
Thatcher and colleagues
58
administered a comprehensive
diagnostic evaluation to 162 TBI patients within 1 to 21
days after injury. Diagnostic evaluation consisted of 19
channel QEEG referenced to age-matched norms, brain-
stem auditory evoked potentials, CT scan, and GCS at
time of admission (GCS-A) and at time of EEG test (GCS-
T). Functional outcome at 1 year following injury was
assessed using the Rappaport Disability Rating Scale
(DRS). The predictive power of each diagnostic measure at
one year following injury was assessed using stepwise dis-
criminant analyses and multivariate regression analyses.
The best single predictors of outcome in both the discrimi-
nant analyses and the regression analyses were EEG
coherence and phase. Discriminant greater than 95.8%
accuracy of prediction of survival outcome 1 year after
injury was obtained.
66
A prospective QEEG study, using
high frequency discriminant, effectively identified 87% of
TBI subjects who had not suffered significant loss of con-
sciousness, across all time periods after TBI and 100% of
subjects within 1 year of TBI.
67
QEEG studies correlate closely with MRI findings. In a
study by Thatcher, Biver and colleagues
29
brain water pro-
ton 1H T2 relaxation times and QEEG coherence were
obtained from two independent groups of closed head
injured patients and a group of normal control subjects.
Statistically significant intercorrelations were observed
between relaxation times of the cortical grey and white
matter and EEG coherence. MRI findings were consistent
with clinical QEEG studies in which (a) white matter lesions
were related to increased delta amplitude and (b) grey mat-
ter lesions were related to decreased alpha and beta fre-
quency amplitude. Lengthened T2 relaxation times in both
the cortical grey and white matter were correlated with
decreased beta and alpha amplitude and increased delta
amplitude and with diminished cognitive function. The
authors interpreted these findings as suggestive of a bio-
physical correspondence between the impaired integrity of
protein-lipid structures of the brain as measured by the
MRI and the scalp-recorded QEEG in TBI.
28
These studies
lend more support for the routine use of QEEG in the eval-
uation of post-concussion syndrome, as suggested in
cross validation studies reported next.
Thatcher, North and colleagues
58
evaluated the effec-
tiveness of QEEG in the determination of severity of post-
concussion syndrome. They used emergency hospital
admission records of 105 patients with mild to severe TBI,
15 days to 4 years after injury, to evaluate severity of injury
based on ratings of Glasgow Coma Scale (GCS), Loss of
Consciousness (LOC) and Post Traumatic Amnesia (PTA).
Using 16 of the highest-loading QEEG variables on each
factor that differed significantly between severe and mild
TBI by univariate t-test, a multivariate discriminant function,
discriminated between mild and severe TBI groups with an
accuracy of 96.39%, sensitivity 95.45%, and specificity
97.44%. In addition, the QEEG discriminant score also
identified intermediate severity in moderate TBI patients.
The discriminant function was cross-validated in 503
Veteran Affairs patients with mild to severe TBI. The valid-
ity of the discriminant function as an index of severity of
injury and a classifier of degrees of severity was confirmed
on the basis of significant correlations between QEEG dis-
criminant scores, emergency admission measures, and
post-trauma neuropsychological test scores.
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Studies reviewed so far attest to the high reliability and
discriminant validity of QEEG discriminant functions in
revealing patterns consistent with MTBI or post-concussion
syndrome. These studies also highlight the high correspon-
dence of QEEG with other neuroimaging methods and in
some cases the superiority of QEEG in locating the source
of anomalies, be it lesions or the excessive regional pat-
terns of excessive slow wave activity associated with TBI or
post-concussion syndrome. Coup contre-coup patterns can
be commonly detected through topographic QEEG maps,
and changes in EEG coherences and phase delays point to
regional or global lack of connectivity brought about by focal
or diffuse injuries. These studies lend support to the use of
QEEG as an objective assessment to evaluate whether
there is an organic basis to the symptoms reported by suf-
ferers of post-concussion syndrome who are often dis-
missed as malingerers or as suffering from psychological,
personality or somatization disorders.
COGNITIVE REHABILITATION FOR
POST-CONCUSSION SYNDROME
Cognitive rehabilitation following TBI has been widely
used, consisting of attempts with computer assisted tasks
to restore cognitive skills, therapist-intensive interactions
with cognitive therapy and counselling to help patients
adapt to their deficits. While cognitive therapy may help
provide psychological support and guidance, a search of
the literature, by this author, found that there appears to be
no theoretical concept for cognitive rehabilitation of post-
concussion syndrome, nor is there evidence in the litera-
ture of the effectiveness of cognitive therapy in improving
or redressing the symptoms of post-concussion syndrome
(12 months or more after injury).
Cicerone and colleagues
68
conducted an intensive sur-
vey of the literature and graded the quality of the research
evidence for cognitive rehabilitation following TBI. They
concluded that there was evidence for the effectiveness of
several forms of cognitive rehabilitation for persons with
stroke and TBI and made specific recommendations for the
remediation of attention, memory, functional communica-
tion, and executive functioning after TBI. However, their
metaanalysis was based on 171 studies conducted mostly
within the time period during which spontaneous improve-
ments are known to occur, and did not appear to differenti-
ate between acute and chronic TBI states associated with
post-concussion syndrome. Other studies reviewed next
have found no evidence to support the use of cognitive
rehabilitation when spontaneous recovery is controlled.
A study by Ponsford and Kinsella
5,69
investigated a
remedial intervention program for attention deficits follow-
ing TBI. The study used a computer-mediated attention
enhancement program with 10 severely injured subjects
and consisted of a multiple baseline across subjects
design to compare the intervention with intervention plus
therapist feedback and reinforcement in separate training
phases lasting 3 weeks. However, when spontaneous
recovery and generalization to day to day activities were
controlled for, no significant gains were demonstrated.
Gansler and McCaffrey
70
evaluated an intensive atten-
tion-remediation program based on Posners 4-component
model of attention for adult male TBI patients with chronic
attention deficits. The hierarchically ordered attention-
remediation program using an A-B-A single case design
yielded no clinically significant improvement on attentional
measures, neuropsychological variables, psychological
characteristics, activities of daily living, or subjective rat-
ings of changes in attentional abilities.
Salazar, Warden and colleagues
71,72
recently reported
the results of a prospective controlled randomized trial com-
paring an intensive inpatient cognitive rehabilitation pro-
gram to a home support program for 120 active-duty military
personnel. All subjects had sustained a moderate-to-severe
closed head injury (GCS <=13 or PTA 24 hours or more), or
evidence of focal cerebral contusion or hemorrhage on CT
scan or MRI. All patients received medical treatment as
needed and were randomly assigned to each group: 67
were assigned to an intensive, standardized 8-week, in-
hospital cognitive rehabilitation program and 53 to a limited
home program, consisting of guidance on home activities
and a weekly telephone call from a psychiatric nurse. At 1-
year follow-up, there was no significant difference in out-
come measures between patients in the two groups on
measures of fitness for return to duty, cognitive, behavioral,
or quality-of-life measures. The authors concluded that
these findings emphasize the importance of conducting ran-
domized trials to evaluate TBI rehabilitation interventions.
It could be argued that cognitive therapy requires that
the attentional system, executive functions and memory be
unimpaired. Hence, in post-concussion syndrome and
ADHD, the dysfunctional frontal lobes may interfere with
the effectiveness of cognitive therapy. In contrast, the use
of operant conditioning of the EEG (neurotherapy) offers
hope to significantly restore normal neuronal functioning
and to restore the TBI-associated deficits towards pre-mor-
bid levels.
1,38,39,60,73-75
NEUROTHERAPY
Brainwave activity is believed to be the manifestation of
the electrical activity of columns of cortical neurons driven
by subcortical generators from the thalamus, hippocampus
and septum
76
There is general consensus in neuroscience
that thalamo-cortical oscillations are responsible for the ini-
tiation of timing and transfer of information between vari-
ous structures in the brain.
77,78
According to this view, nor-
mal human neuronal activity, manifested in the EEG, is
self-regulating. “Dysrhythmia” in thalamocortical oscilla-
tions is believed to arise from dysregulation in subcortical
and cortico-cortical circuits that give rise to abnormal EEG
rhythms, such as excesses or deficits in delta, theta and
alpha or beta activity. Such dysregulation is believed to be
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
201
responsible for a range of psychiatric disorders,
40,77-80
and
theoretical mechanisms and scientific rationale for the
effectiveness of neurotherapy in redressing these “dys-
rhythmias” have been proposed,
40,79-81
but are outside the
scope of this paper.
The core symptoms of post-concussion syndrome as
previously discussed include attention deficit disorder,
impulsivity, mood disorders, memory difficulties and
headaches. Each of these are associated with identifiable
neurophysiological brain patterns, mostly associated with
various degrees of excessive slow wave (theta) activi-
ty.
1,33,47,58,65,82
Each of these core symptoms has been shown
to respond positively to neurotherapy. Since excess theta
is causally linked to reduced cerebral metabolism and
brain blood flow (ischemic hypoxia), impaired neurotrans-
mitter synthesis/release and various forms of brain pathol-
ogy, inhibition of excess theta by any means, including
neurotherapy, is likely to improve brain function.
83
During neurotherapy, real-time QEEG is displayed on a
computer in the form of a game. The game software is driv-
en by selected QEEG parameters and the patient is given
contingent audio-visual rewards in the game for producing
less slow wave (theta 4-7Hz) and more fast waves (beta
16-20Hz). There is now significant evidence in the litera-
ture, which suggests that around 80% of ADHD patients
can learn to produce a brainwave pattern with more normal
theta/beta ratios
37,40,81,84-86
by this operant conditioning
process. Evidence of the effectiveness of neurotherapy in
reducing excess theta and redressing TBI associated
deficits are reviewed next.
Neurotherapy Treatment of TBI
and Post-concussion Syndrome
Hoffman and colleagues reviewed and reported on
improvements in clinical symptoms of post-concussion
syndrome using neurotherapy in a clinical setting.
60,73,87
They generally started treatment at least 6 months post
injury, and reported that on average 40 neurotherapy ses-
sions were required for rehabilitation, with control meas-
ures recorded every 5 sessions. Physiological and EEG
measures were quantified and tracked within each session
to monitor training protocol effectiveness. Hoffman et al
60
reported that in around 80% of cases TBI patients were
able to achieve a minimum 70% improvement in symp-
toms. Good clinical results were also obtained with chron-
ic patients years post-injury.
Ayres reviewed her work with 250 TBI patients, sum-
marizing more than two decades of clinical work using real-
time digital EEG biofeedback for cases of head trauma,
coma, and stroke.
74,75
Ayres described specific protocols
used over that period, training primarily to reduce excess
theta activity at locations where that activity was the high-
est. She reported that as the EEG operant conditioning
took effect, evidenced in reduction of theta/beta ratios,
patients reported improvement in energy levels, concen-
tration, memory, reduced sensitivity to light and sound,
reduced incidence and severity of headaches, and reduc-
tion in positional vertigo.
74
Schoenberger and colleagues
88
conducted evaluation
of the potential efficacy of an EEG biofeedback system in
the treatment of TBI using 12 patients 12 months after
injury. All patients initially reported symptoms of post-con-
cussion syndrome with substantial cognitive difficulties,
which interfered with their day-to-day functioning.
Participants were randomly assigned to an immediate
treatment group or a wait-list control group and received 25
sessions of EEG biofeedback. All were assessed at pre-
treatment, post-treatment, and follow-up with standardized
neuropsychological and mood measures. Comparison of
the two groups on outcome measures indicated improve-
ment in subjective reports of depression, fatigue, and other
problematic symptoms, including improvements in occupa-
tional and social functioning following neurotherapy. There
were also significant improvements in some objective
measures of cognitive functioning.
Head injured patients often report tinnitus, a debilitating
disorder of central auditory processing whereby the patient
continuously hears varying degrees of high pitch sounds.
Gosepath et al
89
treated 40 patients with tinnitus with neu-
rotherapy, training to reward alpha-activity and inhibit the
beta-activity while relaxing and orientating to sounds or
music. All patients had a significant reduction on the Gobel
and Hiller tinnitus questionnaire, concurrent with increased
alpha and reduced beta activity. A control-group of 15 per-
sons without tinnitus didn’t register any changes of alpha or
beta activity during the same period.
In a recent European study, Bounias and colleagues
90
reported in a four-part study on a random group of 27
patients, from various hospital centers with vascular, trau-
matic or combined head injuries, treated with neurothera-
py. In part one, Bounias described the use of a meticu-
lously designed method of typological classification of clin-
ical syndromes. Patients were assigned scores on seven
categories of post-traumatic clinical symptoms: motor func-
tions, language, cognitive functions, psychosocial disor-
ders, pain related disorders, neuropsychiatric impairments
and metabolic disorders. Statistical methods were used to
construct patients’ indices of membership to each catego-
ry. In part two, the study reported on individual assessment
pre- and post-neurotherapy, and on treatment outcome
based on the symptom indices. Results indicated class-
average rehabilitation rates ranging from 59% to 87%. For
the most part, patients were required to reduce slow wave
(delta/theta) activity and increase fast wave (beta) activity,
wherever it was excessive in the QEEG. Improvements in
symptomatology were related to improvements in the
QEEG parameters that the patients were trained to
improve.
91
In part three, Laibow et al reported that the
patients also experienced significant improvements in car-
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
202
diac parameters and peripheral temperature in addition to
targeted improvements in brain functions and symptoms.
92
In part four, Bounias and Laibow described an empirically
derived relationship relating length of neurotherapy treat-
ment to the initial load of clinical symptoms and the rate of
rehabilitation.
93
The researchers concluded that neurother-
apy can successfully treat patients with brain injury with
highly meaningful clinical results.
91
Keller
94
investigated the usefulness of neurotherapy in
TBI rehabilitation during the spontaneous recovery phase.
12 patients with moderate TBI were given contingent audio
and visual feedback for increasing amplitude and duration
of beta activity in their EEG at Fz. A matched control group
of 9 patients were given a standardised computerized
attention training program not involving EEG biofeedback.
The treatment group showed statistically significant
changes in their EEG beta amplitudes and in increases in
the ability to sustain beta output, while no systematic
increases were observed in the control group. On atten-
tional measures, patients in both groups improved in their
ability to attend for short durations on a computer task.
However, only the neurotherapy group improved in tasks of
sustained attention and on pencil paper tasks.
Walker and colleagues
95
investigated whether QEEG
guided coherence training was effective in remediating
symptoms of post-concussion syndrome. Twenty-six
patients with persistent symptoms were first evaluated with
QEEG 3-70 months post injury. Neurotherapy protocols
were designed to remedy abnormal QEEG coherence
scores. Significant improvement (>50%) in symptoms was
recorded in 88% of patients (mean = 72.7%). All patients
were able to return to work following treatment. On aver-
age 19 sessions were required, which is half the average
number of sessions required in most studies using ampli-
tude training.
Attention Deficits Secondary to
TBI and Neurotherapy
QEEG studies reviewed by Hughes and John
33
have
found similar patterns of frontal deficits in TBI as in ADHD.
Both exhibit prefrontal hypercoherence and excessive slow
wave (theta and alpha) activity at frontal sites, and similar
dysfunctional parietal patterns.
Using QEEG-derived discriminant functions, Monastra
et al and Chabot and colleagues were able to discriminate
replicably ADHD versus normal children, with a sensitivity
of 90% and a specificity of 94%
96,97
and ADD versus spe-
cific learning disorders with a sensitivity of 97% and a
specificity of 84.2%.
43,98-100
Their most common findings
were of generalized or focal theta/alpha excess mostly at
frontal and central sites. Monastra and colleagues found
that the power ratio of theta/beta measured at the vertex
(Cz) was able to distinguish their large sample of ADHD
children from normals with a sensitivity of 86% and a speci-
ficity of 98%.
96,97
Findings of attention deficits post TBI correlate with neu-
roimaging studies that indicate that the same areas suffer
damage in TBI as in non-TBI subjects. For example, there
are strong correlations between MRI and QEEG studies
suggesting that the same areas are dysfunctional in TBI-
acquired attention deficits and the neurodevelopmental
ADHD population.
101
In order to explore this possibility, Max
et al
102
found, in a prospective study, that increases in atten-
tion deficit disorder symptoms in the first 2 years after TBI
were significantly related to the severity of TBI, and consis-
tent with brain damage. Gerring and colleagues
101
found an
excess prevalence of premorbid ADHD among children who
presented with moderate and severe TBI. Children with
high psychosocial adversity were more likely to develop
ADHD after TBI. These studies suggest that ADHD and TBI
have overlapping organicity and symptoms, with cumulative
effects, with attention deficits and behavioral inhibition
deficit being the major overlapping features.
101
Recent studies have highlighted the degree and nature
of functional similarities between ADHD and mild TBI.
Using MRI and a set of multiple logistic regression models,
Gerring and colleagues
22
determined that the odds of
developing ADHD were 3.64 times higher among children
with thalamus injury, and 3.15 times higher among children
with basal ganglia injury, supporting an association
between acquired ADHD and lesion in either or both the
thalamus and basal ganglia. Chabot and colleagues
43
demonstrated using VARETA on QEEG data of children
with ADHD that the excess theta observed in ADHD
appears to be generated within the septal-hippocampal
pathways of the basal ganglia, while excess alpha is gen-
erated in the thalamus. These findings support the view
that patients with TBI-acquired ADHD symptoms share
common underlying mechanisms with the ADHD popula-
tion that may be redressed by neurotherapy as evidenced
in studies and clinical reports of neurotherapy treatment of
ADHD
103
and TBI.
1
Tinius and Tinius
104
compared treatment effects of neu-
rotherapy in adult male patients with mild TBI and other
adult male patients with attention deficits to a waiting group
control over an equivalent period. Psychological and neu-
ropsychological testing was applied before and after the
treatment period in both groups. After 20 treatment ses-
sions, results indicated significant improvements in atten-
tion and response accuracy scores, and signifiant reduc-
tion in self-report of symptoms in both treatment groups
compared to control. Errors in a problem-solving task
improved only in the mild TBI patient group.
Neurotherapy in the Treatment of Mood Disorders
TBI is associated with frontal and temporal lobe dys-
function and asymmetries, which in turn have been associ-
ated with headaches, seizures, anger outbursts, mood
instability and psychosis.
1,30,39,65,105-112
In particular, anxiety
and depression have also been linked with excessive left
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
203
greater than right (L>R) alpha asymmetry in the frontal
lobes, a pattern associated with a withdrawal and avoid-
ance style of problem solving, negativity and pessimism.
113-
117
On the other hand, R>L alpha asymmetry has been
associated with mania.
118
Neurotherapy has been used
successfully to redress these asymmetries and reverse the
symptoms of depression.
119-125
A recent report of a 5-year
follow-up of 5 severe chronic mood disorder patients, who
had successfully undergone neurotherapy for depression
using an asymmetry correction protocol, indicated that the
treatment effects had been maintained over that period.
Four of the patients were still off medication, and one on
reduced medication.
Neurotherapy and Memory Rehabilitation
Rozelle and Budzynski
126
presented the case of a 55-
yr-old male treated with neurotherapy for 6 months begin-
ning approximately 1 year after a left-side cerebrovascular
accident. The patient complained of hesitant speech with
word finding difficulty and paraphasia, difficulty focusing his
right eye, lack of balance and coordination, poor short-term
memory, poor concentration, anxiety, depression, and tin-
nitus. EEG entrainment feedback was used followed by
neurofeedback to inhibit theta (4-7 Hz) and increase beta
(15-21 Hz) over sensorimotor and speech areas. At the
conclusion of treatment there were significant reductions in
slow-wave activity and theta/beta ratio. Speech fluency,
word finding, balance and coordination, attention, and con-
centration improved. Depression, anxiety, and tinnitus
were also greatly reduced.
126
Thornton
127,128
used neurotherapy to remediate memory
deficits by applying EEG biofeedback to QEEG correlates
of memory function. An activation QEEG database was
obtained with 59 right-handed subjects during two auditory
memory tasks consisting of prose passages and word lists.
QEEG recordings of clinical cases of memory dysfunction
were compared to the normative database to determine
their deviations from the values that predicted success for
the reference group. Neurotherapy protocols attempted to
normalize the values of the specific QEEG variables that
were relatively deviant in the subjects. Thornton presented
3 case examples that indicated the successful use of neu-
rotherapy in subjects with brain injury, with improvements
ranging from 68% to 181% in relation to baseline measures
as a result of the intervention.
Neurotherapy in the Treatment of Headaches
Headaches following TBI can be persistent and chron-
ic in a substantial number of sufferers. A group of 100 chil-
dren, 90 after brain concussion and 10 after contusion
were observed for a period of 12 months. Of these, 83%
reported headaches, 56% acute, and 27% chronic, mainly
tension type headaches, and in 21% the headache per-
sisted during the whole year of observation.
129
QEEG has
been used to assess the underlying neurophysiology of
headache and migraine sufferers, identifying specific pat-
terns of excessive slow wave activity. The QEEG topo-
graphic maps of 100 patients with various types of
headache (classic migraine, non-classic migraine, muscle
contraction, mixed and post-traumatic) were compared to
the topographic maps of 38 normal controls. Patients with
migraine had 11 abnormal markers. Excess theta at O1
and excess alpha at O2 and T6 identified 82% of the
headache patients.
130
In an exploratory study, Siniatchkin et al
131
showed that
EEG biofeedback training was accompanied by significant
reduction of slow wave cortical excitability. This was likely
to have been responsible for the clinical efficacy of the
training; a significant reduction of days with migraine and
other headache parameters was observed. It was suggest-
ed that normalization of the threshold regulation of cortical
excitability during feedback training may account for clini-
cal improvement. The use of EEG biofeedback training to
suppress excess slow wave activity has been shown to
reduce headache,
132
presumably by increasing blood flow.
Excess theta wave activity is causally linked to reduced
brain blood flow (ischemic hypoxia) and metabolism,
impaired neurotransmitter biosynthesis, and numerous
types of brain pathology.
83
Consequently, reduction of
excessive theta activity by EEG biofeedback is likely to be
associated with the exercising and normalization of self-
regulatory mechanisms that lead the brain into more nor-
mal functioning and reduction of symptomatology.
79,80
Reviews of the usefulness of various peripheral and
EEG biofeedback modalities for a variety of symptoms,
including biofeedback for headaches, were carried out by a
number of authors. These studies have supported the use
of biofeedback for headaches, and hightlight the need to
use the technique most appropriate to the etiology.
133-138
For
example, Glueck and Stroebel
137
reviewed the use of vari-
ous types of biofeedback: EEG, temperature, Skin
Conductance Response (SCR) and EMG and general
relaxation techniques. They described specific biofeed-
back conditioning techniques for the treatment of patients
with vascular headaches, muscle contraction headaches,
and Raynaud’s disease and suggested that the choice of
suitable treatment must be carefully tailored to the needs of
the individual patient.
EEG biofeedback was used to treat 13 patients, aged
18-68 yrs, suffering chronic post-traumatic headache and
cognitive dysfunction. EEG biofeedback consisted of train-
ing to inhibit 4-7Hz theta activity and increase 15-18Hz
beta activity. All patients reported improvement in anxiety,
depression, and irritability, and those subjects who com-
pleted 30 sessions reported significant global improvement
in headache and improved cognitive dysfunction.
132
The effectiveness of EEG biofeedback in cases of ten-
sion headache was evaluated using pre- and post-meas-
ures of EEG-alpha, electromyography, galvanic skin
response, a visual analog scale, an anxiety scale, and a
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
204
behavior disorder checklist. Twenty sessions of EEG
biofeedback training were given to the experimental group,
followed by post-assessment. Post-assessment for the con-
trol group was carried out after an equivalent treatment-free
period. Results indicated a significant reduction of
headaches in the experimental group and improvements in
anxiety.
139
A double blinded study of biofeedback for
headaches showed significant improvement in symptoms
140
QEEG is particularly useful in the assessment of diffi-
cult cases of headaches. For example, Soriani and col-
leagues
141
reported a case of an 8-year-old boy with recur-
rent migraine auras without headache, precipitated by
minor head trauma. Aura was characterized, besides other
brain-stem signs, by confusional state. Soriani found an
uncommon EEG pattern, characterized by diffuse continu-
ous beta activity, recorded during the episodes, which sug-
gested that recognition of this finding may prevent misdi-
agnosis and the inappropriate prescription of medication.
QEEG studies can help to identify the underlying neu-
rophysiology associated with headaches, as different pat-
terns suggest different treatment approaches or biofeed-
back protocols. For example, a pattern suggestive of corti-
cal irritability may be more effectively treated through sup-
pression of fast wave activity, while a pattern of excess
slow wave activity would respond better to suppression of
theta. The choice of biofeedback protocols and modalities
should be individually determined based on assessment
using well established principles of applied psychophysiol-
ogy, which help determine whether the headaches have a
vascular or muscular tension etioligy, or are due to specif-
ic brainwave patterns.
Further Research
A major review of the scientific literature and clinical use
of neurotherapy was published in the January 2000 edition
of Clinical Electroencephalography.
1
Authors reviewed
Neurotherapy in Anxiety Disorders, including PTSD,
142
Attention Deficit Disorder,
103
Affective disorders
125
Seizure
disorders
143
and post-concussion syndrome.
1
The editorial
opinion by Neurology Editor, Frank Duffy, M.D., stated:
“The
literature, which lacks any negative study of substance,
suggest that Neurotherapy should play a major therapeutic
role in many difficult areas. In my opinion if any medication
had demonstrated such a wide spectrum of efficacy it would
be universally accepted and widely used.”
144
Duffy suggested that it would be desirable to have dou-
ble blind placebo controlled studies of neurotherapy.
However, in practice it is impossible to give sham feedback
without the clinician knowing it, and patients quickly learn
that the sham EEG is not their own when eye blinks and
movements are not related to artifacts in the EEG. It may
also be unethical to give sham feedback over 3 to 4 months
to a vulnerable population on account of the possible harm
to the client due to induced learned helplessness. Lubar
reviewed his early work, conducted in the 70s, when ethics
approval was more relaxed. In those studies he demon-
strated in several ABA design controlled studies of
Neurotherapy for ADHD that the treatment effects were
reversible and contingent with the training and not a place-
bo effect.
34
It is imperative to note that in the reviewed studies,
improvement in symptoms correlated only with changes in
the EEG features being trained, for example, reduction of
theta/beta ratio in attention deficits and reversal of frontal
alpha asymmetry in depression. Consequently, one could
argue that neurotherapy treatment protocols should target
dysfunctional brain patterns identified in the QEEG topog-
raphy as they relate to the patient’s difficulties. Choice of
protocols can be made with more confidence when there is
convergence between neuropsychological findings, deficits
and abnormal Z scores in QEEG patterns compared to nor-
mative databases.
Meanwhile, more studies that control for spontaneous
recovery and that compare treatment effects should be car-
ried out in varied clinical settings with larger groups of sub-
jects. Funding for such studies is likely to be difficult to obtain
unless Government instrumentalities can become involved.
CONCLUSION
A number of controlled and uncontrolled studies and
anecdotal reports reviewed in this paper suggest that neu-
rotherapy may be an effective and cost efficient method of
treating patients with mild traumatic brain injury. The length
of treatment or number of sessions may be related to the
initial severity of injury, and further studies may elucidate
the most effective protocols for specific abnormal patterns
seen in the QEEG of TBI patients. The neurotherapy stud-
ies, while not substantial in number, nonetheless stand in
contrast to the nearly complete absence of published stud-
ies of the effectiveness of cognitive rehabilitation or of
other therapies in the remediation of post-concussion syn-
drome. The relative efficacy of neurotherapy in the treat-
ment of post-concussive syndrome warrants the continued
use of this treatment modality. The role of quantitative EEG
or QEEG to help guide the neurotherapist in choosing
which EEG variables and locations to target for biofeed-
back has been proven to be of value in the literature as
reviewed in this paper. No comparative studies of which
EEG variables may be more or less effective have been
published as of this date. Currently, all of the studies cited
in this review share in common a quantitative and objective
approach to variable selection.
CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
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CLINICAL EEG and NEUROSCIENCE ©2004 VOL. 35 NO. 4
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... Patients with mTBI consistently present symptoms of impaired cognition/attention [20,[42][43][44][45][46]. Supporting these behavioral abnormalities, a review paper from Duff [47] demonstrated how mTBI patients express significantly increased magnitude (i.e., power) of slow-wave (delta/theta) EEG across large-scale networks and decreased alpha/beta power. These findings are reinforced by EEG and MRI studies showing positive correlations between increased delta power and white matter lesions plus cognitive dysfunction in PCS [25,28,48,49]. ...
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(1) Background: Mild traumatic brain injury produces significant changes in neurotransmission including brain oscillations. We investigated potential quantitative electroencephalography biomarkers in 57 patients with post-concussive syndrome and chronic pain following motor vehicle collision, and 54 healthy nearly age- and sex-matched controls. (2) Methods: Electroencephalography processing was completed in MATLAB, statistical modeling in SPSS, and machine learning modeling in Rapid Miner. Group differences were calculated using current-source density estimation, yielding whole-brain topographical distributions of absolute power, relative power and phase-locking functional connectivity. Groups were compared using independent sample Mann-Whitney U tests. Effect sizes and Pearson correlations were also computed. Machine learning analysis leveraged a post hoc supervised learning support vector non-probabilistic binary linear kernel classification to generate predictive models from the derived EEG signatures. (3) Results: Patients displayed significantly elevated and slowed power compared to controls: delta (p = 0.000000, r = 0.6) and theta power (p < 0.0001, r = 0.4), and relative delta power (p < 0.00001) and decreased relative alpha power (p < 0.001). Absolute delta and theta power together yielded the strongest machine learning classification accuracy (87.6%). Changes in absolute power were moderately correlated with duration and persistence of symptoms in the slow wave frequency spectrum (<15 Hz). (4) Conclusions: Distributed increases in slow wave oscillatory power are concurrent with post-concussive syndrome and chronic pain.
... 23 Increasing reports of using QEEG to identify and track mTBI over time during the period of recovery are appearing in the literature. 14,15,[24][25][26] The ability to identify individuals that are likely to have a more prolonged recovery can help guide more aggressive treatment efforts earlier in the course of recovery. With improved EEG application techniques, there may soon be a strong argument for performing baseline QEEGs prior to the start of each season, just as other types of testing are currently being performed. ...
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Concussion is a common brain injury. The American Academy of Neurology provides a definition of concussion: “Concussion is a traumatically, or biomechanically, induced alteration of brain function. Emphasis is placed on a pathophysiological process, or functional disruption, as opposed to anatomic, structural, or tissue injury.”. The incidence of mild traumatic brain injury (mTBI) is estimated at 200 per 100 000. The Centers for Disease Control and Prevention (CDC) estimates 3.8 million sport and recreational mTBIs occurring in the United States each year. A more recent CDC assessment estimates 2.5 million concussion injuries in high school sports alone. The controlled environment and opportunity for direct surveillance and observation has made the sports arena the scientific “wet lab” for the study of mTBI natural history, short- and long-term consequences and opportunities to intervene. Quantitative EEG methods have been utilized in the assessment and management of mTBI and lends to provide a cost-effective procedure that has the sensitivities needed to identify pathology where routine visual inspection of the EEG has failed.
... Whilst the participant is not doing this by subjectively altering their thoughts (Othmer et al., 2005), they are required to understand the concept and attend to the task (May et al., 2013). NFT has been reported to improve executive and cognitive functions, memory, attention, motor recovery and seizures following mild, moderate and severe TBI (Tinius and Tinius, 2000;Walker et al., 2002;Duff, 2004;Thornton and Carmody, 2005;Tan et al., 2009), migraine (Stokes and Lappin, 2010), depression (Choi et al., 2011;Linden et al., 2012), anxiety (Hammond, 2005), OCD (Surmeli and Ertem, 2011;Koprivova et al., 2013), and schizophrenia (Surmeli et al., 2012). NFT has also been shown to enhance fractional anisotropy, gray and white matter volume in moderate TBI (Munivenkatappa et al., 2014) and normal participants (Ghaziri et al., 2013). ...
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Background: Mild traumatic brain injury (mTBI) results from an external force to the head or body causing neurophysiological changes within the brain. The number and severity of symptoms can vary, with some individuals experiencing rapid recovery, and others having persistent symptoms for months to years, impacting their quality of life. Current rehabilitation is limited in its ability to treat persistent symptoms and novel approaches are being sought to improve outcomes following mTBI. Neuromodulation is one technique used to encourage adaptive neuroplasticity within the brain. Objective: To systematically review the literature on the efficacy of neuromodulation in the mTBI population. Method: A systematic review was conducted using Medline, Embase, PsycINFO, PsycARTICLES and EBM Review. Preferred Reporting Items for Systematic Reviews and the Synthesis Without Meta-analysis reporting guidelines were used and a narrative review of the selected studies was completed. Fourteen articles fulfilled the inclusion criteria which were published in English, investigating an adult sample and using a pre- and post-intervention design. Studies were excluded if they included non-mild TBI severities, pediatric or older adult populations. Results: Thirteen of fourteen studies reported positive reductions in mTBI symptomatology following neuromodulation. Specifically, improvements were reported in post-concussion symptom ratings, headaches, dizziness, depression, anxiety, sleep disturbance, general disability, cognition, return to work and quality of life. Normalization of working memory activation patterns, vestibular field potentials, hemodynamics of the dorsolateral prefrontal cortex and excessive delta wave activity were also seen. The studies reviewed had several methodological limitations including small, heterogenous samples and varied intervention protocols, limiting generalisability. Further research is required to understand the context in which neuromodulation may be beneficial. Conclusions: While these positive effects are observed, limitations included unequal representation of neuromodulation modalities in the literature, and lack of literature describing the efficacy of neuromodulation on the development or duration of persistent mTBI symptoms. Better clarity regarding neuromodulation efficacy could have a significant impact on mTBI patients, researchers, clinicians, and policy makers, facilitating a more productive post-mTBI population. Despite the limitations, the literature indicates that neuromodulation warrants further investigation. PROSPERO registration number: CRD42020161279.
... The arguments around this are due to disparities in techniques between laboratories as well as post-processing of data producing different interpretations based upon the algorithms employed (Nuwer 1997). Despite progress in a number of areas of research, including qEEG for concussion and post-concussion syndrome (Duff 2004), there is continued debate about the diagnostic validity of qEEG, and it is suggested that further studies are required to corroborate and refine data collection and post-processing methods (Haneef et al. 2013). ...
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The aim of this chapter is to provide an overview of the non-invasive techniques that are used to assess neurophysiological function in humans during exercise.
... Fortunately, other noninvasive imaging modalities that lie outside the traditional standard-ofcare (for persons not diagnosed as concussed) may also reveal measurable changes in brain health with HAE exposure. Quantitative EEG (QEEG), which is more portable and affordable than MRI, has been extensively applied for detection of alterations in brain health, proving highly effective for detection of concussion (134)(135)(136)(137). However, limited effort has been directed at QEEG categorization of subjects who have been exposed to repetitive HAEs in the absence of symptoms, so there is yet little evidence whether QEEG provides a strong match to the gold standard currently represented by MRI. ...
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... The difficulty in assessing an individual with PCS highlights the need to develop reliable physiological biomarkers in quantifying underlying mechanisms contributing to PCS fatigue. Previous studies have reported on electrophysiological changes, using (EEG or qEEG) with PCS (Duff, 2004). However transcranial magnetic stimulation (TMS) is unique given the technique has the capacity to quantify corticomotor excitatory and intracortical inhibitory synaptic potentials, via motor evoked potentials (MEPs), driven by neurotransmitter activity, allowing for understanding of neurophysiological mechanisms in context with functional observation assessments (Hallett, 2000;Kobayashi and Pascual-Leone, 2003;. ...
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Concussion injury results in a rapid onset of transient neurological impairment that can resolve quickly, or sometimes evolve over time, but usually resolve within seven to ten days. However, a small but noticeable cohort (~10%) of individuals continue to experience persistent lingering effects, particularly fatigue, and recognized as post-concussion symptoms (PCS). This study explored neurophysiological mechanisms in people with persistent PCS. Studies involved using self-report post-concussion fatigue scale, transcranial magnetic stimulation (TMS) and somatosensory stimulation in those with diagnosed PCS (n=20; 36.1 ± 14.0 yr., 4 female; mean time post-concussion 15.4 ± 7.6 months) to fully recovered individuals (n=20; 33.8 ± 6.6 yr., 2 female; post-concussion 12.9 ± 6.6 months) and healthy controls (n=20; 37.7 ± 8.0 yr., 3 female). PCS participants demonstrated a significantly higher self-report fatigue (score: PCS - 20.2[95% CI 17.4-22.9], Recovered 6.2 [3.1-9.3], Control 2.75 [0.6-4.8]). PCS participants showed a worsening of reaction time (F2,57=4.214; p=0.020) and increased reaction time variability (F2,57=5.505; p=0.007). Somatosensory differences were observed for amplitude discrimination (F2,57=5.166; p=0.009), temporal order judgment (F2,57=4.606; p=0.014) and duration discrimination (F2,57=6.081; p=0.004). Increased intracortical inhibition in TMS single pulse suprathreshold stimulation (110%: F2,57=6.842; p=0.002; 130%: F2,57=4.900; p=0.011; 150%: F2,57=4.638; p=0.014; 170%: F2,57=9.845; p<0.001) and paired pulse protocols was also seen (SICI: F2,57=23.390; p<0.001, and LICI: F2,57=21.603; p<0.001). Using non-invasive stimulation techniques, this novel study showed increased cortical inhibition and compromised central information processing, suggesting neural mechanisms underpinning ongoing fatigue, allowing for potential clinical rehabilitation strategies.
... Treatment then was provided until symptoms were resolved, and the LCI returned to normal. In the absence of a baseline LCI, treatment was provided until symptoms were resolved, and the LCI stabilized at the lower level [1][2][3][4][5][6][7][8][9][10][11][12][13]. ...
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Panic disorder (PD) has been linked to abnormalities in information processing. However, only little evidence has been published for sensory gating in PD. Sensory gating describes the brain’s ability to exclude stimuli of low relevance from higher level information processing, thereby sustaining efficient cognitive processing. Deficits in sensory gating have been associated with various psychiatric conditions, most prominently schizophrenia. In this case-control event-related potential study, we tested 32 patients with PD and 39 healthy controls in a double click paradigm. Both groups were compared with regard to pre-attentive (P50), early-attentive (N100), and late-attentive (P200) sensory gating indices. Contrary to a hypothesized deficit, PD patients and healthy controls showed no differences in P50, N100 and P200 values. These results suggest that sensory gating seems to be functional across the pre-attentive, early-attentive, and late-attentive time span in this clinical population. Given this consistency across auditory sensory gating indices, further research aiming to clarify information processing deficits in PD should focus on other neurophysiological markers to investigate information processing deficits in PD (eg, P300, error-related negativity or mismatch negativity).
Article
Objective: To examine the effectiveness of EEG biofeedback in the treatment of chronic post-traumatic headache and cognitive dysfunction. Design: Patients were to receive at least 30 sessions of EEG biofeedback, with training to inhibit 4 to 7Hz theta activity and produce 15 to 18Hz beta activity. P-300 cognitive evoked potentials were to be done before and after treatment was complete, along with self-reports. Setting: This was considered a pilot study at an outpatient headache clinic. Patient Selection: Thirteen adult patients (nine female) with both post-traumatic headache and cognitive dysfunction of at least 6 months duration. All subjects had been injured in automobile accidents with loss of consciousness of less than 30 minutes. Main Outcome Measures: Follow-up P-300 cognitive evoked potentials measured for latency, amplitude, and topography. Self-report measures for post-traumatic headache and cognitive function using a before- and after-symptom list. Results: Only three patients completed all 30 treatment sessions. These patients all reported significant global improvement in headache and cognitive dysfunction. These cases are presented in detail. Two of these patients also showed improved P-300 latencies. Five patients showed some improvement and five reported no significant change near the 15-session mark and chose to discontinue (despite being advised there not be any change until 20 to 30 sessions). All patents reported improvement in anxiety, depression, and irritability. Conclusions: EEG biofeedback appears to be possibly effective for some individuals with post-traumatic headache and cognitive dysfunction. Methodological difficulties are discussed in using this treatment, some of which became apparent in this study.
Chapter
This chapter focuses on assessing and treating open head trauma, coma, and stroke using real time digital electroencephalogram EEG neurofeedback. The chapter is organized into separate sections devoted to the nature, diagnosis, and EEG neurofeedback treatment of head trauma, coma, and stroke. EEG is malleable in cases of open head injury, coma, and stroke. Real-time digital EEG feedback technological advances now enable permanent changes in the EEG pattern, often with improved neurological function and emotional well-being. The author considers two clinical factors to be of utmost importance in the field of neurofeedback: (1) practitioners of EEG neurofeedback need to be familiar with brain anatomy and physiology; and (2) they should always observe the raw EEG, whether analog or digital, and constantly view in real time the minute-by-minute voltage changes and the evolving EEG pattern during training.
Chapter
This chapter describes the clinical use of an alpha asymmetry NeuroFeedback Protocal in the treatment of mood disorders. The chapter states that the relationship between mood disorders and cortical asymmetry was first describedwhen it was observed that damage to the left frontal lobe results in symptoms of depression. A striking finding is that differences in frontal brain asymmetry discriminated populations of depressed and non-depressed subjects. Theories of emotion and anterior cerebral asymmetry led to an investigation of an alternative way to treat depression. It was learned that normal subjects can be trained to modify their brain waves by changing their frontal alpha asymmetry. The transition was made from the theoretical foundations and experimental studies to the practical applications when depressed persons were trained to change their frontal alpha asymmetry to resemble the asymmetry pattern found in non-depressed persons. Taking these factors into account, one feels that the crucial next step for research is to demonstrate that appropriate control cases do not improve clinically as much as cases given the specific asymmetry protocol do. Although the treatment proved successful, the patient was still depressed at the end of the neurotherapy sessions as measured by the MMPI-2 and the BDI. The novel approach to the treatment of depression is in its infancy. Based on initial findings, it seems that alpha asymmetry neurofeedback is a promising alternative adjunctive treatmentor mood disorders.