Neuropsychological Assessment in Clinical Practice: Test Interpretation & Integration
by Gary Groth-Marnat
A Monthly Summary of News and Events
Vol. 4 No. 9 - September 2001
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One interpretation of the new findings is that the placebo effect is much less important than has been thought, and that the whole matter of placebo controls has been vastly overdone. This interpretation is of course controversial. Another interpretation, however, is that the paper simply reintroduces common sense into the discussion. The placebo effect is simply not operative at a similar level across the board, as has been represented (say 30%), but is much more of an issue in some disorders than others. For example, one does not expect much of a placebo effect in such conditions as dementia, Parkinson's, Alzheimer's, cerebral palsy, medically uncontrolled seizures, or disorders of articulation. Thus if a technique is devised which shows some benefit for these conditions, the placebo hypothesis is not the first thing that comes to mind as an explanation, and hence ruling out the placebo effect should not have to be the first burden of research. That would be a waste of scarce resources. Similarly, if the issue is an increase in measured IQ in ADHD children with neurofeedback training, the placebo hypothesis is simply not in play. Individual outcome measures are quite sufficient to establish the finding.
On the other hand, it remains true that the power of suggestion is operative for many conditions, in particular some of the conditions of disregulation that are also addressed with neurofeedback. In these cases, the 'expectancy effect' may need to be tested for explicitly. This is certainly the case for something like depression, where both spontaneous recovery and the placebo effect are assumed to be operative. One suggested remedy for the placebo problem is to identify the 'placebo responders' in a preliminary phase of the research and remove them from the study. If, however, there is a finite recovery probability per unit time for essentially everyone, then this approach only appears to ameliorate the placebo problem. One could imagine taking the same approach to a hunk of radioactive material. Eliminating the 'early decayers' from the sample does not alter the statistics of subsequent decay. Attempting to eliminate placebo responders does not guarantee a separation of the issues between subsequent spontaneous recovery and the placebo response.
When it comes to ADHD, numerous studies have made the case for a certain placebo response in medication studies. This has even caused some to propose that a 'sugar pill' trial should ethically always precede the administration of stimulant medication even in clinical settings. If there is indeed a large placebo effect here for ADHD, that case should prevail. But hold on. One of the difficulties in working with ADHD children is that they are typically not troubled by their own behavior. After all, they do not self-refer! So why should a placebo effect even be operative here? Most likely one is dealing here with the 'natural variability of the disorder,' rather than with a true placebo response or with spontaneous recovery from the condition. On some days, some children will find themselves on one side of the cutoff, and on a later occasion they may find themselves on the other side. Tracing out the natural variability of the disorder should therefore scope out the dimensions of any presumptive placebo effect as well. When this is done with measures such as the TOVA, considerable consistency of response is observed over time. This means that significant changes in TOVA measures, obtained consistently over a short period of time with neurofeedback, do not yield to a placebo explanation. Hence, they do not require a placebo cohort for their validation.
It is noteworthy that the multi-site, multi-modal study of ADHD that was completed and published a year or more ago did not include a placebo cohort. This speaks louder than words to the proposition that those who were in charge of the experimental design at the NIH did not consider the placebo hypothesis viable any more with respect to ADHD. It appears that the hypothesis is only dragged out these days when it is necessary to flog neurofeedback. This seems to me intellectually dishonest. At a minimum, a double standard appears to be operative when it comes to pharmacological and behavioral interventions. This is ironic because the placebo control really lends itself very well to pharmacological studies, and only poorly to behavioral interventions.
Anecdotal Data
A trial was recently held in England which involved a historian who comes close to being a "Holocaust denier." He finds it important to make the case, for example, that Adolf Hitler left no documentary evidence of his ever having ordered mass exterminations. And he dismisses the evidence of Holocaust survivors as anecdotal, and therefore unreliable. This man represents himself as maintaining the highest standards of evidence in his profession of historian.
Recently a restaging of his trial was shown on PBS. I was struck by the similarity of his position to that of our chief critic: The categorical rejection of anecdotal information; the breast-beating profession of fealty to the highest scientific standards; and the relentless defense of a simply absurd position. I realized that Holocaust deniers and neurofeedback deniers are kin under the blanket. Something besides the facts themselves must be animating the protagonists.
Anecdote is the lifeblood of history; and the life of a clinician can be thought of as one anecdotal case after another. Every clinical case is seen in the prism of the clinician's collective prior experience, and the expectations for every client are set on that basis. If these expectations are consistently violated with neurofeedback, outside of the bounds of the "natural course of the condition," then attention should be paid. The neuropsychologist Elkhonon Goldberg once said, "The career of every clinician is punctuated by a few formative cases." Of course anecdote matters.
The validity of neurofeedback as a viable therapy is now a settled issue for a number of psychopathologies. Only ignorance and/or a skewed value system stands in the way of its general acceptance.
Siegfried Othmer
News & Reviews
NEW BOOKS
Neuropsychological Assessment in Clinical Practice: Test Interpretation & Integration
by Gary Groth-Marnat
Bipolar Disorders: Basic Mechanisms and Therapeutic Implications
Finding Out About Asperger's Syndrome, High-Functioning Autism and PDD
PMS, Perimenopause, and You: Guide to Emotional, Mental, & Physical Patterns of a Woman's Life
Treating Adult Children of Alcoholics: A Behavioral Approach
Nonverbal Perceptual and Cognitive Processes in Children With Language Disorders
Neuroimaging of hyperactivity
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Review of imaging papers suggest minor structural changes in frontal and caudal areas, esp. on right side, with hyperactivity, and functional studies are consistent with this; yet imaging for diagnostic purposes remains in the future.
Psychosocial functioning after TBI
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At 6 mo and 1 yr post-injury, ) 1/4 of TBI patients suffer from depression with emotional contrl problems most distressing. 70% lost job, 30% lived back with parents, and 38% had relationship breakdown
Depression and emotional control in brain injury
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At 6 mo and 1 yr post-injury, 1/4 of TBI patients suffer from depression with emotional control problems most distressing. 70% lost job, 30% lived back with parents, and 38% had relationship breakdown
Brain metabolic changes associated with symptom factor improvement in major depressive disorder.
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Improvement in cognitive disturbance in depression is associated with increasing dorsolateral prefrontal cortex metabolism.
Predicting Relapse to Alcohol and Drug Abuse via Quantitative EEG
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Enhanced amount of high frequency (19.5-39.8 Hz) beta activity was observed in patients who later relapsed compared to those who maintained abstinence and controls.
Frontal lobe changes in alcoholism: a review of the literature.
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A review of literature supports the concept of frontal lobe pathology in alcoholism.
Thought disorder in attention-deficit hyperactivity disorder.
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Thought disorder in childhood may reflect impaired development of communication skills.
Measures of psychopathology in children with complex partial seizures
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The Schedule for Affective Disorders and Schizophrenia for School-Age Children identifies psychopathology better than the Child Behavior Checklist in children with seizures.
Cognitive neuroscience of aging: contributions of functional neuroimaging.
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Brain activity tends to be less lateralized in older adults than in younger adults.
Psychophysiological marker of ADHD--defining the EEG consistency index.
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Further validation of an QEEG correlate of transitions between tasks for identifying ADHD.
Upcoming Courses
Prerequisites:
All Adv. classes require successful completion of the 4 Day Comprehensive Beta/SMR.
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Conferences for Neurofeedback Clinicians & Researchers | ||
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| CONFERENCE | LOCATION | DATES |
| SNR - http://www.snr-jnt.org./NewsPlus/2001/2001-sched.htm | Monterey, CA | Oct 27-30 |
Pay Attention: Ritalin Acts Much Like Cocaine
Excerpt from JAMA Aug 22/29, 2001
Methylphenidate (Ritalin), which is taken daily by nearly 6 million American children, acts much like cocaine, though at a much slower pace, according to recent neuroimaging research.
Surprisingly, methylphenidate was found to be a more potent dopamine transport inhibitor than cocaine. A typical dose given to children blocks 70% of dopamine transporters compared to 50% for cocaine. "The data clearly show that the notion that Ritalin is a weak stimulant is completely incorrect," said Nora Volkow, MD, psychiatrist and imaging expert at Brookhaven National Laboratory. However, methylphenidate takes an hour or so to raise dopamine levels whereas inhaled or injected cocaine hits the brain in seconds. However when injected as a liquid, methylphenidate sends a jolt that "addicts like very much," Volkow said. "They say it's like cocaine."
This research has provided a model of the mechanism underlying ADHD: Apparently, children with ADHD have underfed attention circuitry; they produce weak dopamine signals, so that usually interesting activities provides fewer rewards. At the same time they face random, distracting neuron firing. This background noise interferes with concentration, making the child easily distractible. Methylphenidate increases the signal and reducing the noise. Nonetheless, the long-term dopamine effects of taking methylphenidate for years, as many do, are unknown. "Could chronic use of Ritalin make you more vulnerable to decreased dopamine brain activity as cocaine does?" Volkow wonders. "It's a key question nobody has answered."
For complete letter, see http://jama.ama-assn.org/issues/v286n8/ffull/jmn0822-1.html