What's New in Neurofeedback
A Monthly Summary of News and Events
Vol. 4 No. 5 - May 2001
This newsletter is sponsored by EEG Spectrum International Intl, Inc.,
a leader in providing clinical service and training professionals.
Past issues are available at www.eegspectrum.com/newsletter/
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The opinions related in this newsletter reflect those of the author only.
Copyright (C) 2001 by EEG Spectrum International Intl, Inc. All rights reserved.
Announcements
In the Spotlight
How Well is Functional Neuroimaging Functioning?
Last month marked the 11th anniversary of functional magnetic resonance imaging, or fMRI, the most successful neuroimaging technique to date. Last month also marked a transition in the history of neuroimaging itself: EEG, the granddaddy of all brain imaging technology, was surpassed by the upstart in number of papers published. Around 75,000 journal papers had been published in EEG and in fMRI. The field of EEG required 70 years to reach this plateau; fMRI required a mere 132 months to achieve so much ink.
Dozens of scientists contributed to development of MRI and related neuroimaging techniques, but the official birth of fMRI, it you could call it that, took place in Murray Hill, New Jersey. In April 1990, Ogawa, Lee, and colleagues working at AT&T Bell Laboratories published their investigation of how oxygenation altered MR images in mice and rats. Like much of science its conception took place at another time and on another continent. One hundred years earlier Roy and Sherrington (1890), working out of London, published "On the regulation of blood supply of the brain" in which they suggested that neural activity was accompanied by a regional increase in cerebral blood flow. From this speculation has emerged a cottage industry of cognitive neuroscience in 2001. Both PET (positron emission tomography) and fMRI take advantage of local changes in blood flow and blood oxygenation associated with increased or decreased neural activity, but fMRI does it non-invasively (i.e., without radioactivity), using high powered magnets.
One reason for the rapid success of fMRI was that it utilized machines (MRIs) already widely install in hospitals and other medical facilities. It also provided a good compromise between spatial sensitivity and temporal resolution. Yet fMRI is not without its drawbacks. First and foremost is the elements it measures: whereas EEG assesses neuronal activity by measuring neuronal (electrical) activity, fMRI measures vascular activity (or blood flow) and blood oxygenation. Other drawbacks include technical and physical constraints: required stillness of the head (which makes speaking and other large movements problematic), detection through differences (e.g., subtraction method), an inherent time lag in hemodynamics (up to 4 to 6 seconds), and other non-specific influences on blood flow (respiratory fluctuations, heart rate changes).
A final issue with fMRI (both a strength and weakness) is the amount of information derived from each recording session. A single recording can generate one gigabyte of data. In comparison, QEEG recordings generate less than a percent as much data per comparable session. Data reduction is essential for both fields. Investigators quickly learn to limit their analysis or face opening too many doors. As with QEEG, our limited understanding of brain function makes a sensitive measure noisy. A recent paper examines the strengths and pitfalls associated with fMRI for ADHD populations.
According to neurosurgeon Joseph Bogen (pers. communication) fMRI has to date shown us very little we didn't already know from other imaging techniques. The only new knowledge generated out of billions of dollars spent so far on this technique is the surprising activation of the cerebellum during cognitive function. But perhaps that is a pessimistic viewpoint shared by few. fMRI is extremely popular among psychologists and neuroscientists. In "Incoherence of neuroimaging studies of ADHD", Baumesiter and Hawkins (2001) attempt to collate and compare all relevant structural and functional neuroimaging on ADHD populations. There is a desperate need for some order in the world of neuroimaging, particularly functional neuroimaging. With more than 800 fMRI papers published every month, it's nearly impossible to separate the good from the bad, the wheat from the chaff.
Baumeister and Hawkins not only seemingly share Bogen's skeptical point of view, particularly in relation to ADHD, they might go a step further and argue that the supposed strength of the tool is undermining its actual application and muddying the field of investigation. The problem lies with noise: inconsistency, unreliability, the overall iack of replicated findings. All techniques are affected by "investigational noise", but fMRI appears to suffer at the extreme. Though it's not as clear as the authors would state the case, they argue that no neuroimaging finding has been consistently observed across ADHD studies.
They do perform a useful service in collating study results, a service desperately needed to make sense of all the neuroimaging publications flooding the datasphere nowadays. For instance, they review a series of five investigations into caudate nucleus size and morphology, six structural studies of of the seven sections of the corpus callosum, nine studies which identified frontal lobe dysfunction, and seven which also examined temporal lobe function. Altogether, they identify numerous findings but little similarities between labs.
Functional imaging studies include resting and challenge conditions. This point is often glossed over by the authors when the mass together incompatible findings across studies. It's not surprising to find that certain frontal lobe function in ADHD adults doesn't vary from controls during rest but does during specific cognitive "stresses," as they call them. This incompatibility of recording conditions may account for much of the apparent incoherence among studies, particularly for the frontal lobe effects. But it cannot explain incompatibility structural neuroimaging findings.
The authors provide a handful of data tables to strenghten their argument, but a different set of eyes may see another story altogether. In structural imaging of the corpus callosum, for instance, the splenium is found to be smaller in ADHD patients compared to controls in half the studies listed. Studies of the genu, isthmus, and other corpus callosum sections show only one or two positive findings among 4 or 5 negative (non-significant) ones. Yet one cannot help but notice that of the 8 significant differences depicted from 42 comparisons depicted, not a single study reported greater size for ADHD patients; all 8 reported smaller sections compared to control. A sign test, about the simplest statistical test possible, find 8 out of 8 highly significant. So despite all the noise, the variety of subjects used, the shadings of diagnoses and comorbidities presumably included in six independent samples, as well as the variety of methodology and sampling techniques applied, ADHD is often association with size reductions in the corpus callosum. The exact opposite conclusion of the authors.
A similar pattern is witnessed in the caudate nucleus studies. Only 5 of 13 comparisons were significant, but all were in the same direction (i.e., smaller in ADHD populations). And whereas morphology asymmetry of the caudate nuclei was present in 4 of 5 studies for controls, four of five studies found no asymmetries in ADHD populations.
Finally the vast majority of frontal lobe studies reported lower activity in certain areas in ADHD patients compared to controls. The handful of studies reporting greater activity in specific frontal areas in ADHD subjects were all isolated finding, neither supported contradicted by another study. Yet nearly all reduced activity findings associated with this disorder were confirmed by other studies.
The authors are not blind to these patterns, they are simply underwhelmed by the reports to date. Where is the compelling evidence for biological mechanisms of ADHD? How can other scientists blithely refer to neuroimaging studies as support for their biological hypotheses when the picture is hardly clear?
Functional MRI is a powerful tool, creating instant enthusiasts in most scientists who encounter it. With this tool we can peer into the brain and watch it work, we can isolate a single nucleus or system -- the amgydala, the hippocampus -- and analyze its contribution to cognition and emotion. We can witness the mind's processes as they unfold with remarkable clarity. Or can we? Has power seduced us? The brain is more like a river than an insect under the microscope. Amorphous, ever changing, undefinable when viewed too close. Our efforts to measure its currents and resolve its riverbed must proceed carefully if we are too avoid the subtle distorting power of flowing waters.
"Biologic tunnel vision," the authors call it: neuroimaging tools obscuring non-biological
contributions to a condition. It's not unusual in science to believe in expensive tools, that these tools reveal more about the human condition than, say, a series of simple questions and answers. Yet how a child interacts with a mirror or how a patient responds to a set of questions can disclose more about one's psyche that any non-invasive probing.
DK
Related reading:
- Roy, C. & Sherrington, C. (1890) J. Physiol. (London) 11, 85-108
- Ogawa S, Lee TM, Nayak AS, Glynn P. (1990). Oxygenation-sensitive contrast in magnetic resonance image of rodent brain at high magnetic fields. Magnetic Resonance Medicine, 14, 68-78.
www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?form=6&db=m&uid=2161986
- Baumeister AA, Hawkins MF. (2001). Incoherence of neuroimaging studies of attention deficit/hyperactivity disorder. Clinical Neuropharmacology, 24, 2-10.
www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?form=6&db=m&uid=11290875
News & Reviews
NEW BOOKS
Handbook of Functional Neuroimaging of Cognition
by Roberto Cabeza
PET and fMRI findings in attention, visual recognition, semantic memory, episodic memory, and working memory; and the effects of aging and impairment on brain activity during cognitive performance.
-www.amazon.com/exec/obidos/ASIN/0262032805/top100
The Neurophysics of Human Behavior: Explorations at the Interface of the Brain, Mind, Behavior, and Information
by Mark E. Furman, Fred P. Gallo
Advances a unified theory of brain, mind, behavior, and information.
-www.amazon.com/exec/obidos/ASIN/0849313082/top100
Pharmacotherapy for Mood, Anxiety, and Cognitive Disorders
by Uriel Halbreich
Pioneers in the development of treatment modalities explain the underlying mechanisms of treatments for mood and cognitive disorders.
-www.amazon.com/exec/obidos/ASIN/0880488859/top100
Developmental Disorders of the Frontostriatal System: Neuropsychological, Neuropsychiatric and Evolutionary Perspectives
by John L. Bradshaw
Proposed common origin in the function and dysfunction of the brain's frontostriatal system that contributes to a handful of conditions including depression, schizophrenia, ADHD, Tourette's Syndrome and OCD.
-www.amazon.com/exec/obidos/ASIN/1841692263/top100
Prozac and the New Antidepressants : What You Need to Know About Prozac, Zoloft, Paxil, Luvox, Wellbutrin, Effexor, Serzone, Vestra, Celexa, St. John'
by William S. Appleton
Describes each new antidepressant on the market, the side effects, and who should be taking them.
-www.amazon.com/exec/obidos/ASIN/0452281644/top100
Essentials of Chemical Dependency Counseling
by Gary W. Lawson
For clinicians or clinicians in training: covers all aspects of counseling including legal and ethical issues, family counseling, counseling those reluctant to recover and harm reduction.
-www.amazon.com/exec/obidos/ASIN/0834218240/top100
Depressed Child and Adolescent: Developmental and Clinical Perspectives
by Ian M. Goodyer
Discusses normal development and psychopathology, response to clinical treatment; for clinicians.
-www.amazon.com/exec/obidos/ASIN/0521794269/top100
Epilepsy and Sleep: Physiological and Clinical Relationships
by Dudley S. Dinner
Argues that many sleep disorders are in fact due to the undiagnosed condition of epilepsy; for clinicians, psychiatrists, and sleep disorder specialists.
-www.amazon.com/exec/obidos/ASIN/0122167708/top100
Cognitive Neuroscience : A Reader
by Michael S. Gazzaniga
An overview of this new and growing field via a collection of readings ranging from the earliest articles discussing brain plasticity to recent research in executive functioning.
-www.amazon.com/exec/obidos/ASIN/063121660X/top100
Encyclopedia of Drugs, Alcohol, and Addictive Behavior
by Rosalyn Carson-Dewitt
Written primarily for non-experts.
-www.amazon.com/exec/obidos/ASIN/0028655419/top100
Strong Feelings: Emotion, Addiction, and Human Behavior
by Jon Elster
Interrelation between three explanatory approaches to behavior (and its motivations) are explored: neurobiology, culture, and choice.
-www.amazon.com/exec/obidos/ASIN/0262550369/top100
JOURNAL PAPERS
Long-term effects of stimulant medications on the brain
:
Treatment of ADHD with amphetamine-like stimulant medications for extended periods of time during child development may carry negative consequences (e.g., increase in use of illicit drugs, higher incidence of mania, psychosis, etc.)
Role of functional neuroimaging in the neuropsychology of depression.
:
Dorsolateral prefrontal cortex, particularly in the right hemisphere, are key brain structures in emotion/cognition interactions in negative mood states.
Advances in functional neuroimaging underlying neuropsychological dysfunction.
:
Strengths and limitations of the neuroimaging techniques (e.g., PET, fMRI) are discussed, including integration with EEG and MEG.
Neural activity related to drug craving in cocaine addiction.
:
Craving-related activation of a network of limbic, paralimbic, and striatal brain regions, including amygdala, nucleus accumbens, and anterior cingulate cortex.
EEG power, frequency, asymmetry and coherence in male depression.
:
Depressed males show a pattern of aberrant inter-hemispheric asymmetry and a profile of frontal activation in QEEG measures.
Prefrontal-subcortical and limbic circuit mediation of major depressive disorder.
:
Psychomotor retardation was associated with decreased left prefrontal activity and impaired sustained attention was associated with right prefrontal and parietal dysfunction.
Brain imaging in posttraumatic stress disorder.
:
Dysfunction of the anterior cingulate, with a failure to inhibit amygdala activation, may characterize PTSD
Diffuse cortical reduction of neuronal activity in unipolar major depression
:
Regional cerebral blood flow or glucose metabolism indicate a diffuse cortical rather than regionalized (e.g., hypofrontality) reduction of neuronal activity in unipolar major depression.
Incoherence of neuroimaging studies of ADHD
:
Review of neuroimaging of recent ADHD studies finds no specific abnormality in brain structure or function convincingly demonstrated.
A history and review of quantitative EEG in traumatic brain injury.
:
Reviews history and significance of conventional EEG and how Quantitative EEG (QEEG) is used in a clinical setting.
On the role of prefrontal cortex glutamate in OCD and ADHD
:
OCD is a hyperglutamatergic and ADHD hypoglutamatergic condition, with prefrontal brain regions being especially affected.
Events & Locations
Upcoming Courses
Woodland Hills, CA
- 4-Day Beta/SMR - May 17-20
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Prerequisites:
All Adv. classes require successful completion of the 4 Day Comprehensive Beta/SMR.
* Advanced Practicum requires 150 hours direct NF clinical experience.
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More info at www.eegspectrum.com/course
Conferences for Neurofeedback Clinicians & Researchers |
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| CONFERENCE | LOCATION | DATES |
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| SNR | Monterey, CA | Oct 27-30 |
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Last Word
Waiting for V
While we await the fifth edition (V) of the APA's Diagnostic and Statistical Manual of mental disorders, better known by its acronym DSM, scheduled to be published in 2007, we might spend some of this time discussing what we have, what we will get, and what we want from the APA.
Although numbers vary depending on one's criteria, at last count the DSM (IV) contains 410 diagnoses, a 530% increase since inception. The DSM was first published in 1952 and contained 60 diagnoses. Its first revision DSM-II was published 16 years later in 1968 and contained 145 diagnoses, more than double the original. (The 60s was a mentally trying time...) DSM-III was published in 1980 and bumped up diagnoses to 231. Its major revision DSM-IIIR added 10 disorders per year for 8 years, and finally we arrive at the present incarnation, DSM-IV, published in 1994 and containing 410 disorders. Obviously psychiatry is a growth industry. And yet 1994 is, psychologically-speaking, a distant memory. Extrapolating from past publications, we must now have 595 disorders to speak of and treat. By publication date 2007, we will have to add 190 on top of this increase. When will all this madness stop!
Obviously such extrapolations, like those from the Congressional Budget Office, are apt to reflect anything BUT reality the further into the future one projects. Still that doesn't stop the government so it shouldn't stop me.
Future historians may study DSMs for sociological perspective, as ideological statements by the psychiatric community of the time, and they will have to explain why we reach quadruple digits (1,000) in 2013. Were we half as sick in 2006 and 16 times sicker than a century ago? By year 2064 we attain quintuple digits -- 10,000 conditions -- which is about one condition per psychiatrist alive today. By year 2114, ten times more; by 2165, one million disorders, and by year 2370 and using UN moderate population projections, the DSM-XXIII will contain 11 billion disorders, one per planet inhabitant. Imagine the conversations at psychiatric conferences (which will engulf entire counties and account for 70 % of GDP): "What condition did you treat him for?" "Oh, a bad case of John Jacobs." "Never heard of it." "You should, he lives on your street."
(The nonsense is almost over...) Unfortunately if one can extrapolate into the future, the past is also vulnerable. According to DSM trends, in year 1900 Sigmund Freud, at the pinnacle of his career, only had a mere six mental health conditions to deal with. How difficult is that? But more disturbing is the final extrapolation: the very first mental health condition struck the world's population sometime in 1856. The year of Freud's birth.
Coincidence or not?
