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Neurofeedback and Autistic Spectrum
Study on Autistic Disordered Children in a Public Charter School Setting. Completed under the auspices of the Office of Mental Health/Mental Retardation. Click here to read the report.
Biofeedback and Alzheimer's
Sponsored research supported by the Helen Bader Foundation studyied the impact of stimulation driven EEG biofeedback on the cognitive and behavioral symptoms of people struggling with early stage Alzheimer's dementia.
Neurofeedback and Children with ADHD
The Philadelphia Office of Mental Health sponsored a study of neurofeedback's efficacy with children in the public mental health system with ADHD and conduct disorder. We were challenged to show that neurofeedback could be provided effectively in a community mental health and residential treatment context. Please review our findings by clicking here.
Neurofeedback, Anxiety and Opiate Addiction
We completed a pilot study in collaboration with Thomas Jefferson Medical College's Dept. of Psychiatry and Human Behavior in 1996 on the effects of alpha-theta biofeedback on anxiety symptoms in a methadone-maintained population. The results of all the above activities are available in our research section.
Neurofeedback and Alzheimer's
Our report was completed in 2009, results were presented at the 2009 International Conference on Alzheimer's Disease (ICAD) in Vienna, Austria.
This trial involved the use of EEG biofeedback training to reduce the symptoms of dementia. Subjects participated in 40 sessions of biofeedback training conducted twice weekly with quantitative EEGs (QEEG) and neuropsychological testing conducted before and after the block of 40 training sessions. Read the report here Neurofeedback Treatment for Early Stage Dementia.
Previous studies have shown that dementia is associated with quantitative EEG (QEEG) abnormalities including a reduction in the dominant alpha frequency. The purpose of this study was to test whether EEG biofeedback (neurofeedback) training to normalize abnormal EEG activity could improve measures of memory and executive function. Participants were randomly assigned to immediate treatment or to a waiting-list control group. All participants received neuropsychological and QEEG assessments before and after treatment or control conditions. Each participant’s pre-treatment QEEG was compared to a normative database, and neurofeedback protocols were customized to reward EEG changes at significantly deviant frequencies and locations. Treatment consisted of 30 or more neurofeedback sessions. Fifteen subjects have completed treatment to date. Compared to eleven controls, pre- and post-treatment scores displayed significant improvements in verbal memory (mean Mini Mental Status Exam [MMSE] orientation and recall, Memory Assessment Scales’ [MAS] list and prose memory, p=.024); visual memory (mean MAS Visual and Rey Figure recall, p=.017); Behavioral Rating Inventory of Executive Function (mean self and informant General Executive Composite, p=.036); Immediate Visual and Auditory (IVA) continuous performance test response control (p=.027). Trends toward improvement were seen in the MMSE (p=.072) and psychiatric distress measured by the Symptom Checklist 90-Revised (p=.085). A number of executive function measures did not significantly improve, including the IVA Attention, Wisconsin Card Sort, and Delis-Kaplan Executive Function System subtests including Trails, Design Fluency, Color-Word, Sorting, 20 Questions, and Word Context (with the exception of verbal fluency, p=.047). In the treatment group, the standardized mean treatment effect on variables that improved (at p<.10) correlated significantly with the pretreatment MAS Global Memory index (r=.71, p<.01). In the control group, this correlation was -.063. These results support QEEG-based neurofeedback as a “probably efficacious” treatment for dementia. The correlation of efficacy with pretreatment memory shows the importance of learning and memory in neurofeedback’s mechanism of action, and suggests that this treatment is more strongly indicated for mild or early stage cases.
This study measures whether executive and memory symptoms in dementia can be effectively treated by neurofeedback training to increase frontal cerebral blood flow (CBF) and normalize abnormal EEG rhythms. Neurofeedback training has shown efficacy or possible efficacy for treating a variety of central nervous system mediated disorders. However, this is the first controlled study of neurofeedback to improve executive symptoms in persons with dementia. Executive symptoms can include problems with attention, impulsivity, planning, organizing, strategies of learning and remembering, apathy, judgment, and insight.
In EEG biofeedback, an individual’s real-time EEG is presented continuously as a visual or auditory signal, and desired variations are rewarded. For example, a reduced peak alpha frequency (PAF) has been commonly observed in dementia (Passant et al., 2005; Chan et al., 2004; Yenner et al., 1996). A recent double-blind controlled study (Angelakis et al., 2007) showed that neurofeedback rewarding increased peak alpha frequency (PAF) improved cognitive processing speed and executive function in a small sample of normal elderly adults.
However, not all dementia patients show a reduction in PAF. Often, an abnormally high average amplitude in the slow (0-8 Hz) EEG frequencies is present. EEG coherence, a measure of the number and strength of connections between locations, may be reduced. While abnormalities in the frontal leads are most commonly associated with executive symptoms, abnormalities at other locations may be clinically significant. Often, multiple abnormalities may be observed. For instance, excessive slow wave activity might be associated with attentional difficulties, while increased high beta (22-30 Hz) activity can be associated with excessive emotional arousal, which exacerbates the primary attentional problem.
A standard practice in neurofeedback therapy is to analyze a baseline quantitative EEG (QEEG) during an initial assessment, and build custom neurofeedback protocols designed to reward the normalization of each client’s individual abnormalities (Lubar, 2004). Another standard practice is to train multiple criteria during the same session. Thus, a participant may be rewarded for increasing PAF, decreasing slow wave amplitude and high beta wave amplitude.
Research also suggests that impaired cerebral blood flow (CBF) plays an important role in dementia. While a number of studies show that regulation of CBF can trained with biofeedback, very little clinical efficacy research has been published about CBF biofeedback. The present study would be the first controlled clinical efficacy study of hemoencephalography biofeedback.
Spilt et al. (2005) hypothesized that neurodegeneration and dementia are largely secondary to pathologies of CBF. For example, Alzheimer’s patients with brain damage (regions of MRI signal hyperintensity) have increased oxygen extraction per mL/min. That is, blood supply rather than demand seems to be the problem. Oxygen extraction would be expected to be the same if reduced blood flow were secondary to tissue damage (Spilt et al., 2005; Yamaji et al, 1997).
When compared to elderly controls with optimal cognitive function, patients with dementia did not differ significantly from elderly controls with respect to the number of cerebral infarctions. Demented patients showed significantly more white matter lesions and cerebrospinal fluid, but a reduction in cerebral blood flow had the largest effect. After the effect of reduced blood flow was included, the effects of white matter lesions and CSF were insignificant.
Single photon emission computed tomography (SPECT) studies have shown cerebral blood flow to be significantly reduced in the frontal and temporal regions in frontotemporal dementia (FTD) patients (Miller et al., 1997; Read et al., 1995). The anatomical distribution of reduced CBF corresponds to the pattern of neuropsychological deficits (McMurtray et al., 2006).
Recent studies have suggested that individuals can learn to increase CBF through biofeedback. Yoo et al. (2006) showed that participants given feedback of fMRI activity while listening to music were able to significantly increase the mean blood oxygenation in the auditory cortex. Another study (deCharms et al., 2005) trained participants to change fMRI activity in the rostral anterior cingulate gyrus (RACG), a region implicated in pain perception. Control conditions included sham feedback or feedback from a different brain region. When a noxious thermal stimulus was applied, participants had decreased pain sensation when trained to decrease RACG activity and increased pain sensation when trained to increase RACG activity. In another phase of the study, eight chronic pain patients reported decreased pain after down-training fMRI in the same region.
FMRI costs more than $1000 per session, which places this form of therapy beyond the reach of most patients. However, it is possible to provide CBF neurofeedback for the outermost 1.5 cm of cerebral cortex with a relatively inexpensive device that uses the refractive properties of oxygenated hemogoblin to red and infrared light (Toomim et al., 2004). A light source is attached to the scalp (typically on the forehead) with a headband, 3 cm away from an infrared sensor, which detects the relative absorption by oxygenated blood. This procedure is known as hemoencephalography or HEG. Toomim et al. (2004) showed that ten sessions improved impulsivity scores on the Test Of Variables of Attention (TOVA) in 28 patients of diverse psychopathology. Carmen (2004) provided frontal HEG to 100 migraine patients, and found that 90% of those who completed at least six sessions reported significant improvement in migraine symptoms. In a single case study, Mize (2004) reported that a child with ADHD showed significant improvement on the IVA, which improvement persisting into the 18-month follow-up.
While HEG is widely used by clinicians, the few studies of HEG have significant limitations, including the lack of a control group. More peer-reviewed, clinical research on HEG biofeedback training is greatly needed.
Participants will be assessed before and after 30 sessions of neurofeedback with the following.
(1) Memory Assessment Scale (PAR Inc). Assesses short-term and delayed memory for lists, details of a story, figures, names and faces.
(2) Rey-Osterreith Complex Figure Task. Measures visual spatial constructional ability and visuospatial memory.
(3) Wisconsin Card Sort Test. Assesses abstract reasoning and cognitive flexibility.
(4) Integrated Visual and Auditory Continuous Performance Test (IVA). Measures attention and impulse control.
(5) Delis-Kaplan Executive Function battery. Assesses flexibility of thinking, concept formation, problem solving, planning, creativity, impulse control and inhibition.
(6) Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A; self-report and also an informant report by the primary caregiver and/or significant other). This instrument includes a Behavioral Regulation Index assessing symptoms inhibition, shifting, emotional control, and self-monitoring; and a Metacognition Index assessing Working Memory, Initiate, Plan/Organize, Task Monitor, and Organization of Materials.
(7) Symptom Checklist 90-R. This is a comprehensive checklist for co-morbid psychiatric symptoms including Somatization, Obsessive-Compulsive, Interpersonal Sensitivity, Depression, Anxiety, Hostility, Phobic Anxiety, Paranoid Ideation, and Psychoticism. We hypothesize an improvement the Global Severity Index will be associated with improvements in cognitive function.
A quantitative EEG will also be analyzed to assess abnormalities in brain function.
Participants will be randomly assigned into one of three groups: (a) EEG neurofeedback; (b) EEG+HEG neurofeedback combined; (c) a waiting list control group. The waiting list control group is eventually provided treatment and randomly assigned to strengthen comparisons among (a) and (b).
Treatment Available Nationwide
Most testing and treatment sessions will be conducted at the Quietmind Foundation offices at 521 Plymouth Road, Plymouth Meeting, PA, 19462. However, study participants who live in remote locations may be provided with training and equipment for home-based treatment, or assigned to a therapist in their local area. Call 610-940-0488 to discuss the remote treatment option.