Treatment of Attention Deficit Disorder
using
Neurotherapy/EEG Biofeedback
DIAGNOSTIC CODES
314.01 Attention Deficit Disorder with Hyperactivity
314.00 Attention Deficit Disorder without
Hyperactivity
BACKGROUND
Diagnosing an attention deficit disorder is a difficult task. This disorder is a significant problem in the classroom today. Referrals include individuals with the following symptom or symptoms: difficulty staying with a task; difficulty completing an assignment; inability to listen to the teacher; easily distractible; difficulty concentrating; impulsiveness; "acting before thinking;" and shifting from one activity to another without completion. In addition to exhibiting the above symptoms, a second group of individuals appears to be highly active. These individuals tend to be restless and fidgety, always "on the go," and are constantly on the move while awake and during their sleep.
INCIDENCE AND ETIOLOGY
Attention deficit disorders affect approximately seven to ten percent of children before they reach the age of twelve or thirteen. Ten times more common in boys than in girls, it tends to run in families. Recent research indicates it generally appears to be a temporary developmental problem in which a small part of the sensory neurological system appears to lag behind in its development. This lag results in the child's inability to sustain attention to either visual cues, auditory cues, or both. Since they cannot sustain attention to stimuli in the environment for any long period of time, they actually never sense(hear, see, etc.)a great majority of the cues, facts, and ideas in their environment. Therefore, the stimuli never get to their brain to be remembered or retrieved by the child and used in future situations. This disorder may also be related to other physical problems or may be the result of inadequate, disorganized, or chaotic environments. The problem sometimes begins by the age of three and usually comes to professional attention when the child enters school. More severe forms, with a greater number of symptoms, are usually present in younger children. Unfortunately, symptoms vary significantly from child to child; however, the essential features include signs of a developmentally inappropriate attention span and impulsivity.
What is Neurotherapy?
Neurotherapy (also know as EEG Biofeedback and Neurofeedback) is a painless, non-invasive treatment that allows individuals to gain information about their brainwave activity. The information is used to learn to change the brainwave activity.
Clinicians and reserachers who have provided Neurotherapy report that when brainwave activity is changed, symptoms of ADD/ADHD are usually reduced or eliminated.
Available research indicates that individuals with ADD are deficient in beta brainwave activity, while those with ADHD are deficient in SMR brainwave activity. Both individuals with ADD and ADHD often have elevated theta brainwave activity when compared to those without the disorder.
Neurotherapy at Psychological Services is being used as an alternative or adjunct to the more traditional approaches of treating ADD/ADHD (i..e. medication and behavior management)
What is Neurotherapy?
Neurotherapy (also know as EEG Biofeedback and Neurofeedback) is a painless, non-invasive treatment that allows individuals to gain information about their brainwave activity. The information is used to learn to change the brainwave activity.
Clinicians and reserachers who have provided Neurotherapy report that when brainwave activity is changed, symptoms of ADD/ADHD are usually reduced or eliminated.
Available research indicates that individuals with ADD are deficient in beta brainwave activity, while those with ADHD are deficient in SMR brainwave activity. Both individuals with ADD and ADHD often have elevated theta brainwave activity when compared to those without the disorder.
Neurotherapy at Psychological Services is being used as an alternative or adjunct to the more traditional approaches of treating ADD/ADHD (i..e. medication and behavior management)
How is Neurotherapy Performed?
Computerized biofeedback equipment (an electroencephalograph) is connected to the patient by sensors that are placed on the scalp and ears. These sensors are safe, do not prick the skin, and are painless.Dr. Overcash administers Neurotherapy in order to help the patient learn to change brainwaves to desired activity levels.
How Successful is Neurotherapy?
Some clinicians who have adminstered Neurotherapy to patients with ADD/ADHD report improvements in school performance, social relationships, and self-esteem, increased intelligence, and a reduction in oppositional behavior. In addition, ADD/ADHD students are often attentive, less distratable, less hyperactive, and more in control of their behavior.
The major reason Dr. Overcash is committed to providing Neurotherapy is to help patients for whom other approaches such as medication and behavior management have failed.
Dr. Overcash will assess the patient before, during, and after treatment ot objectively determine whether positive results are occuring.
Does Neurotherapy produce Negative side Effects?
Neurotherapy should produce no discomfort nor side effects. In fact, lack of side effects is one of the strengths of Neurotherapy.
How Frequent are Neurotherapy Sessions?
In there initial stages of training, sessions should occur two times/week. As progress is made, sessions can be reduced to once/week and finally to 1-2 sessions/month.
How Long does the Neurotherapy Take?
Neurotherapy is a training process and improvements occur over time. The length varies among patients. Many individuals report intitial progress after 10 sessions. On the average, effective treatment requires about 40 sessions.
Improvements in behavior are usually durable, but a few patients may need booster sessions. There are 10+ year followup studies indicating that the changes in behavior and EEG are maintained.
How to start Neurotherapy?
The evaluation of ADD/ADHD must have been made through objective evaluation and EEG studies by a BCIA certified psychologist or physician. Associated problems must also be identified. This can be done at Psychological Services by Dr. Overcash. The purpose of the assessment is to determine the best type of Neurotherapy to be given and to adjust the treatment as appropriate. Patients must be at least 8 years of age.
Will Insurance Cover the Cost of Neurotherapy ?
Neurotherapy is a relatively new treatment for ADD/ADHD. Some insurance companies do provide coverage, while most do not. We encourage you to contact your insurance company to find out whether your policy covers Neurotherapy (Neurofeedback, EEG Biofeedback) for ADD/ADHD.
Below is a Summary of Research Explaining one Successful Protocol that can be used in the Treatment of Attention Deficit Disorder
The efficacy of EEG biofeedback in the remediation of attentional deficits and specific learning disabilities is evaluated for a study population of fifteen school-age children in a clinical setting using psychological and academic testing. The Wechsler Intelligence Scale for Children--Revised (WISC-R) is used in combination with the Wide Range Achievement Test (WRAT), Peabody Picture Vocabulary Test (PPVT), the Tapping Subtest of the Harris Tests of Lateral Dominance, and the Benton Visual Retention Test (VRT). Behavioral changes are assessed by means of teacher and parental reporting. The training protocol is enhancement of EEG activity in the 15-18 Hz regime, with suppression of excessive activity in the 4-7 Hz and 22-30 Hz regions. Significant improvements in cognitive skills, academic performance, and behavior are found, and confirmed in follow-up. Average improvement in WISC-R full-scale IQ was 23 points. A preference for 15-18 Hz training versus 12-15 Hz training is indicated.
A number of studies evaluating EEG biofeedback for hyperactivity, attention deficit disorder (ADD), and learning disabilities have already yielded evidence of improvement in cognitive skills and academic performance. (Shouse, 1979; Lubar, 1984; Tansey, 1990). The focus initially was on remediation of hyperactivity in cases which were responsive to stimulant medication, and hence were thought to be most obviously traceable to cortical underarousal (Lubar, 1976). This work was grounded on earlier success of EEG augmentation training in the 12-15 Hz region with epileptic seizures of predominantly motor symptomatology (Sterman, 1972). Such augmentation training was then combined with inhibition of excessive activity in the 4-7 Hz region (Sterman, 1974). Viewing hyperactivity as motor disinhibitionmotivated use of the same protocol.
The 12-15 Hz region was identified by Sterman as associated with specific rhythmic activity (referred to as sensorimotor rhythm, or SMR) which governs the setpoint, or the poise, of the motor system (Sterman, 1982a). Subsequently, it was found that cases of attention deficit disorder without hyperactivity (as defined in the DSM III) were also responsive to the training, and that cognitive deficits associated withattentional deficits could be effectively remediated with both 15-18 Hz training (Lubar, 1984) and with 12-15 Hz training (Tansey, 1990).
The more universal applicability of the technique meant that a more generalized model was needed, and the efficacy of both 15-18 Hz and 12-15 Hz training also called into question any simple identification of the mechanism with the SMR rhythm. No comparable rhythm has been identified in the 15-18 Hz regime, which is referred to as "beta" in the following.
The present work is motivated by the need to confirm the previous studies, and to quantify and particularize the benefits in terms of cognitive function and short-term memory which may be attributable to the training. There were differences in protocol, in electrode placement, in instrumentation, and in the role of the biofeedback therapist in the prior studies. This variety in approach also calls foradditional studies which may allow discernment of the preferred protocol. Finally, there has been sufficient anecdotal evidence of a more generalized efficacy of the present EEG training protocol, e.g. for behavioral problems, that a more inclusive model may be required to explain all of the findings.
The previous work supports the hypothesis that deficits in cortical activation and control are observable in the statistics of cortical neuronal activity, as reflected in EEG spectral density distributions and in time domain phenomena such as spikes, other characteristic waveforms, and paroxysmal activity. It is therefore proposed that EEG biofeedback training in general, and beta and SMR training in particular, may effect cortical regulation in a very broad sense when it is used to train the EEG toward more state- appropriate frequency distributions. This is accomplished by impacting on those mechanisms, originating in the reticular formation of the brain stem and mediated by the thalamus and the hypothalamus, which govern states of arousal and level of consciousness, including cortical activation. The mode of generating SMR orother rhythmic brain wave activity via the stimulation of a thalamic gating mechanism was first described by Sterman (1982).
Specifically, the presence of high-amplitude, low-frequency activity is inappropriate for a state of attentive arousal under which the training takes place. Similarly, low amplitude in the beta region appears to be associated with cortical underarousal (Lubar, 1989). Obversely,excessive high frequency activity may be observed in children showing anxiety symptoms (our own observation). Such waveforms yield high amplitude in the upper beta band of 22-30 Hz. The training protocol, in terms of reward and inhibit bands, follows directly from these observations. Extraneous factors impinge as well: head and neck muscle activity intrudes into the beta band, allowing clients to obtain rewards inappropriately, unless such activity is specifically inhibited.
Electrode placement in the present study was bipolar, at sensorimotor cortex, along the Rolandic fissure. Placement was C1-C5, or C2-C6,per the International 10-20 system. An ear ground electrode on the same side being trained was also used. Training was performed on thedominant hemisphere, unless there were hemispheric differences in the EEG, in which case the side showing the larger or more deviant EEGwas trained. Verbal reporting from the client, family, and teachers was used to adjust the training protocol throughout. By way of comparison, Lubar employs a frontal-temporal placement, whereas Tansey uses a large-area electrode at Cz in a monopolar configurationwith an ear reference and ear ground. Our choice of electrode placement was largely historically rooted in the early work of Sterman and Lubar.
Instrumentation was by Neurocybernetics. A two-channel EEG amplifier from Mendocino Microcomputers was used. The signal wasdigitally processed in a PC. The primary EEG trace and the three filtered waveforms are continuously displayed to the therapist in a scrolling or chart recorder type of display. This information is used by the therapist to provide guidance, coaching, and motivation to the client, andhelps the client to begin to associate certain mental states with what is observed in the EEG and in the feedback display. The feedback signalis derived digitally in the PC, and is presented to the client via a second computer, which displays a video game in which the brightness andspeed of a pacman-like object is governed by the beta amplitude relative to a pre-set threshold. If the theta or high-beta (i.e., 22-30 Hz)thresholds are exceeded, the object goes dark and stops. Binary auditory feedback is provided as well.
The training proceeded in sessions of thirty minutes on the instrument (45-minute contact hour), after an initial intake session of an hour and a half, in which the history was taken, baseline EEG records were obtained for both hemispheres, and a training session was conducted. The academic testing was accomplished in a two to three-hour session on another day. At each training session, the last six-minute segment of the EEG record was stored on the client disc, along with an updated history of thresholds and other performance data from every session. A chart recorder output of representative EEG data was also obtained at each training session.
Academic and cognitive skills testing encompassed the full WISC-R, the PPVT, the WRAT, Benton VRT, and the Tapping Sub test of the Harris Tests of Lateral Dominance. The selection was made partly on the basis of the broad familiarity with these tests among educators,psychologists, and educational therapists, who will serve as the primary referral source for this type of training in the foreseeable future.
The subject population had the following characteristics: Of the fifteen subjects, fourteen had been diagnosed as having attention deficit disorder. Of these, seven had prominent symptoms of hyperactivity, and of these, two were on medication for the condition. Seven subjectswere identified as having specific learning disabilities; of these, four were identified with dyslexia. Six of the subjects were characterized byoppositional/defiant disorder, and two by conduct disorder. Five of the children reported chronic headaches. And thirteen of the group reportedvarious sleep disorders, including two cases of sleep anxiety (inability to fall asleep in one's own bed or room), four cases of sleep walkingand sleep talking, and three cases of nocturnal enuresis. Mood disorders were common as well, with three cases of chronic anxiety, and fourof childhood depression or dysthymia. One subject exhibited obvious motor tics.
Training was conducted for an average of 35 sessions, at a rate of 2-3 sessions per week.