ADHD is a
pervasive lifelong disorder of great significance. It affects perhaps as high as 10
percent of the population depending on which review article one reads and how it's
classified and how it's characterized (Whalen & Henker, 1991). ADD/ADHD overlaps with
other disorders. Attention Deficit Disorder (ADD) comes in three forms,
inattentive,hyperactive and combined. Unfortunately it's been classified as Attention
Deficit/Hyperactivity Disorder (ADHD) but in the new 1994 DSM-IV ADD and ADHD are
classified more separately and there are even different subtypes. The term hyperkinesis,
an older term which is still used represents Attention Deficit with hyperactivity. The
overlap of both ADD & ADHD is as high as 70% with specific learning disabilities (LD)
(Hynd, Marshall & Gonzales, 1991). There are over 250 different kinds of LD (Hooper
& Willis, 1989). Also in many individuals ADD/ADHD and LD overlap with conduct
problems (Barkley, 1990). The Attention Deficit Disorder without hyperactivity is
sometimes referred to as ADD-, to use Barkley's (1990) classification, and it tends to
overlap more with anxiety disorders as well as learning disabilities. The Attention
Deficit Disorder with hyperactivity, ADD+, also overlaps with learning disabilities but it
is also more concurrent with oppositional defiant disorder (ODD).
ODD is diagnosed behaviorally when the individual, often a child, purposely does not
follow rules, does not see the significance of them and therefore doesn't believe they are
important. If this is not corrected or treated, it can evolve into a conduct disorder.
Conduct disorder is more severe and more premeditative and even has more purposeful
destructive behavior than the ODD. If the conduct disorder is not brought under control,
especially in late adolescence and early adulthood, it can evolve into a much more serious
disorder known as antisocial personality disorder. Many individuals who have antisocial
personality disorder spend part of their time in prison and some with conduct disorder do
also, but when there is only oppositional defiant disorder, they usually have not reached
that point in the legal system. There is a great deal of overlap of this whole
constellation with some other disorders such as depression and anxiety Some ADD/ADHD
children have movement or tic disorders ranging from benign tic disorders to the more
severe Tourette's Syndrome. Occasionally they may have seizure disorders and there is a
higher incidence of substance abuse in the ADD and ADHD population than in the non-ADD/HD
population.
There is evidence, from Kenneth Blum and colleagues (Noble, Blum, et al., 1991) that
there is a strong genetic component in this whole constellation of problems located on
chromosome 11. They've identified the series of alleles that are associated with and ADHD
that lie close to another set that are associated with alcoholism, depression, and
Tourette's Syndrome. Blum has designated a constellation of these disorders as the
"reward deficiency syndrome ". This may be one of the reasons why these
disorders sometimes occur together. He also postulated that many of the addictive
behaviors including gambling, and risk taking are symptoms of reward seeking. In ADD/HD
the reward valence of stimuli habituates rapidly. We find in our evaluation of children
with ADD/HD that it's very common to be able to follow it back one to three generations in
the family. In doing an intake evaluation, one should ask to what extent the disorder is
seen in other family members particularly in males since it is between 3 and 5 times as
common in males as in females (Lubar, 1990).
There are some considerations about criteria for ADD/HD listed in DSM IV (1994) that
require elaboration. The main deficit as far as behavior is concerned is difficulty in
task completion, particularly if the task is perceived by the child, adolescent or even
adult as irrelevant for them. So, for example, if you tell the child, I want you to go
home and do the 50 math problems on page 100, the child will probably not get the work
done. A common excuse is "there is no homework tonight" or "I lost the
assignment on the way home", or if the assignment is brought home, there'll be a
pitched battle between the child and parents over each math problem. The child will plead
"I want to go out and play", "I want to watch TV." The parent may say,
"If you do the next problem, I'll give you a nickel, if you don't do the next one,
I'll send you to your room." This kind of behavior goes on and on and then the
assignment may get done, very sloppily and then the next day, it doesn't get turned in.
The child either doesn't return it, destroys it, or loses it.
Consider this scenario: The mother is called into the principal's office because the
child is not getting the assignments done and the principal says "your child has
attention deficit disorder" and the parent says "that's not possible. My child
will come home and sit in front of a TV set for 4 hours, play Nintendo or play in the
arcade with his friends for hours without stopping. He also likes to build models all the
time, beautiful models, and does it very meticulously, how can you say my child has an
attention deficit disorder?" The answer is that attention deficit disorder is
extremely selective, it is not global. ADD children are not necessarily distractible, they
are only distractible for something that they don't see the point in doing. This is only
one aspect of ADD/HD behavior, the other is that in regard to the child's life space, the
child is living now, everything is right this minute. If you say to the child, "now
look, you've got to get this homework done, you have an exam this week, if you don't get
these problems done, you're going to have difficulty getting through the exam." The
typical response is "oh that exam isn't till Friday, why do I have to do it today,
Monday? I'll do it Thursday night." The child does not process the consequences of
behavior. These are some of the aspects of ADD/HD that are not really well pointed out in
the current DSM-IV.
ASSESSMENT
Common tools used to determine diagnoses and comorbidities include extensive
interviewing and family history, medical history, and, in some cases, detailed medical
workups involving EEG, neurological scanning (MRI or PET) techniques, bloodwork, and
sometimes, genetic studies. Psychodiagnostic tools such as the MMPI and metrics designed
specifically for children can be useful as part of the assessment of possible thought and
affective disorders.
Neuropsychological measures are particularly useful for assessing organic brain
dysfunction and Specific Learning Disabilities. These techniques include but are not
limited to the Halstead-Reitan battery, Luria Neuropsychological battery, Wechsler
Intelligence Scale for Children (WISC-R) or WISC-III) or the Wechsler Adult Intelligence
Scale-R (WAIS-R), Woodcock Johnson Psychoeducational Evaluation-Revised (WJ-R), and other
Neuropsychological and achievement measures.
For the behavioral-observational assessment of ADD and ADHD, there are excellent rating
scales available. These include Barkley (1987) Conners' Parent and Teacher Questionnaire
(Conners 1969), Hawthorne, Achenbach Child Behavior Checklist, the Child
Activity/Attention Profile of Edelbrock, Home and School Situation Questionnaire, and
others in development. Many of these are checklists filled out by parents or teachers and
often include items based on the DSM categorization of ADHD, One should employ the same
checklist before and after an intervention to determine the extent that an intervention
has affected the behaviors described.
The selection of treatments that have been used as standard are the stimulant
medications more for children who have Attention Deficit with hyperactivity. For example,
the use of amphetamine sulfate (Benzedrine) was first prescribed by Bradley in 1937. These
are sometimes supplemented by tricyclic antidepressants, alpha blockers and in rare cases,
anti-psychotic medications. There are no medications for children with only learning
disabilities, such as dyslexia, dysgraphia, dyscalculia, receptive disorders or expressive
disorders not in the constellation of ADD or ADHD.
Two main hypotheses have been developed to explain how stimulants may be useful to
these children.
A) the low arousal hypothesis of Satterfield and Dawson (1971) and further elaborated
by Satterfield, Lesser, Saul and Cantwell (1973).
B) the Noradrenergic Hypothesis developed over years and elaborated by Zametkin et al.
(1990)
Basically, the two hypotheses propose that children with ADHD experience low arousal.
This low arousal comes about as the result of decreased impact of sensory stimuli in all
modalities, acting upon the central nervous system mechanisms for sensory integration and
resulting in the child engaging in stimulus seeking behavior. Self-stimulation and object
play are primary features of the hyperactive (hyperkinetic) syndrome (Lubar and Shouse,
1976; Lubar and Shouse, 1977 and Shouse and Lubar, 1978.) Children with hyperactivity
often exhibit intense but brief interest in new stimuli., rubbing objects against their
bodies, smelling them, tasting them if they can. They often engage in other
stimulus-seeking behaviors, including excessive movement, picking up one object after
another and then examining it, spinning around, running from place to place within a room.
If in a room with minimal stimulation, they will often fall asleep after a short flurry of
activity.
This stimulation-seeking behavior may be based upon decreased noradrenergic activity,
particularly in the brainstem reticular formation and possibly in the basal ganglia as
well. Heilman et al., (1991) proposed that in many of these individuals, both adults and
children with this disorder, a defect in response inhibition and particularly in the
nigro-striatal frontal system exists, more on the right side of the brain than the left
side. Motor restlessness may reflect not only frontal lobe dysfunction but also possible
impairment of the dopaminergic system as well. However, Malone. et. al.(1994) proposed
dual neurochemical mechanism which is somewhat different in that they view ADHD related to
increased presynaptic release of norepinephrine particularly for the right hemisphere and
decreased left hemispheric dopaminergic transmission. They further postulate that
methylphenidate acts to increase the dopamine available and to inhibit the release of the
excessive norepinephrine. The dual effect of the medication is to decrease the
overstimulation due to the norepinephrine and to increase attention which is mediated by
the dopamine system.
We also think of arousal 1) Mediated by connections from the brainstem reticular
formation, which receives inputs from all the sensory modalities except olfaction 2) the
transmission of this information to the diffuse thalamic (reticular) projection system,
and 3) the basal forebrain. These input systems, in conjunction with the basal ganglia and
the cerebellum, which is involved in programming the output of the motor cortex, are all
affected by decreased noradrenergic activity. Norepinephrine is produced by a very
important brainstem nucleus, the locus coerulus. This nucleus has extensive projections
with these mesiolimbic-striatal and forebrain systems. The neuroanatomy of these systems
is not only complex, but the resulting neurochemical dysfunctions and/or neuropathology
associated with them is also quite complex. The latter include both movement and affective
disorders. As will be discussed later, these neurochemical and neurophysiological
abnormalities are reflected in EEG measures, in regional brain metabolism, and
event-related potential measures for individuals with ADD/HD.
The other common treatments for ADD/HD are behavior therapy using complex schedules of
punishments and rewards, (Barkley, 1990, ) cognitive behavior therapy, , individual
psychotherapy and family systems therapy. Regardless of what treatment is employed,
whether it's neurofeedback, behavior therapy, drug therapy, and all the possible
combinations with and without family and psychotherapy, there is one sad reality, ADD and
ADHD are not curable at this point in time. That doesn't mean however, that they can't be
dealt with. Diabetes is not curable but one can become asymptomatic with proper
management, live a normal long life and not suffer any significant consequences, if the
diabetes is not too severe. There are many other disorders that can be treated to the
level of becoming asymptomatic. The hope for ADD and ADHD is that one can experience long
symptom-free periods and maybe permanently become relatively asymptomatic, except under
extreme conditions of demand or stress. But for the present it appears that ADD/HD is a
pervasive, lifelong, neurophysiologically based disorder.
The disorder of ADD/HD manifests itself in the form of poor educational achievements,
inappropriate emotional behavior, and all of the problems seen in terms of compliance,
academics, etc., but the problem is not a primary emotional disorder, an educational
disorder, nor a behavioral disorder; it is neurophysiological. This means that ADD/HD is
reflected in the way in which the child, adolescent or adult is processing information.
The way in which his or her brain is processing input is affecting the way the individual
perceives the world and therefore responds to it. This disorder also involves a decrement
in motivation or persistence of effort to be able to complete tasks which are perceived as
boring, irrelevant or to difficult. Our point of view in working with this disorder is
that if we can change the underlying neurophysiology, perhaps we can effect a more long
term change in this disorder. This is the reason why behavior therapy has not been
particularly successful. It works very well while it's being done. You can set up complex
schedules of time outs, and reinforcements for behaviors and you say to the child,
"Okay, you have 25 long division problems, if you get them done, we're going to go
out to your favorite restaurant for dinner." Half an hour later, they're done
perfectly. The next night, "I'm not going to do the homework." What is the
parent going to do now? There is very little carryover of the seemingly potent reward. The
hope is that if you continue to do the behavior therapy, from age 6 to somewhere around
age 16, finally the message will get through and the child will develop insight as an
adolescent and will be able to self-integrate the task-appropriate behaviors without
continuous reinforcement or punishment. But very often, that's not the case.
Stimulant Medications & Guidelines
The stimulant medications are powerful for many children with hyperactivity, and 60 to
70% of children on medication show a very marked improvement of the hyperkinetic component
of the syndrome and may perform better educationally. Currently, three primary stimulants
are used in attempting to restore neurochimical balance. Dextroamphetamine is commonly
used in younger children. Methylphenidate (Ritalin) and pemoline (Cylert) are commonly
used with children from six on into adolescence and even adulthood. Adults and children
who have extreme difficulty with organizational and planning skills or impulsive behavior
may respond positively to small amounts of tricyclic antidepressants such as imipramine or
norpramine. Imipramine has more side effects than norpramine. For some children, when
impulsive behavior also becomes very aggressive, clonidine, an alpha adrenergic blocker,
is sometimes helpful. Between 60 and eighty percent of children with ADHD show varying
degrees of positive response to these medications when they are administered properly. In
the ideal response cases, the child no longer exhibits all components of hyperactivity nor
any great attention problems. Patients who have this ideal response can stay on their
medication regimens for extended lengths of time without any significant adverse side
effects. Other patients respond partially to the medications and may exhibit a variety of
side effects, including anorexia, mood changes and varying degrees of sleep disturbance.
Ritalin sometimes produces an almost totally flattened affective response in some
children, and they are described as "zombie-like" by parents or others who know
the child. This kind of response would warrant a change in medication or a non-medication
alternative. .
The twenty-five percent of children who do not respond to medications are usually not
good candidates for neurofeedback, though there are exceptions, particularly children who
had allergic, toxic or medical reactions to the medications. Of the twenty to twenty-five
percent of children who do not respond to medications well, there are a number of possible
reasons:
1) serious side effects, such as gastrointestinal disturbances, 2) urinary problems ,
3) seizure activity, 4) headaches, 5) increased tic activity ( particularly a possible
problem with Ritalin), or , 6) unacceptable changes in affect and emotional behavior .
One of the main problems with stimulant medications is that as soon as the medication
is out of the system, the ADD/HD behaviors return. If one is using a very short term
medication such as methylphenidate or Ritalin, the poor behaviors will reappear within 3
to 6 hours after the last dose is given. Then you have to give the drug in the morning,
again at noon, and maybe another small dose in the afternoon just to get through the
homework. Use of a time-release form is one solution to this, but this is not always as
effective as separate doses. If you don't give the medication during weekends, or on
vacation, ADD/HD behaviors return. Parents often despair in taking their hyperactive
children on vacation because they say they are unmanageable. Some of the experts in the
field such as Wender (1985) believe that it doesn't matter if they're 8 or 80 years old,
you keep them on medication all the time every single day, even during vacation periods.
Since the disorder is not curable, the idea is to alter the distribution of
neurotransmitters in the brain and maintain the appropriate behaviors pharmacologically.
Unfortunately, pharmacologic treatments do not seem to have a long term carryover. If
you've had a child on Ritalin for 10 years, and you try to phase the child off you may
find that the behaviors will continue to be maintained for approximately 3 months and then
the child starts to go downhill and then maybe you have to put the patient back on
medication (Whalen & Henker, 1991).
The other fallacy that was in the older literature is if the child has hyperkinesis or
is hyperactive, if you don't do anything, it will go away (Swanson & Kinsbourne,
1979). What will happen in many cases is that the hyperactivity does decrease, but the
attention deficit becomes worse and so then you have an adolescent or a young adult who
has ADD+ characteristics. They start failing their courses in high school, or they get
thrown out of school. They can't go to college or during college, they can't get through
and have to leave. If they get a job, they very often get fired because they don't meet
the employment demands, or they get in power struggles with peers or superiors. I've had
ADD adults who come in and talk about their marital situation saying, "I've been
married 4 times," and then I ask, "Do you have an idea of what some of the
problems may have been that caused this to happen? They'll say "Yes, I got bored with
the relationship, it wasn't interesting anymore. I found somebody else." Their
ability to stay in any particular setting is very difficult. They will often go from job
to job, from location to location, sometimes from marriage to marriage, exemplifying the
aspects of this pervasive disorder. Sometimes children with ADD\HD will perform well up to
about grade 3 or 4, if they're very bright, and then they will become worse and worse
until eventually they just can't make it as the demands of school become greater.
Subtypes of Individuals with Attention Deficit/Hyperactivity Disorder
Children and adults with ADHD often experience comorbid difficulties including
Oppositional Defiant Disorder, Conduct Disorder, Anxiety Disorder, substance abuse,
depression, and in some cases, tic or movement disorder. To further complicate matters,
between 50 and 70 percent of children with ADHD also experience learning disabilities.
Barkley (1990) has already pointed out that children with ADHD may experience primary
difficulties in terms of attention, impulse control or impulsiveness or hyperactivity. He
has also pointed out that ADHD usually can be diagnosed before the age of 7 and is
sometimes also associated with distractibility, poor planning, poor rule following
behavior, and inability to engage in sustained activities for any significant period of
time. Whereas some individuals are described as hyperactive, others are described as
hypoactive or lethargic, easily bored, disinterested in most play activities and extremely
disinterested in school-related activities. Children who have specific learning
disabilities, may also be classified in terms of specific areas of disability such as
subtypes of reading disability. Flynn and Deering (1989) and Flynn, Deering, Goldstein,
and Rahbar (1992) have described two subtypes of dyslexics-- , diseidetic and disphonetic.
The differentiation is based on a classification by Boder. The question arises whether the
different subtypes of ADHD with or without learning disabilities, conduct disorder,
oppositional defiant disorder, depression, etc., can also be characterized as somewhat
neurologically distinct and if they are neurophysiologically distinct, it is important to
tailor the Neurofeedback treatment for the neurophysiology that is presented by these
different subtypes.
Recently Amen, Paldi, Thisted (1993) have been evaluating ADD using brain SPECT imaging
(single proton emission cerebral tomography). SPECT scan is a technique similar to a PET
(positron emission tomography) scan. SPECT scan measures cerebral blood flow and
indirectly brain metabolism and has the advantage that it involves less radiation than PET
scan, is less expensive, and allows for a longer data collection period while the tracer
is being distributed through the nervous system. There appears to be a high correspondence
between the findings reported by our group using quantitative EEG and topographic brain
mapping and the SPECT scan findings. Both the quantitative EEG and the SPECT scan findings
indicate that for the most part ADD/HD is a disorder which involves deactivation of the
prefrontal lobes (reduced blood flow,) particularly during an intellectual or academic
stress task. In other words, the more the child tries to concentrate, the poorer they
perform on academic tasks and the more they show slowing or decreased cortical metabolism
particularly in frontal and central areas. One of the advantages of SPECT and PET scan
over EEG is that they allow us to examine what is happening in subcortical structures as
well as changes in the cortical surface in terms of blood flow and cortical activity. The
Amen et al. study of 54 children who met the DSM-III-R criteria for ADHD were compared
with 18 controls. Their work then identified the following subtypes:
(1) frontal lobe deactivation without other findings: This is the more classic ADHD
individual who responds best to stimulant medication if pharmacotherapy is the treatment
chosen. These individuals show marked decreased frontal lobe metabolism, particularly
during academic tasks as compared with a resting eyes open baseline. EEG studies show
excessive slow activity .
(2) A second subtype is represented by temporal lobe dysfunction. These individuals
will often have deep temporal lobe dysrhythmias or epileptiform activity, and still
experience an Attention Deficit Disorder which seems to respond best to anticonvulsants
sometimes combined with Ritalin if pharmacotherapy is chosen.
(3) A third subtype is ADHD with homogeneous cortical suppression. These individuals
tend to respond to antidepressants in combination with Ritalin. The main difference
between this subtype and the first subtype is that individuals with this type of disorder
have more widespread cortical deactivation than the stimulant responders alone. Very often
these individuals will respond well to tricyclics such as Desipramine or Norpramine.
(4) A fourth subtype are individuals who actually have increased activity in the
anterior medial aspects of the frontal lobes. This refers to an anatomical region known as
gyrus rectus or the region which lies in front of the septal region. These individuals are
also hyperactive, distractible and restless. This pattern is also associated with
Obsessive-Compulsive Disorder and overfocusing to the point of being unable to complete a
variety of tasks hence experiencing a type of attention deficit in which there is an
inability to shift attention and excessive overattending to often irrelevant details.
(5) There is a fifth subtype which is characterized as ADHD with hypofrontality at rest
but normal frontal activity with the challenge of intellectual stress. These individuals
are also distractible, impulsive and restless but there are also extremes of more
oppositional-defiant behavior than some of the other subtypes. They also tend to respond
well to methylphenidate (Ritalin).
Overall, the Amen et al. study found that in 87% of the cases, there is prefrontal lobe
deactivation with intellectual stress (65%) or decreased activity in the prefrontal lobe
at rest (22%). In our own work with quantitative EEG, we have some preliminary evidence
that suggests that individuals that show more slowing in the right prefrontal lobes
experience difficulties with impulse control and often act inappropriately in social
situations but show good organizational skills. Children with left prefrontal lobe slowing
tend to have poor organizational skills but are more appropriate in social settings and
children with right posterior parietal slowing tend to be of the lethargic, hypoactive
category and often complain that everything is "boring".
In a more recent study by Henriques & Davidson (1991), it has been shown that
individuals experiencing reactive or monopolar depression have more left frontal alpha
than right frontal alpha activity whereas nondepressed individuals tend to have more right
frontal alpha activity than left frontal alpha activity. The overlap of hypofrontality in
terms of theta activity and perhaps excessive left frontal alpha activity might represent
a type of individual who experiences ADHD and depression as well. To make matters a little
more complicated, it is well known from the research of Peniston and Kulkosky (1989) that
many individuals experiencing alcohol addiction and certain other types of chemical
dependency experience increased beta activity and decreased alpha and theta activity. This
pattern was shown originally by the work of John et al. (1988).
One final point regarding the neurology of ADD\HD and associated disorders is that many
of the executive functions including planning, judgment, appropriateness of behavior in
social settings, is mediated not only by the prefrontal cortex but by the frontal pole and
the area underneath the frontal pole known as the orbitalfrontal cortex. The
orbitalfrontal cortex has extensive projections to the amygdaloid complex and other
structures within the limbic system which have been known for nearly a century to strongly
mediate emotion and motivational states. The orbitalfrontal cortex is one of the
organizing cortical areas for the control of emotional behavior through the limbic system
and ultimately through the output systems of the autonomic and skeletal motor pathways. It
is most unfortunate that we cannot reach this area of the brain in terms of neurofeedback
strategies. The orbitalfrontal cortex is for all practical purposes inaccessible via
surface EEG; however, it is a region of the brain which is very sensitive to medication
effects and perhaps individuals in which SPECT and PET scans show abnormalities in this
region are really better candidates for pharmacotherapy than a neurofeedback approach. In
contrast, those patients that show excessive EEG dysfunction in the superior frontal
cortex or the midline central cortex are much better candidates for neurofeedback
interventions which can train individuals to produce more optimal patterns of EEG
activity.
The Neurophysiological Hypothesis underlying the Neurofeedback Model
If ADD/HD are associated with neurophysiological dysfunction, particularly at the
cortical level and primarily involving prefrontal lobe function, and if the underlying
neurophysiological deficit can be corrected, the child with ADD/HD may be able to develop
strategies and insights (paradigms)
which non affected individuals already possess. Using these paradigms, the ability to
organize, plan and understand the consequences of inappropriate behavior is facilitated.
This results in a stronger carry over of the effectiveness of time-outs, rewards and other
behavioral approaches. Medication needs may actually decrease if by changing cortical
functioning we can also show a change in brainstem functioning, such as brainstem or
cortical event related potentials or measures of sensory integration. The long term
effects of Neurofeedback have already been documented (Tansey, 1990; Lubar, 1991,Lubar
1995).
In conclusion, this technique, which leads to normalization of behavior, can lead to
normalization of neurophysiological dysfunctional behavior in the ADHD child, and can
produce long term consequences
in social integration, academic achievement and over-all life adjustment.
A Rationale For Neurofeedback
A primary problem the ADD/HD individual experiences is difficulty completing long,
repetitive tasks which are perceived as boring. This includes much of the activity which
occurs in the school setting, including homework. Another characteristic is difficulty
accepting that socially appropriate behavior is governed by rules and rule-following
behavior are essential to progress through the developmental milestones needed to become a
fully functional adult. Individuals who cannot follow these rules may ultimate develop
Oppositional Defiant Disorders, Conduct Disorders , or in the worst cases, Antisocial
Personality Disorders. Not all ADD/HD children are inevitably on this pathway as a
consequence of their behaviors, but there is a higher incidence of these problems
particularly in the ADHD population. Poor motivation and rapid habituation to the reward
properties of stimuli are additional common characteristic of the ADD/HD population. For
that reason. toys and play activities do not remain interesting for very long for these
children. Thrill-seeking behavior is sometimes also seen in ADHD adolescents.
Stimulant medications such as Ritalin (methylphenidate) , Cylert (pemoline) or
Dexedrine (amphetamine sulfate) are primarily used to increase arousal or the impact of
stimulation. However, there is very little clear evidence that these medications,
particularly Ritalin, change cortical function.(Swartwood,1994). Parents commonly complain
that the child, even with the medication, does better in school, concentrates better, is
less hyperactive, but still has trouble getting work done, still has difficulty following
the rules and understanding why, when they act inappropriately, that the behaviors have to
be corrected. These latter problems are caused because of altered cognitive functioning
and to a great extent, problems with frontal lobe functioning. The frontal lobes, as
discussed previously, are the executive portions of the brain and they have decreased
metabolism in ADD adults and probably in ADD children, plus decreased fast EEG activity
and excessive slow wave activity. With Neurofeedback we are attempting to change cortical
functioning as well as arousal functions. We attempt to establish a cortical EEG signature
template which responds similarly to that of non-ADD/HD individual in the situations and
circumstances which cause problems for ADD/HD adults, adolescents and children. Many
neurofeedback trainers, report that once neurofeedback is implemented with this
population, when they misbehave and the behavior is pointed out to them, they can readily
move to correct it and they don't repeat the inappropriate behavior as much once they
understand why the behavior was not acceptable. Essentially, ADD/HD children trained with
neurofeedback often experience long-term transfer of training to home and school settings
because they begin to cortically function more like non-ADD individuals in that
rule-following behavior increases, inappropriate social behaviors decrease, impulsiveness
decreases, and motivation levels improve. Our own earliest studies in the 1970s
showed the carry over of effects into school settings (Lubar and Shouse, 1977).
Quantitative EEG, Brain Mapping and Electrode Placement
A question raised by the literature on QEEG is whether one needs an extensive
neurological assessment before neurofeedback training or is brain mapping sufficient? In
our work, we are basing our electrode placements on studies of blood flow and imaging. We
have placed most of our electrodes bilaterally, halfway between CZ and FZ (FCZ), and
halfway between CZ and PZ (CPZ). The reason for using these particular placements is that
based on 19 channel topographic brain mapping, these locations represent the areas where
the highest ratios of theta to beta activity are seen which we believe, at this time, to
be the most relevant neurophysiological correlate especially for ADD. The success rate
with this particular set of placements has been found to be very high by our group and
many others who are using this protocol for training and because the signal has less
artifact there. I wish to encourage both clinicians and researchers to consider other
sites based on the individual neurophysiology that is presented and to do the training
either with bipolar or referential electrode placements over those sites where EEG
assessments indicate that abnormal activity is more focal and particularly if it is not
along the midline. If the greatest amount of dysfunction is in the orbital frontal cortex,
the best locations for recording this activity would be FP1 and FP2; however, eye roll and
blink and frontal EMG artifacts make these sites virtually impossible to use. If one were
treating depression, perhaps placing electrodes at either F3 and F4 or C3 and C4 or some
intermediate point between F3 and C3, and F4 and C4 would be acceptable in terms of
changing alpha ratios between left and right hemispheres. These same locations utilizing a
combination of feedback to change alpha distribution and to decrease the amount of theta
activity and increase the amount of beta activity might be ideal for working with ADD/HD
individuals who also are depressed This protocol might be the analog for individuals who
are placed on a combination of stimulants and tricyclic antidepressants. Individuals who
show the slow lethargic pattern which is sometimes localized on the right posterior
parietal region around P4 might be trained in that location with electrodes perhaps at C4,
P4, the bipolar placement or to change the ratio of theta-beta activity in the right
parietal region with respect to the left parietal region in order to equalize distribution
of this activity between the two hemispheres. Individuals with significant hyperactivity
would benefit considerably from training the sensorimotor rhythm (SMR) with bipolar
placements at C1-C5, or referential placement at C3 with linked ear references. This
should be done for 20-30 sessions before using the midline placements for theta-beta
training to increase attention, focusing and executive functions. The combination of SMR
and theta-beta training may take as long as 40-60 sessions but the long term results are
well worth the effort.
One final point which is of relevance in regard to electrode placement is the question
of generalization. We have seen in more than a dozen cases in which training was carried
out along central cortex with electrode placements either at CZ, PZ or halfway between FZ,
CZ (FCZ) and halfway between CZ, PZ (CPZ) pre-post training changes in the theta-beta
ratios in all 19 standard electrode locations. Although the changes are greatest in the
central cortex, they can even be seen in occipital and temporal regions where small
improvements are noted. This indicates that even with a central location electrode
placement, the effects of the neurofeedback are experienced in widespread cortical areas.
The issue of whether there is generalization from locations off the midline to all other
locations is unknown at the present time and represents a researchable question. At the
present time, I do not recommend electrode placements that employ summation of activity
from multiple sites. The algebraic sum of EEG activity from multiple sites bears no
resemblance to the activity seen at each site individually and may result in
feedback which might be either irrelevant or perhaps even injurious.
Filter bandpass considerations
The question also arises as to which band passes are appropriate. We find that in
working with children, typically we'll reinforce increasing beta activity between 16 and
20 Hz. and decreasing theta activity between 4 and 8 Hz. This has worked for the majority
of patients. However, above the age of 14, we find that there are many individuals that
show excessive alpha activity and lack of alpha blocking. With these individuals we often
train to decrease activity between 6 and 10 Hz., high theta low alpha, and increase beta
activity between 16 and 22 Hz., 16 and 24 Hz., or even 18 and 24 to 26 Hz. These decisions
are based on spectral analyses to determine whether there are areas in which there is
decreased beta activity or increased alpha and/or theta activity during task specific
conditions. It is probably difficult to train activity above 28 Hz. with conventional
feedback systems because of the overlap of the EMG spectrum and the possibility of
training individuals to increase certain types of muscular activity in order to achieve
reinforcement for these higher frequencies.
The essential requirements for neurofeedback instrumentation include very accurate
signal processing with the ability to show changes of one tenth of a microvolt , for
threshold-setting purposes. Software should always allow the clinician or researcher to
observe the raw signal and how it is processed so as to produce reward or inhibition of
the signal and to observe the relationship between changes in events in the raw EEG and
the feedback. Excellent systems employ both analog and digital processing. Such systems
have been described in detail previously (Lubar and Culver, 1978 and Lubar, 1989).The
absolute requirement of seeing the raw signal and exactly how it is processed and what in
the raw signal activates the reward and inhibits is paramount for fine tuning of the
protocol in terms of the duration, amplitude, and frequency of the relevant signals. The
displays should be so complete that one could use a signal generator with a 0.1uv
sensitive voltage divider to evaluate the accuracy and response time of the system.
Without this type of display there is no way other that blind faith to know if your
feedback device is providing accurate analysis of the raw signal and appropriate feedback.
Regulatory agencies and third party payers have the right and power to demand
accountability in this regard.
Activities During Training Sessions
The neurofeedback trainer must simultaneously meet specific physiological criteria.
These include: 1) increase either sensorimotor rhythm (SMR) between 12 and 15 Hz
(especially if hyperactive) or 2) beta activity, often defined as 16-20 Hz, while at the
same time, not producing theta, movement or EMG activity. The goal is to increase the SMR
or Beta activity, duration , prevalence and, if possible, amplitude, while simultaneously
decreasing the amplitude and percentage of theta and gross movement, as detected by EMG
activity. The subject or patient has to be very alert, but also relaxed and quiet to do
this.
Staying on task, often documented by poor performance on continuous performance tests
such as the Gordon Diagnostic system or the TOVA (Test of Variables of Attention,) is one
of the main problems of children and adults with ADD/HD. ADD/HD children are able to play
Nintendo or computer type games for long periods of time because the games change the
demands to new tasks every few seconds. But there is no significant transfer to homework
or other situations which are long, continuous, repetitive and/or boring, such as school
related tasks. Neurofeedback essentially involves engagement in a continuous performance
type task under an altered EEG state which is like a non ADD person's EEG for significant
periods. Training the children this way. to stay on task for extended time periods, in the
"normalized EEG state seems to work, enabling transfer of the skill to situations
away from the neurofeedback setting.
Recording EEG and Artifact Considerations
Recording EEG through the human scalp is not an easy task in one respect. Electrodes
are placed on the scalp, and so they are recording activity from the skin, such as skin
potential changes or electrodermal activity, then underneath the skin, there are several
layers of muscle producing EMG. Next you have to record through bone, hence there is
further attenuation of the EEG, especially the higher frequency components. As a result,
what we are struggling with primarily are non-EEG artifacts. There is EMG artifact, which
is part of the signal, starting from as low as 12 Hz. and ranging to greater than 500 Hz.,
although most of the EMG spectrum is between about 30 and 150 Hz. This is why a lot of EMG
machines for both EMG recording and feedback will have a frequency range of 30 to 150 Hz.
The other thing that we are concerned about is EKG, electrocardiogram, because this is a
very powerful artifact that is often seen in the EEG. The EKG artifact is more prevalent
as we get older because the EEG amplitude becomes smaller. EKG is occurring from the
electrodes that are picking up activity from underlying pulsating blood vessels in the
scalp. The reason EEG becomes smaller as we get older is because the skull becomes thicker
as do the meninges and the connective tissues between the skull and the scalp, and the
skin layers. Also, the amplitude of neurological activity decreases.
Trying to get a perfect multichannel recording of 19 or even 32 channels becomes very
difficult in adults. One might think children are going to be very difficult to record
from but I've obtained some of the most ideal recordings from children because their EEG
signal is so large that these artifacts are less of a problem. If you're recording from
frontal locations in addition to these others you also pick up ocular artifacts, blinks,
and electroretinal activity. If you examine the EEG, you sometimes see these large
excursions, that look like slow wave activity, however, it's often simply an eye roll. Eye
movements and blinks are in the delta range from 0 to 4 Hz.; but they're seen in the
anterior half of the scalp. If recording from any leads from the lateral surface,
temporal, lateral frontal, parietal, posterior, specifically F3, T3, T5,P3,F4,T4,T6,P4,
invariably we pick up muscle activity from the masseter muscles, temporalis and with every
swallow. Every time that happens, even to a small degree, we get a burst of very fast
artifact activity which appears in the EEG that can create problems in terms of signal
processing, sometimes leading to feedback for non-EEG activity. If you record from the
posterior half of the scalp, then we pick up EMG activity, from the occipitalis,
trapezius, and supraspinal muscles.
The question is how do you get "clean" EEG from an individual? We spend a lot
of time, especially if we're going to do quantitative topographic brain mapping, trying to
clean up all these signal problems, with relaxation, or through positioning of the head.
Sometimes you have to hold the head of the individual or use pillows to stabilize their
head, so that you can minimize these artifacts. If you record from the central locations
along the midline, such as FZ, CZ, or PZ, then you can get relatively pure EEG.
We have chosen a particular set of locations for training with our ADD and ADHD
population which are far less prone to artifact. One location is halfway between CZ and
FZ, and the other location is halfway between CZ and PZ. These two points represent the
two locations on the head where there is less EEG to artifact than anywhere else.
Referential Versus Bipolar Recording For Training
Another point relative to feedback is an unresolved issue, concerning the difference
between what is called referential or monopolar recording and bipolar. When you employ
referential recording, what you're asking is what is the activity at a particular point on
the head as compared with some point that is electrically neutral? The way we usually do
this is to place a reference electrode on each ear lobe. Essentially you are examining the
relationship between activity at CZ or some other point while making the assumption that
the ears are neutral or act as a ground so any activity we see in that EEG recording,
represents the activity at that point. This approach is good in terms of knowing what's
happening at each point and differentiating the activity at each point from any other
point. However, the energy is maximal right under the electrode and it decreases with the
square root of the distance from the electrode so that the activity surrounding CZ, the
central location falls rapidly as we move away from CZ. If we have a montage where we have
one electrode with ear references that we use for feedback, you have to realize that what
you're really going to be influencing is a limited area around the electrode and probably
activity occurring more than a centimeter from that electrode will have relatively little
effect. There is then the theoretical question of whether training at that one point can
have very much effect on behavior, although it is being done and some clinicians are
getting good results with that type of recording.
Since referential recording for feedback purposes is very prone to artifacts, another
alternative is bipolar recording. Bipolar recording depends upon the algebraic subtraction
of activity between two points. From an electrophysiological point of view or neurological
point of view, we don't know exactly what that means, yet nevertheless training that type
of activity seems to work very well for many different disorders. Bipolar recording has
two advantages: one is that we are actually influencing activity over a larger area and
that of course seems to be advantageous. Maybe it affects the spread of activity because
if we're looking at activity of apical dendrites in layer 1 of the cortex, since that
activity is linked to many cortical areas, it's going to have more of an influence on
other regions of the brain.
Another advantage of bipolar recording is that anything which is occurring in both
channels at exactly the same time the same amplitude and completely in phase is subtracted
out. This is called common mode rejection. If you clench your jaw, there will be a burst
of activity in temporal electrodes and if it occurs at the same time and in phase at both
electrode locations, much of this EMG will be subtracted out. Certainly EKG is a problem
when electrodes are placed over blood vessels in different scalp areas. EKG is usually
rejected or decreased as common mode activity. Eye rolls and eye blinks will also be
reduced. However, if one is interested in pure alpha conditioning and if you have your
electrodes at 01 and 02, the alpha which is in phase and coherent between these locations
would be factored out. So that's a consideration that might lead to the use of a monopolar
referential montage in alpha signal detection and neurofeedback training.
The concept of phase and coherence may be of considerable importance for what we are
trying to accomplish. Phase is measured in degrees of lead or lag between the signals of
the same frequency. For example if two 10 Hz sine waves rise and fall in each cycle at
exactly the same time then they are in phase and the phase angle between them is zero
degrees. If one wave reaches a maximum when the second wave reaches zero voltage then they
are out of phase by 90 degrees. If one wave reaches its maximum positive voltage when the
second wave reaches its minimum voltage then they are 180 degrees out of phase. Coherence
is a measure of the degree to which the phase angle between two waves of the some
frequency (not amplitude) remains constant over time, regardless of the phase angle
between the two waves. Coherence is similar to a correlation coefficient and in this sense
ranges from 0-1.0. If two waves of equal amplitude and frequency are recorded with a
bipolar electrode montage and these waves are in phase then the resultant amplitude will
be zero due to these being common mode signals. However if these two waves are 180 degrees
out of phase then the resultant amplitude will be twice that of each wave measured
separately. Since a considerable amount of neurofeedback concerns either increasing beta
or decreasing theta activity in conjunction with ADD/HD or teaching individuals to
increase alpha and theta activity for treatment of addictive behaviors (Peniston &
Kulkosky, 1987), it is important to determine whether bipolar or referential recording and
training is appropriate.
Figure 1 presents a scatter plot showing the relationship between the relationship of
theta to beta activity in 32 cases for both
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Insert Figure 1 About Here
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referential and bipolar recordings. Each individual represented in the figure had 3
electrodes placed on their cranium at CZ and halfway between FZ and CZ and halfway between
CZ and PZ. The bipolar and referential recording was done with the eyes open while the
individual was fixating on a photograph placed 24 inches in front of them. The photograph
was 2 X 4 inches in size and because of its size, produced minimal eye movement.
Referential recording was done first in half the subjects and then the bipolar recording,
each recording lasting for 90 seconds. The order was reversed in the other half of the
subjects.
The figure clearly shows that there is a strong linear equivalent relationship between
bipolar and referential theta-beta ratios. In other words, individuals tended to have
approximately the same theta-beta ratios whether the recording was done using the bipolar
montage or the referential montage. This has some very specific implications for
neurofeedback training. First, the study indicates that the amount of common mode
rejection in the bipolar recording is not of significance in that if there was
considerable rejection of common mode EEG signals, then the ratios for bipolar recording
should be very different from those for monopolar recording. The second implication is
that the decision as to whether to use a referential montage at CZ or bipolar montage with
electrodes placed halfway between FZ and CZ and halfway between CZ and PZ should be based
on the behavior of the individual. If we are working with a child who is very hyperactive,
then we would want to have common mode rejection of movement artifacts and EMG. In this
case bipolar recording would be preferable. If the individual is primarily ADD without
hyperactivity, then referential recording with an electrode placed at CZ could be used.
However, linked ear references must be employed. It is interesting that in the many groups
that are using the theta-beta paradigm for Attention Deficit Disorder, those employing
monopolar and bipolar recording montages are obtaining approximately equal results. If
using a bipolar montage, inter-electrode distance must be measured for every session and
should remain plus or minus 1 mm., since signal magnitude depends on inter-electrode
distance. Accurate electrode placement is essential if reliable conclusions about the
learning taking place are to be drawn.
Figure 2 shows the alpha-beta ratio relationships for referential and bipolar
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Insert Figure 2 About Here
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recordings with the eyes open. Notice there is also a linear relationship but there is
much more scatter. The reason for this is as follows: if for a particular individual with
a bipolar montage, the two signals are in phase, there will be considerable common mode
rejection. In that particular case, the referential ratio will be much higher than the
bipolar ratio. If the individual's alpha activity is out of phase a bipolar recording will
result in larger amplitudes of alpha activity and therefore the bipolar ratios will be
higher than the referential ratio. There are individuals on the graph who represent both
conditions. The decision then to use referential or bipolar recording in training a
decrease in alpha-beta ratios should be based on measures obtained both ways to determine
whether common mode rejection is of importance. And then, one should go with the greatest
ratio for a decrease and the lowest ratio to train for an increase.
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Insert Figure 3 About Here
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Figure 3 shows a different representation of this type of data. In this figure the
actual percent power of theta, alpha, and beta activity is represented for all subjects.
It can be clearly seen that there is virtually no difference between the actual amount of
theta and beta activity obtained with either montage. In the case of alpha, however, there
is greater alpha power obtained in the bipolar montage than in the referential montage.
This would tend to indicate that most alpha activity recorded along the midline between FZ
and PZ is out of phase leading to a greater amplitude in the bipolar recording condition.
Table 1 summarizes the relationships between a variety of bipolar and referential
measurements in terms of their correlation coefficients. Even though for some measurements
the correlation between referential and bipolar measurements may be as high as .9, it is
still important to employ both types of measurements in determining for a specific
individual whether training should be undertaken with referential or bipolar electrode
placements. One final point and that is that the data presented here is only valid for
central locations. New databases would have to be obtained with reasonable numbers of
subjects using both types of recording for any other locations on the cranium. Therefore,
decisions as to whether to record bipolar between locations 01 and 02 or referentially at
OZ or bipolar for locations F3 and F4 versus referential recording at FZ or similarly
recording between C3 and C4 as opposed to a referential recording at CZ is unknown at this
time and will await development of databases similar to the one shown here for the central
midline locations.
A third approach which hasn't been done systematically but it's theoretically possible
is instead of subtracting the activity from two electrodes, adding the activity. So for
example you might place an array of electrodes at F7, F8, C3, C4, and CZ, and train the
summated activity from all of these at the same time. From a theoretical point of view, we
do not know what is being recorded but the idea behind that kind of a montage is try to
train large areas of the brain at one time. A few people such as Fehmi (1980) and Tansey
(1991) use a 1 x 6 centimeter electrode soaked in saline. It is very difficult to assess
what is being added, or subtracted with such an electrode. Therefore regardless of what
type of recording you use, always observe the raw signal and how it is being processed for
feedback applications.
EEG Signal Processing: Analog Hardware Vs. FFT Software
How is EEG activity processed in order to produce feedback? There are actually several
techniques. When you use an active band-pass filter, what you do is to isolate the
particular frequencies that you're interested in. So, for example, if we are trying to
train activity between 16 and 20 Hz., and this is not rhythmic activity, it will be mixed
with other EEG frequencies. I can design a filter which oscillates so that activity in the
middle frequency which is 18 Hz. will maximally drive the filter output. The highest
output amplitude of this filter will be for activity between 16 and 20 Hz. Outside of that
range, the filter will be less active and will not significantly respond to EEG one octave
above or below the center frequency. Next we set an amplitude threshold in microvolts so
that as long as the activity detected by the filter is above that threshold, we will start
a sampling counter chip or circuit, e.g., counting at a certain rate, e.g., sampling at
128 times a second. Then when the criterion threshold is met, such that as long as the
filter output is above this threshold, for example, 7 microvolts, and we accumulate 50
samples in a 0.5 second period, feedback will be triggered. This type of signal processing
is very fast, especially for higher frequencies. With a careful choice of filter roll-off
(measured in decibels per octave) very rapid response without activation of the filter to
harmonics can be established. With a very accurately designed system of reward and inhibit
channels we can fine tune it to almost do a "pattern"analysis. This means that
one can observe a particular relatively sinusoidal pattern in the raw EEG for theta,alpha.
beta, smr, gamma etc. of a specific amplitude and duration and provide feedback whenever
that pattern or a close approximation to it occurs. If we really believe that specific
patterns are associated with different, learning, cognitive, or emotional states then we
need to employ systems with this capability.
Another technique is based on Fourier analysis,which is derived from a theorem that was
developed by Joseph Fourier in 1822. It states that you can take any complex wave form or
any periodic wave form in the frequency spectrum from 0 to many megahertz and decompose it
into a series of sine and cosine waves. If we calculate the period of all the sine and
cosine waves, take the inverse of their periods, we can calculate the frequency of all the
components in the complex wave form. This technique has been utilized by the music
industry where it is called additive synthesis. One type of synthesizer employs a large
number of sine wave and cosine wave oscillators at different frequencies, combine them
together into a very complex wave form, which simulates a flute, a clarinet, or a human
voice. The only disadvantage of Fourier analysis is that it takes time to make the initial
calculation so that the shortest length of time or epoch that you can use reliably to
calculate a Fourier transform is about 2 seconds. If you employ less than 2 seconds, you
lose some of the lower frequencies. The way to get around this problem is to use a
shifting time window. This works pretty well but there is still an initial delay. We can
calculate the output during that first two second period and update it every 0.1 seconds.
This provides a moving average which follows the EEG better although there is a lag
initially. The faster the computer, the better it works so that if you're going to use a
machine that uses this type of analysis, a recommendation is to employ as a minimum a
486-33 megahertz computer with math coprocessors. If you use anything below that, then
there's going to be a significant feedback lag. For example, if you close your eyes, some
alpha activity appears on the screen and after a delay of greater than 0.5 seconds, the
feedback occurs. If you're looking at the screen, you may see an alpha burst and then
after the delay the feedback occurs. According to classical conditioning theory, the
contingency between the conditioned and the unconditioned stimulus should be less than
half a second. If you're using an active band pass filter, the delay between the filter
response and the raw signal event can be as little as 0.1 seconds especially for higher
frequencies.
There is no really perfect signal processing device for feedback at the present time.
The ideal system, which doesn't exist yet, would be based on a true pattern analysis. That
would be ideal because it could be programmed to "see" a specific configuration
in the EEG, and then you give feedback only for that configuration. Such a pattern
analysis would be based upon matching a stored template even if it contained complex
waveforms with mixed frequencies and amplitudes.
Electrode Preparation
For training the sensorimotor rhythm, place the electrodes at the international 10-20
locations C3 or C4. To locate these two points, you must locate CZ, the vertex by applying
a tape measure from the nasion below the top of the bridge of the nose where he forehead
is indented to the inion, just underneath the occipital condyle, that bump at the back of
the head, Mark half the distance with a dry marker, such as is used on white boards. Then
place the tape from the preauricular notch of the left ear through this marked spot to the
preauricular notch on the right ear. Half the distance again is measured, The CZ is
located where the two cross. When CZ is located, then 20% of that total distance from ear
to ear is calculated. That distance is then marked from the vertex toward the left ear and
the right ear along the line between the two ears. This is the location of C3 and C4,
We have found that for Beta training,, the best location is a point 10% of the total
distance from nasion to inion, in front of CZ and behind CZ. These two points are halfway
between FZ and CZ and halfway between PZ and CZ and are correctly referred to as FCZ and
CPZ. Once the locations are marked, remove the marking dot with Omniprep, a gel containing
a small amount of pumice. (Available FUTUREHEALTH Inc or (Available D.O. Weaver Company,
Aurora Colorado) Next, place a small mound of electrode paste over the cleansed spot.
Either 10-20 conductive paste, or Nihon Kohden paste(Elefix) can be used. Next, push the
electrode down on the mound until the paste extrudes through the small hole in the middle
of the electrode. Our preference has been to use Grass E5SH electrodes or, in some cases,
the smaller E6SH, electrode. Finally, a small cotton ball is pressed down on top of the
electrode in the mound of paste. This completes the electrode application on the head. For
the ear placement, a Grass Instrument Co. ear clip electrode is used. This consists of two
cup electrodes placed in a small plastic holder. The ear is cleaned by rubbing it with
Omniprep, wiping the Omniprep off, and then placing some electrode paste in the cups of
the electrode and placing the ear clip on the ear. Children as young as age six have
tolerated this procedure very well.
Typically, an experienced therapist can do the entire electrode connection in two
minutes or less. When the session is ended, simply remove the electrodes by lifting them
from the head. The paste is removed with either a mild warm water soap solution or
isopropyl alcohol. Patients tolerate the electrode removal with no difficulty. It is
advisable to describe the electrodes as sensors, which is less threatening, particularly
with children.
Electrode Care & Sources of Artifact
Regardless of the method of signal detection and processing used, make sure your
electrode leads are as short as possible and also make sure that your electrodes are
stationary. The impedance between electrodes and the skin surface should really be
preferably less than 5K ohms. We also must be very careful about offset voltages in the
electrodes, that can create amplifier problems. If you have gold or silver electrodes, and
they eventually become electroplated, will act like a little battery between the electrode
and the scalp. That can happen, if you take the electrodes off and keep them in water a
few hours and then clean them. If you have a feedback system that depends upon EEG signal
that is symmetrical around a zero voltage reference, and the electrode acts like a
battery, an offset voltage is imposed on the EEG. This distorts the signal and the signal
processing circuits in the instrument might only be processing a portion of the signal
which may even be truncated with square wave components. Fourier analysis of a square wave
has odd harmonics therefore you will obtain a very distorted signal; we might reinforce
events that do not exist in the EEG. With a band pass filter, the sharp cutoffs on square
waves will cause the filter to "ring" or oscillate and this will result in false
feedback. So what you have ending up with is feedback that has very little if any
relationship to the original wave form. If the wave form is offset enough so that it is
totally out of the amplifier range, the amplifier may respond by producing random noise.
Offset should be less than plus or minus 30 millivolts for most systems to respond with
fidelity.
You can have excellent impedance, and get poor recordings because the offset is too
great or you can have perfect offset and high impedance and get poor recordings so both
criteria have to be met. When a session is done, take the electrode off the scalp, wipe it
off with a Q tip very carefully or wipe it off with a piece of cloth, or if you put it in
water, hold the electrode so water can't get up under the electrode collar. Use a
toothbrush just to get the excess paste off and then wipe the electrode dry as soon as you
can after
you use it. I've used the same electrodes daily for eight years by taking good care of
them.
Neurofeedback for ADD/ADHD
Neurofeedback, a form of EEG biofeedback, has developed very rapidly. We were the first
to develop this methodology for treatment of hyperactivity, learning and attention
problems in the middle 1970's; but in the last 5 years, there's just been a burgeoning of
interest in this area. There are more than 450 groups we know of that are using
Neurofeedback, treating this complex of disorders. They are obtaining very impressive
results with many patients. Some clinics claim success rates from 70 to 90%. That seems
extremely high because medications are effective for about 60 to 70%, sometimes 75% with
multiple medications. Behavior therapy seems to be effective for about 40 to 50% of the
children. With Neurofeedback, if you choose the children, adolescents or adults properly,
there is long term carryover. After you phase them out of treatment, some patients may
need some occasional booster sessions. We have followed 51 individuals for up to a 10 year
period and find that the behavioral changes assessed by the Connors Parent Scale have been
maintained long after the treatment was over (Lubar, 1995). The data was from a
retrospective study by independent survey. Many of our former patients have said, "If
I hadn't had that experience 5 or 8 or 10 years ago, I would've never made it. It was the
biofeedback that made a difference in my life." Some of them were even able to
eliminate stimulant medication. Neurofeedback, especially as part of a multimodal
treatment, holds the promise of long term carryover.
Patient selection is extremely important. Our Position Statement regarding who is
appropriate for Neurofeedback treatment for ADD/ADHD is a living document which was
developed empirically(Lubar, 1995). If practitioners follow these guidelines carefully,
they will derive maximally positive results from a majority of the patients they treat.
Occasionally someone will report that they treated an extremely hyperkinetic child and it
worked well. Probably the most dramatic example of an exception to that set of guidelines
was a boy we worked with in our summer program 5 years ago. This child was very
hyperkinetic, was on Ritalin, and was having considerable difficulties in school. Based on
our current guidelines, we probably wouldn't have worked with such a child. His parents
were very insistent and they stated that they knew it was a risk, that it might not work,
but wanted to try it. The child responded incredibly well, so well that he went off of all
medication. He's never gone back on it and is now an honor student in junior high school.
It was just a stroke of luck that his mother was a freelance writer. She told us that she
was going to wait a year or two to see if this EEG treatment really works, and if it did,
write an article about it and send it to a popular magazine. The neurofeedback worked so
well that she wrote the article that appeared in Woman's Day in September of 1991 which
produced an explosion of interest in Neurofeedback Treatment for ADD/HD.
DATABASES
The determination of whether an individual is appropriate for a particular treatment
employing neurofeedback is based on many factors one of which is whether they present
neurophysiological evidence that they are functioning outside of the normal range. In
order to determine this, databases need to be established for different disorders for
which neurofeedback is currently being used. An excellent normative database has been
developed by Thatcher and his colleagues (1987) for normal controls of all ages from near
birth through to senescence. The original purpose of that database was to determine
whether an individual with a closed head injury differed significantly from matched normal
controls. However the Thatcher database may have other applications besides closed head
injury, one of which may be assessment of ADD/HD. When individuals with a particular
disorder are compared with a normative database, the questions that might be asked are
whether they differ in terms of the percentage of power in different frequency bands for
different locations. Also are there abnormalities in terms of coherence and phase
relationships in different regions. The Thatcher database is designed to measure these and
even more complex questions. Figure 4 presents some data extracted from our previous study
(Mann, Lubar, et al., 1991).
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Insert Figure 4 About Here
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In this figure, power ratios are presented for a group of 27 controls with an average
full scale WISC-R IQ of 107 and a group of 25 matched individuals with pure Attention
Deficit Disorder without hyperactivity with a full scale WISC-R score of 102.5. These
children were between the ages of 9 and 12 years old with a mean age of 10.55. Measures
were taken under 3 conditions: (1) a baseline eyes open condition ,during reading material
which was grade and comprehension level appropriate and during reproduction of figures
from the Bender Visual Motor Gestalt Test. The data was normalized by log transform and
power ratios were computed for the ratio of theta (4-8 Hz.) to beta (13-21 Hz.) and the
ratio of alpha (8-12 Hz.) to beta (13-21 Hz.). The figure shows that the individuals with
Attention Deficit Disorder without hyperactivity experience higher theta-beta and
alpha-beta ratios for all conditions combined. More detailed analysis also showed that the
greatest differences were during the drawing task than during the reading task and
relatively minor differences occurred during the eyes open baseline task. These task
related differences were highly significant and have been reported in our previous paper.
(Mann, et. al, 1992). The main point of the diagram is that individuals with Attention
Deficit Disorder without hyperactivity experience more theta and alpha activity with
respect to beta activity.
This database was gathered on a particular instrument with a particular software
program (Stellate Systems, Westmount, Canada) and the actual ratios obtained are matched
for that brain mapping system. Data was also collected on another group of more than 60
individuals ranging in age from 7 to 11 and two older groups, 12 to 14 year olds, and 15
to 55 year olds. The total number of individuals in the entire study is greater than 100.
This latter data was analyzed using the Lexicor Neurolex 24 channel system and is
presented in another publication (Lubar, 1995). The basic finding that theta and alpha
activity is increased with respect to beta appears to hold for individuals that have an
attention deficit disorder without hyperactivity. Since the actual ratios obtained may
differ somewhat depending on the instrument used and the way in which power is calculated,
it will eventually be necessary to develop conversion factors that can be used to
translate from one quantitative EEG mapping system to another. Eventually it should be
possible to obtain ratio data as well as absolute power data that can be comparable across
a variety of different EEG systems. It is important to emphasize that the data presented
here only applies to Attention Deficit Disorder without hyperactivity. Individuals with
ADHD may very well show different patterns. Current research to address this issue is now
in progress in our laboratory.
Individuals with other comorbidities such as depression, substance abuse, oppositional
defiant disorder may show other different patterns in terms of absolute power, ratios, and
the distribution of activity. The development of comprehensive databases for all of these
disorders will take years. This then raises the practical question, how do you know
whether an individual is appropriate for neurofeedback
treatment?
Screening Appropriate Candidates for Neurofeedback
The first consideration should be based on behavior and history. Does the individual
experience significant academic, organizational and social adjustment difficulties? Has
the individual been independently evaluated as having Attention Deficit Disorder with or
without hyperactivity, oppositional disorder, conduct disorder, or other comorbidities by
a variety of measures including psychometric, behavior rating scales, and academic
performance. Note that reaction to medication is not included as a criteria since
stimulant medications will improve cognitive functioning on a short term basis for most
individuals, regardless of whether they have an attention deficit disorder or not. Once
databases are established and published, if an individual experiences increased theta or
alpha activity with respect to beta which is more than 2 standard deviations from the
control group, then they may also have a neurophysiological marker for the disorder and
might be a good candidate for neurofeedback interventions. However, there may be
individuals whose ratios may still be within the normal range and may be good candidates
for neurofeedback if it can be shown within 10 to 15 sessions that they are
experiencing significant improvements in the areas that most typically demarcate their
disorder.
Neurofeedback Treatment Caveats
If neurofeedback treatment is to be undertaken, it must be emphasized that the average
number of sessions is between 30 and 50 and comprehensive treatment requires, if not
demands, the integration of neurofeedback with a variety of other treatment protocols
which often also includes medication and in addition requires a long term follow-up.
Patients must be weaned from the treatment gradually and followed for several years on an
occasional basis to ensure that the gains that they have attained are not lost. Patients
should not be given false hope that a small number of sessions is going to drastically
remediate their disorder and it should be emphasized at the present time there is no
definitive cure for ADD/HD its comorbidities regardless of the treatment protocol! The
purpose of neurofeedback is to help them function more like non-ADD individuals which may
or may not result in the reduction of medication and hopefully will result in better
academic, cognitive and social functioning. At the present time there are no comprehensive
replicated studies indicating that small numbers of sessions (less than 25) lead to long
term success. Until this is established claims regarding this possibility should be
undertaken with extreme caution, otherwise they border on a gross misrepresentation of
what can be accomplished with neurofeedback regardless of the frequencies and locations
trained, or whether the training was done with referential or bipolar montages or by a
particular manufacturer's feedback system. The fact remains that Attention Deficit
Disorder is one of the most complex disorders that is treated with EEG or other forms of
biofeedback and requires an enormous amount of effort both on the part of the patient and
the therapist.
One further question that is often raised in conjunction with neurofeedback treatment
for Attention Deficit Disorder is whether there is any relationship between success in
training and degree of change in the EEG. Some recent data from our laboratory and clinic
indicate that there is potentially a strong relationship between these measures. This data
is presented in Figures 5 and 6.
Figure 5: Pre-Post Training Theta Beta Rations Eyes Open 11 Cases Good Learners with
EEG changes
------------------------------------
Insert Figures 5 and 6 About Here
-------------------------------------
Figure 6: Pre-Post Training Theta Beta Ratios Eyes Open Six Cases No EEG Learning
Changes
We have obtained data on 17 children and young adults who had undergone neurofeedback
training where we were able to do a complete 19 location quantitative EEG on the same
individuals before and after training. Six of these individuals were not able to learn the
task and 11 of them were able to learn the task very well. Figures 5 and 6 show the
difference between the good learners and the poor learners in terms of theta-beta ratios
mapped over 19 different locations. It can be seen that the 11 individuals who were able
to learn were able to decrease their theta-beta ratios by at least 30% particularly in
those locations that are most related to ADD, specifically C3, FZ, CZ, PZ, and C4. In
Figure 6, the data is presented for the 6 cases who were not able to learn. These
individuals showed no changes in their pre and post brain map data.
The relationship between the brain map data and learning is shown in Figure 7 in terms
of a histogram of correlation coefficients. --------------------------------
Insert Figure 7 about here
--------------------------------
The figure illustrates that the good learners showed almost a -.6 correlation between
the percentage of theta over sessions as compared with no change in the percentage of
theta for the poor learners. In terms of microvolts, the good learners showed almost a -.4
correlation over sessions whereas the poor learners showed less than a -.2 correlation.
And finally in terms of the percentage of beta, the good learners were able to increase
their beta with a correlation over sessions between percent beta and session number of
approximately +.6 whereas the poor learners showed less than a +.3 correlation of
increased percent beta over sessions. These data are of some significance in that they
relate training on a day to day basis over 30 to 50 sessions with changes in multichannel
topographic EEG and further strengthen the argument that when an individual is able to
either decrease the percentage of theta or the microvolt levels of theta or increase the
percentage of their beta activity during the course of neurofeedback, this is correlated
with improved performance and also to changes in the underlying neurophysiological markers
that appear to be associated with Attention Deficit Disorder particularly without
hyperactivity.
Identifying Candidates for Neurofeedback
Based on our published position statemant(Lubar, 1995),any individual between the ages
of 7 and 45 (there is less documentation and research with those above 45, though we have
worked successfully with people above that age) , with a primary diagnosis of ADD/HD with
above average to low average intelligence is a candidate. If co-morbidity with the
following conditions exists, then neurofeedback should not be offered:
-Learning disabilities without ADD or ADHD as a primary problem, unless a QEEG has been
done to specify regions where the EEG and neuropsychological testing has indicated
possible dysfunction.
-Significant seizure disorder where medications interfere with learning (i.e. sedating
medication)
-Hyperkinesis, where multiple medications or high dosages with monotherapy have been
ineffective
-Childhood Psychosis
-Mental Retardation
-Severe Depressive or bipolar illness
-Dysfunctional families who refuse to participate in indicated therapy
Aspects of living Which Can Be Improved with Neurofeedback
Attention, focus & Concentration
Impulsiveness
Mild hyperactivity
Task completion and organizational skills
Planning for the future rather than living for the present
Increased self-esteem
Higher intelligence test scores
Improved behavior and learning
Improved Parent-Teacher rating scale scores
Greater realization of innate potential
Better job performance
Improvement in school grades
When the above criteria are used to select candidates for therapy and treatment, the
majority of
patients completing treatment experience long term maintenance of the treatment gains.
Integrating Neurofeedback with Academic and Cognitive Skills
Children in a typical session are provided a baseline without feedback and this is
compared with their performance while combining feedback with reading, math, writing,
spelling and other academic skills as well as EEG biofeedback when used by itself. By
building in the academic skills training within the Neurofeedback session, this prepares
the student to use the skills directly in homework and in school settings. If the
Neurofeedback is done only in isolation, many children will not learn how to apply the
technique in real situations.
This raises another theoretical point which has been in the biofeedback literature ever
since the late 1960's, i.e., whether awareness or direct perception of the
psychophysiological change is necessary in order for learning to occur. Kamiya (1979)
showed that it is possible to obtain autoregulation of the EEG alpha rhythm without
necessarily being aware of how learning took place. There is an extensive literature
dealing with autonomic control without awareness. However, in our direct experience with
more than 500 individuals in neurofeedback settings, I believe that at least for younger
individuals some degree of awareness of process is necessary. It is important to help the
child to develop strategies so that they can tell you what it feels like when they produce
beta or inhibit alpha and/or theta and can demonstrate that they can do this without
receiving feedback on demand. Individuals who can do this will experience greater
carryover of the effects than those who have no idea how they are able to change EEG
activity. With adults, in contrast, it may not be necessary to be specifically aware of
exactly what strategies one uses. Children will often tell us when they concentrate on
point scores on displays and imagine the numbers increasing, they receive more feedback.
Sometimes using color displays, they imagine the colors changing, e.g., on a color wheel
or in a figure moving through a maze and as they imagine a change is going to take place,
it does; this event is paired with feedback for producing the appropriate pattern. Once an
EEG change has been paired with feedback enough times, eventually it becomes almost
reflexive. If I ask a patient to raise their arm, they can do this successfully without
telling me the processes they go through to do it. They just say, "I did it."
They can't describe muscle by muscle and nerve by nerve exactly how the action was
initiated or what stopped it. This is true of all automatic motor learning and it's
probably true of a great deal of autonomic conditioning as well but it takes a great many
repetitions before entrainment occurs to the degree that awareness is no longer a critical
factor.
Integration of Neurofeedback with Ancillary Therapies
Attention Deficit Disorder with or without hyperactivity has been shown to be
exceedingly complex and often associated with significant comorbidities discussed
previously in this chapter. It is clear that there is no single monolithic treatment
approach which is highly effective for dealing with this disorder. This includes
Neurofeedback, psychotherapy, behavior modification, cognitive behavior therapy,
attribution therapy, medication or any other single approach. There are numerous studies
that have compared various therapeutic procedures, e.g., Reid & Borkowski (1987) have
looked at the relationship between cognitive behavioral self-control techniques and
attribution training for ADD/HD children. The rationale is that these children often
interpret the cause of their successes or failures to be uncontrollable and external,
leading to beliefs of helplessness and poor self-efficacy or self-esteem. In children that
perceive themselves as helpless, failure events lead to a deterioration in the quality of
their performance and their ability to maintain performance under stressful conditions.
However, research has shown that teaching children who feel helpless to attribute their
failures to controllable causes of insufficient effort then giving them the experience of
empowerment by helping them with successful experiences leads to increased motivation and
improved performance.
In our clinical program, we examine the influence of both antecedent (general
historically based attributions relating to self-concept) and program-specific
(domain-specific attributions of success or failure on a task) attribution training in
combination with self-control training for the maintenance and generalization of newly
acquired strategic behaviors. We have found that attribution training which involved
helping the child become aware of the role of personal effort in success or failure on a
task was much more successful than simply the use of cognitive behavioral approaches. When
children learned that they had control over situations that led to failure and that by
changing those strategies, they could change failure to success, they were much better at
being able to modify certain aspects of their ADD/HD behavior than when simply reinforced
for "doing the right thing". Reid and Borkowski’s results showed general
short term success in strategy-based learning, attributional beliefs, and more reflective
self-control. These effects persisted at a 10 month follow-up despite a decrease in their
size and scope. The two main problems that have plagued cognitive behavioral treatments,
maintenance and generalizability, were significantly improved by including attributional
training in the approach.
The main point of the Reid and Borkowski study is that it represents one of the only
behavioral approaches that has shown any degree of success. Other behavioral approaches
such as operant control of behavior through standard behavior modification techniques have
poor carryover and relapse occurs as the complex schedules or reinforcement are
discontinued. As far as medication is concerned, it by itself also is not sufficient.
Recent studies done by Satterfield and his colleagues found that individuals who are
placed on Ritalin alone showed very poor long term outcome in terms of ADD/HD behaviors
and oppositional defiant behaviors. Many individuals who had been incarcerated as young
adults had a history of ADD/HD and had been placed only on medication with no other
attendant therapies. As a result of these findings, Satterfield now believes that the
integration of medication with psychologically based procedures is absolutely essential.
The same caution holds for Neurofeedback. Although there are over 450 groups now claiming
very high rates of success with Neurofeedback, it must be emphasized that unless the
Neurofeedback is integrated with educational approaches, assessment of specific learning
disabilities, behavioral approaches and when needed medication, it is very unlikely that
long term changes will persist.
In our retrospective study of 52 patients (Lubar, 1995) followed for up to 10 years, it
was found that the greatest area of maintained success was in the specific categories as
assessed by the Connors Behavior Rating Scale dealing with school performance, completion
of tasks, better peer and family relationships. We now believe that the reasons for the
greatest improvements lying primarily in the categories that have to do with academic
success was because we build into the program for these children academic training as part
of the Neurofeedback session.
Family Dysfunction
Another reason for integration of Neurofeedback with other therapies is that a majority
of children who experience ADD and ADHD come from dysfunctional families, specifically in
the sense that most of these children do not live with both of their biological parents.
In more than 70% of the cases that we have worked with, there is a stepparent and in many
cases, the ADD/HD child has been adopted by non-ADD parents who blame their behavior
either on their poor genetics or on some other kind of biological defect and therefore
respond to their difficult behavior through punishment. ADHD children as a group are often
physically and emotionally abused more than non-ADHD children, at home, in school, as
adolescents and adults in work settings, and by peers and colleagues. All of this leads to
a desperate feeling of inadequacy which if not dealt with as part of a treatment also
reduces the overall success of the program. Which type of intervention to use depends to a
great extent on the training of the therapist. Some therapists tend to be more behavioral,
others psychodynamic, some may be more cognitive behavioral or rational emotive.
Ultimately it is the skill of the therapist and their ability to put themselves into the
ADD/HD individual's place, whether it be a child, adolescent or adult, and see the world
as they
see it, that leads to their ability to develop the appropriate transference for a
successful outcome.
Integrating Medication & Neurofeedback
There are many children, especially those with ADHD, that need to be on stimulant
medication at least part of the time. Without medication, their hyperactivity would be so
pervasive that they would be unmanageable in any therapeutic situation. There are other
individuals for whom their comorbidities such as depression, impulsiveness or even
obsessive behavior need to be dealt with in a pharmacological manner. For this reason it
is totally inappropriate to promise a parent or an ADD/HD individual that the purpose of
treatment is to free them from medication. The purpose of the treatment is to obtain
better control of the various aspects of this syndrome than medication and other means
can, and to be able to recognize how it is creating problems for them and how to cope with
it. If in the process of the training they are able to reduce their medication and
maintain the same level of control that they had with a full medication regimen, then
medication reduction trials could be considered in conjunction with the referring
physician or medical specialist.
Sometimes stimulant medication can be reduced partially and in some cases, it can be
phased out completely. This is ideal if it should occur but by no means should it be
promised to a perspective client or parent of a client. There are other cases in which the
stimulant medication may be reduced or eliminated entirely but it is essential that the
patient remain on a tricyclic antidepressant, alpha blocker or in some rare cases an
antipsychotic if indicated, or even an anticonvulsive medication. Just as neurofeedback is
a powerful adjunctive treatment used in combination with other treatments, it is equally
accurate to say that psychotherapy or medication are also powerful adjunctive treatments
that need to be used in conjunction with neurofeedback in most cases. A multicomponent
model is by far the most successful approach that has been developed at the present time
because ADD and ADHD is a multifaceted and a very complex disorder.
Medication reduction should be undertaken in conjuction with an appropriate physician
or specialist. We've found that for Ritalin, the best regimen is to reduce it gradually,
even though it quickly clears the system. Take , as an example, a child on 20 milligrams
of Ritalin in the morning, 10 mg at noon, and 5 mg, in the late afternoon. The medication
reduction strategy might proceed as follows: 20 mg, 10 mg, 0 mg,; then 20 mg, 5 mg,; then
10 mg, 5 mg,; then 5 mg, 5 mg,; then 5 mg, 0 mg,, then 0. The stepwise reduction should be
carried out every four to seven days. If, in the process of medication reduction, the
patient appears to be losing control over hyperkinesis or impulsiveness, stop the
medication reduction at this point, or perhaps increase the medication.
Cylert is usually administered in a dosage of 37.5 mg once or occasionally twice a day.
Medication reduction can consist of simply stopping the afternoon dose and then , if
possible, stopping the morning dose two weeks later, Amphetamine can be reduced in much
the same manner as Ritalin.
Sometimes medication reduction can appear to work very well for one or two months, and
then the child begins to show signs of needing medication again. When this occurs one can
reintroduce the medication if requested by parent, school or physician. Many children with
ADHD are able to completely eliminate medications with follow-up times of 6 years or
longer without reintroducing medication. These are the most fortunate outcomes and
probably represent one end of a continuum.
Other medications commonly are used in treating ADD/HD comormidity problems such as
impulsiveness, depression and seizure and tic disorders, These include desipramine
(Norpramin) and imipramine (Tofranil) which are often prescribed for depression and
occasionally for impulsiveness, Clonidine (Catepress) is an alpha blocking agent also used
for the management of aggressive or assultive behavior These medications, particularly the
tricyclics, take several weeks to reach maximum blood levels. A similar time is needed to
clear the body. Medication reduction must be carried out more slowly and under careful
medical supervision.
Informed Consent and Financial Considerations
At the present time, there are many third party payors, including managed care insurers
that are covering biofeedback treatment under the CPT code 90908. The reason for this is
because this approach has been shown to be very effective clinically. However, while in
the short run, it is an expensive treatment, often involving between 30 to 50 or more
sessions. Over the long term it still can be the most cost effective approach for the
group of disorders discussed in this chapter. . In addition the patients might require
other interventions such as family therapy, behavioral approaches, or integration of the
technique with pharmacotherapy. Its important to develop an informed consent that clearly
describes the realistic expectations and limitations of the technique.
Practitioners should be urged to follow the guidelines of the position statement that
has been described previously (Lubar, 1995), and reviewed earlier in this chapter.( See
section of evaluating candidates). An appropriately designed informed consent should state
that EEG Neurofeedback treatment for any specific disorder cannot be guaranteed to produce
a successful outcome, that biofeedback interventions including Neurofeedback as well as
psychotherapeutic interventions or behavioral interventions are not an exact science but
depend upon the appropriateness of the client and their willingness to commit themselves
to treatment and its goals, and is dependent on the ability of the patient-client and the
practitioner to work together in order to achieve these goals. Informed consent should
state the approximate number of sessions that will be involved in the treatment, e.g.,
treatment may involve approximately 50 sessions over a period of several months with long
term follow-up. It is also important to state that the practitioner cannot guarantee the
treatment will be a success , especially if the patient stops the treatment before it is
completed or does not engage in follow-up sessions or consultations when necessary. It is
also important to elaborate that EEG Neurofeedback is a safe treatment, does not involve
any internal sensors, does not produce any known negative side effects but it is a
powerful adjunctive technique that must be integrated with other approaches to be
maximally effective. It would be appropriate in the consent form to state that there are
currently approximately 450 practitioners or organizations currently using Neurofeedback
and that overall the results are very promising in terms of improved grades, test scores,
better behavioral adjustment but that in any individual case, these results cannot be
guaranteed. Furthermore, the consent form should include a statement that the results of
treatment will be available to the patient and/or their parents at any time and that these
results may be made available to the third party payers if payment from another source is
desired The practitioner also has the option in the consent form of stating that the
results of the treatment might be utilized in research but that the individual patients
would not be identified in research protocol and that the data would be used primarily for
statistical purposes. It is also necessary for the patient to be told that if the results
are to be reported in a research study, even though individuals are not identified, that
they would be asked permission for this specific purpose and may be asked to sign an
additional consent form in that regard. Many journals now require that authors sign a
certificate of compliance with APA ethical principles.
Very often children in treatment will require school interventions. These interventions
may consist of meetings with teachers for classes where problems may have arisen in terms
of behavior and performance, or with school psychologists, or even the principal. It is
important that the practitioner explain at these meetings the purpose of the treatment,
how it is integrated with other conventional treatments and is also an opportunity for the
practitioner to inform the school about Neurofeedback services and in what ways they may
be helpful. Very often school psychologists, counselors and teachers are good referral
sources.
One question that many parents of patients ask is whether the school is responsible for
payment if their child is engaged in a psychological intervention, and does this include
Neurofeedback? At the present time, this is not clear. Some schools in some states are
paying partially for psychological interventions for ADD/HD children. This is something
that needs to be investigated by the practitioner in their own locale.
Certification of neurofeedback-neurotherapy providers
Other questions that may arise regarding EEG biofeedback, Neurofeedback or Neurotherapy
whether the treatment is carried out by the health care practitioner or by individuals
supervised by the health care practitioner. At the current time, certification procedures
are being developed. The recently formed Academy of Certified Neurotherapists has
developed guidelines for certification of practitioners and trainees who employ EEG based
treatment for a variety of different disorders. Individuals engaged in Neurofeedback are
strongly encouraged to become certified. At present the Academy of Certified
Neurotherapists has negotiated a contractual arrangement to serve as a specialty
certification under the Biofeedback Certification Institute of America (BCIA). If the
health care provider can, under their State licensure or through certification guidelines
supervise therapists (this might include graduate students who are entering the health
care provider professions), then they need to state in the consent form that their
supervisees will be carefully monitored throughout the treatment program for the client or
patient..
Treatment of ADD/ADHD in Adults
It is clear that ADD/ADHD is a lifelong disorder. It does not go away in adulthood. The
only thing that may change is that the Attention Deficit Disorder with hyperactivity may
evolve more toward an Attention Deficit Disorder without hyperactivity. At least 70% and
perhaps as many as 90% of children with ADD/ADHD experience significant problems as they
approach adolescence and adulthood. Because this is a neurophysiologically based disorder,
it is unlikely that it ever really goes away. As mentioned previously, ADD adults have
great difficulty with planning which is often reflected in poor job performance,
interpersonal skills, and sometimes even marital relationships are severely compromised.
In the adult, there is more likely to be a reactive depression because of repeated
failures and inability to meet sometimes unrealistic standards set by the individual. ADD
individuals do not like to admit that they have a significant disability. They will often
try to compensate for their disability by overwork, impulsive behaviors, and in some
cases, addictive behaviors become a significant problem. As far as the neurophysiology of
ADD/HD is concerned, as we approach adulthood, the amount of fast (beta) activity in the
EEG increases with regard to slow activity. The dominant occipital rhythm which is less
than 8 Hz. for young children becomes established as the alpha rhythm in adults and by age
12-14, reaches its adult level and remains relatively constant in terms of frequency until
advanced age. Beta activity continues to increase particularly in the frontal regions
until approximately age 20-25 when it also stabilizes. Some adults show excessive slow
activity in the theta bandpass just as children do but more often, one should look for
increased alpha activity during academic tasks as one of the signs that there may be an
attention deficit disorder. Normally alpha activity blocks or decreases when one is
engaged in active processing. The greatest amount of alpha activity is seen when
individuals are resting with their eyes closed or even in an eyes open situation when they
remain in a relatively blank mind relaxed state. As soon as they engage in any kind of
complex mental activity such as mental arithmetic, reading, writing or other types of
cognitive challenges, alpha activity decreases and more beta activity appears. In the
initial assessment of adults who have Attention Deficit Disorder with or without
hyperactivity, note whether they show alpha blocking and increased beta activation with
academic or cognitive challenges. If they don't it may be necessary to extend the inhibit
frequency band pass from 4 to 8 Hz., which is the theta region, to include some of the low
alpha activity as well. We often train adults to block 4-10 Hz. activity or 6-10 Hz.
activity and to increase beta activity between 16 and 22 Hz. or even 18-24 Hz. This is
because beta activity in adults is faster than beta activity in children. We have found
that blocking alpha in ADD adults can be extremely helpful and has very much the same
effect as blocking theta activity in children.
Addiction Considerations
The work described previously by Peniston and his colleagues indicates that many
alcoholics show increased beta activity and decreased alpha and theta activity.
Individuals with Attention Deficit Disorder, on the other hand, have almost the opposite
pattern. They experience too much slow theta activity or alpha activity and decreased beta
activity. There is also an increased frequency of alcoholism or other types of substance
abuse in the ADHD population. The question often arises if you can teach an ADD\HD child
to increase beta activity, do you make them more prone to alcoholism? At this present time
it is not possible to answer this definitively because for children with ADD/HD,
relatively few have been followed into adulthood. However, the possibility of increasing
likelihood for alcoholism through training is unlikely. Even in the work with alcoholics,
it has been found that it is unwise to allow a client to leave a session after only having
been trained to increase slow activity and inhibit beta. The reason for this is that this
low arousal of training leads to an increase in hypnogogic activity and can result in
disorientation, particularly when the person has to go out into a world where there is
traffic, driving responsibilities, and other activities that require rapid shifts in
attention. The best approach is to train the alcoholic individual to first increase the
slow activity in conjunction with abreaction and to facilitate the development of
anti-alcoholic messages and then toward the end of the session to be able to increase beta
activity so that they can be alert in demand settings.
Essentially, in working with both children with ADD/HD, and substance abuse disorders
in both adolescents and adults, it is important thing to be able to shift EEG activity
into the appropriate pattern for the activity that is to be engaged in. Hence, ADD
individuals need to increase levels of fast activity in demand situations and if they
wish, to increase slow activity for purposes of daydreaming and imagery in situations that
are purely relaxation oriented or when they are not required to meet schedule demands.
Alcoholics and individuals with other types of substance abuse for which the Peniston
protocol is appropriate need to use the alpha-theta training to help them maintain
anti-abuse images but need to be able to shift into beta in demand situations. Essentially
then all forms of EEG feedback as well as other types of feedback have to be learned in
terms of their utilization in task appropriate situations. Even in cases of regulation of
skin temperature or EMG activity, sometimes it is necessary to increase blood flow to the
extremities, sometimes it may be actually desirable to decrease blood flow or to increase
EMG activity in certain muscle groups or decrease it in others, depending on the setting.
At the present time then, it does not appear that training individuals with ADD/HD
increase beta activity and decrease theta activity makes them more susceptible to alcohol
or drug abuse.
Current and Future Research Needs
In closing this chapter, I would like to point out some needs in the research area that
must be addressed if Neurofeedback for ADD/HD is ever going to be embraced by the
mainstream health care establishment as an effective treatment. Over and over again we
have been told that no matter how convincing our clinical results appear to be, even with
follow-up, there is always the possibility that placebo effects account for success. In
many ways we are being held to a much higher standard than other treatments have been held
in the past. An excellent article by DeGood (1993) explores the question of whether
biofeedback produces specific effects and in the case of pain, are these effects
site-specific? He points out that although biofeedback has been used for the management of
pain for many years and particularly for the management of muscle contraction and migraine
headaches, even where the effects of the biofeedback training are as strong as those
obtained with medication and where there has been documented improvement in literally
thousands of patients with long term follow-up..."evidence of specific effects in
mechanism has been inconsistent." "Changes in muscle tension are not always
correlated with changes in tension headache, nor are skin temperatures reliably related to
the level of migraine discomfort." "To date however it appears that biofeedback
for headaches may produce a nonspecific therapeutic effect that is at least as powerful as
the specific effects associated with medication."
This exemplifies a very important standard that we are being asked to meet. One end of
the continuum is stated by Furedy (1987). His published specific view is that because
biofeedback approaches involve physiological feedback, it is essential to show that the
mechanism of action is a specific physiological mechanism and not due to some kind of
psychological change or some vague change in arousal mechanisms. In conjunction with the
work described in this chapter, Furedy would argue that unless we can show that the
Neurofeedback produces very specific changes in the EEG that can be documented and that
these specific changes are linked to the degree of behavioral change in the individual
with ADD/HD or for the individual with a substance abuse problem, then in fact the
biofeedback has produced only some kind of vague nonspecific placebo effect. Our recent
paper (Lubar, Swartwood, Swartwood, & O'Donnell, 1995) demonstrates specificity in
that only those ADD/HD children who were able to significantly decrease microvolts of
theta over sessions were able to experience significant improvements in T.O.V.A. scores.
There are researchers who believe that we must show with controlled outcome studies
involving either double blind or matched groups design that only those individuals who are
successful in Neurofeedback training are the ones that show changes in behavior ratings,
school performance, academic achievement, and other measures of improvement. Further, we
must demonstrate that individuals who do not change their EEG do not show these changes.
For these critics the fact that literally thousands of children have benefited from
Neurofeedback in terms of the various behavioral and academic achievement measures is
irrelevant unless attendant neurophysiological and neurological changes have also
occurred. Why do we who espouse neurofeedback approaches have to meet higher standards
than have been met for the treatment of headache or pain mechanisms for which literally
thousands of individuals have achieved success even though the underlying physiological
mechanism is not always clearly established and in some cases, totally unknown? If one
examines the Physicians' Desk Reference (PDR) there are many drugs including Ritalin
(methylphenidate) in which the statement "mechanism of action unknown" is
clearly stated yet the drug is used, and used quite successfully. Mechanisms of action of
many anesthetics are not even known; nevertheless they are essential for surgical
interventions. I've already discussed this controversy in considerable detail (1992).
The two most common experimental designs that can be used to separate out Neurofeedback
effects from nonspecific and other treatment effects are the matched groups design and the
double blind crossover design. The double blind crossover design is inappropriate as I
stated in my Biofeedback Newsletter article (1992) because for part of the treatment
individuals, especially children who are vulnerable to the effects of failure are exposed
to treatment conditions which could actually make them worse. This could lead to them
dropping out of treatment early and feeling that they had only experienced another failure
in a long line of failures that they are already coping with. A matched groups design is a
much better approach. In this design one suggestion is to have a group which receives only
EEG Neurofeedback, a group which receives EEG Neurofeedback plus a second intervention
such as behavior therapy or psychotherapy, a third group which receives a form of behavior
therapy or psychotherapy as the only intervention, and perhaps a waiting control group, or
a control group which receives only some kind of attention training, such as computer
games or cognitive rehabilitation tasks. I would already predict that the results of the
Neurofeedback will be weaker in this type of design than it would be if integrated into a
multicomponent dynamic treatment process.
Fortunately several matched groups design studies have been presented or published
recently. Scheinbaum,Zecker,Newton, and Rosenfeld (1995)in a controlled study compared a
Neurofeedback trained group of 8-12 year olds with a "cognitive control therapy"
group on a variety of measures including T.O.V.A scores. Only the Neurofeedback trained
group were significantly improved with 6 of 8 children attaining normal test scores. In
the control group only two of six children obtained this degree of improvement. This study
is still in progress. In another controlled study, Cartozzo, Jacobs and
Gervitz(1995),employed a neurofeedback group(n=8) and a control group(n=7). The
neurofeedback group were trained to increase SMR and decrease theta. The control group
played a PAC-Man video game on the same apparatus as the experimental group but without
Neurofeedback . Both groups were given 30 sessions. The Neurofeedback group decreased
their theta by 2.1 uv. and improved significantly in T.O.V.A. and WISC-R scores, whereas
the controls actually increased their theta by a mean of 3.5 uv and did not improve on
these measures. (Montgomery, and Nagel(1995) and Kade(1995) have presented individual case
studies showing that neurofeedback or neurofeedback combined with cognitive therapy can
lead to significant and objectively measured improvements in EEG measures, school
performance or psychometric measures. These studies should be expanded and/ of published
in peer reviewed journals now that they have been presented at a national meeting and
published in that meetings conference proceedings(Conference Proceedings of the
Association for Applied Psychophysiology and Biofeedback. 26th Annual Meeting. Cincinnati,
Ohio, March,1995).
Recently, Rossiter and La Vaque(1995) published a potentially important paper in a peer
reviewed journal. They compared 23 children and adults given only 20 sessions of
neurofeedback for increasing SMR or beta while decreasing theta with a control group of 23
participants given only stimulant medication. The dependent measure was T.O.V.A. scores.
The EEG treatment was just as effective as the medication in terms of improvements
obtained both in for the continuous performance measure and improvement assessed by
questionnaire. It would have been interesting to see if the usual 40 session treatment
regimen would have resulted in even more improvement in T.O.V.A. scores than attainable
with the medication. Since the latter measure is often used to titrate medication levels
it appears that with between 20-40 sessions the neurofeedback matches or surpasses the
results obtained with medication alone, Clearly, however EEG biofeedback cumulatively
facilitates the use of medications, behavior therapy, cognitive interventions, and these
other interventions facilitate the use of Neurofeedback. Overall, combining them seems to
produce a very powerful outcome that affects positively most of the measures that are
currently used in terms of academic achievement, behavior ratings, etc. If more studies
continue to obtain positive results and are well published much of the controversy
surrounding Neurofeedback may begin to abate as it becomes a more mainstream treatment for
Attention Deficit Disorder.
Just as neurofeedback helps those that are struggling with a neurophysiologically based
disorder, neurofeedback also offers the promise of helping all of us to function at a
higher level in terms of academic achievement by enhancing the EEG activity associated
with complex processing. In my own research my collages and I are beginning to explore the
QEEG patterns associated with complex processing and exploring new protocols for enhancing
these processes. As these new directions lead to new applications with the changes that
are occurring in the health care field we can begin to move beyond the disease-disability
model to the realm of expanding our human potential.
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Figure Captions
Figure 1 Comparison of theta-beta percent power ratios in the same subjects with
referential vs. bipolar recordings. Electrode placements are the same as in Figure 1.
Figure 2 Comparison of alpha-beta percent power ratios in the same subjects with
referential vs. bipolar recordings with placements the same as in Figures 1 and 2.
Figure 3 Percentage of theta, alpha and beta recorded referentially with an electrode
at CZ and linked ear references and with a bipolar montage and with electrodes placed
halfway between FZ and CZ and halfway between CZ and PZ with ear reference.
Figure 4 Comparison of theta-beta and alpha-beta ratios in a group of 9-12 year old
individuals with Attention Deficit Disorder without hyperactivity and matched controls.
Controls and the ADDs were matched on the basis of IQ and socioeconomic status.
Individuals with Attention Deficit Disorder without hyperactivity experienced
significantly higher theta-beta and alpha-beta ratios. Those presented here are averaged
over 16 locations.
Figure 5 Pre-, post-training theta-beta ratios average for 5 eyes open conditions
before and after training for individuals who showed significant improvement during
neurofeedback.
Figure 6 Theta-beta ratios for 6 individuals who were unable to show improvements in
measured parameters during neurofeedback training. These measured parameters consisted of
percentage of theta reduction, microvolts of theta reduction, and percentage of beta
increase.
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