On Depression
Author: Dr. Siegfried Othmer
The current issue of Biological Psychiatry offers a trenchant
study titled “Are There Differences in the Symptoms that Respond
to a Selective Serotonin or Norepinephrine Reuptake inhibitor?”
by Jay Craig Nelson, Laura Portera, and Andrew C. Leon (Volume
57(12), June 15, 2005, 1535-1542).
Remarkably, in two sequential, independent, randomized controlled
large-scale studies (253 and 168 subjects) no significant differences
were found in the response of major depression to reboxetine and
fluoxetine. Symptom change was assessed with the Hamilton Depression
Rating Scale (HAMD).
First of all, these results fly in the face of the core belief
system of modern psychiatry, namely that of specificity not only
with regard to diagnosis but with regard to pharmacological remedy.
It also undermines the chemical deficiency model of depression.
That model all along has had little more than the presumptive
“specific efficacy” of selective serotonin reuptake inhibitors
in evidence. Now that tall pole in the tent is gone.
It is truly ironic that the hegemony of the SSRIs has lasted
for the entire duration of the Prozac patent. The superiority
of SSRIs vis-à-vis the earlier medications that targeted the norepinephrine
system as well (the tricyclics) seemed to be established beyond
question. In truth, the driving force has all along been more
a question of side effects rather than raw efficacy, with SSRIs
being “cleaner” and freer of dietary restrictions than the tricyclics.
This paper will make it easier to propose that the clinically
effective drugs serve mainly to “reregulate” the system rather
than to resolve a putative neurotransmitter deficit.
Neurofeedback for ADHD: A Review Paper
The latest issue (June 2005) of the Applied Psychophysiology
and Biofeedback Journal features A White Paper Review of the prior
research on neurofeedback for ADHD:
Monastra, V. J., Lynn, S., Linden, M., Lubar, J. F., Gruzelier,
J., &
LaVaque, T. J. (2005). Electroencephalographic Biofeedback in
the
Treatment of Attention-Deficit/Hyperactivity Disorder. Applied
Psychophysiology & Biofeedback, 30(2), 95-114.
The paper focuses on research performed with three of the standard
protocols:
1) SMR Enhancement with Theta suppression;
2) SMR Enhancement with Beta-2 Suppression
3) Beta-1 Enhancement with Theta Suppression
The Kaiser-Othmer study on 1089 subjects is included in the review.
However, the work is lumped under Protocol 1 (with variation).
Unfortunately, the essence of the protocol is thereby lost. First
of all, the protocol combined all three of the above. It provided
standardly for the inhibition of both theta and beta-2 bands (22-30
Hz). And it provided for both SMR (12-15 Hz) and beta-1 (15-18
Hz) reinforcement according to the demands of the situation. Most
individuals received both kinds of training.
Hence the review gives the impression that a standard protocol
was used as with the other studies. And the essential feature
of balancing right- and left-hemisphere training with hemisphere-specific
parameters (SMR on the right; beta-1 on the left) was submerged.
It is difficult not to get the impression that the introduction
of variability into protocol-based training is considered in some
way a deviation from the ideal. Nevertheless, the White Paper
is to be welcomed. Unfortunately, the paper came too soon to include
the just-published replication by Tom Rossiter. Looking further
back in history, the Cartozzo controlled study could not be included
since it was kept out of the literature. And unfortunately the
large-scale study we sponsored back in 1994-95 at Cal Poly Pomona
never got written up. This was due to the fact that Barkley thoroughly
intimidated the authors of that study when they surfaced their
preliminary results at the 1995 APA meeting in Los Angeles. Perhaps
there is a way to include such data in a future meta analysis.
And when it comes to outcome studies, there is Tamsen Thorpe’s
dissertation, in which she quantified and analyzed the results
from a number of practices that were using C3beta and C4SMR training
with common instrumentation.
There is continuing controversy about whether training effects
necessarily show up in the stationary EEG measures. The authors
report on Lubar’s work with protocol 3 with some 17 children.
6 of these did not show change in EEG variables, whereas 11 showed
change consistent with the design protocol. “Although the association
between learning to control cortical activation and degree of
clinical response was not assessed,” the authors nevertheless
press the “importance of directly assessing neurophysiological
indicators of learning in any evaluation of efficacy.” Remarkable.
One can also relate this back to item one in the newsletter. If
such criteria had been applied to the SSRI’s—i.e. they would be
applied only in the case of a demonstrated deficit, and then only
if the deficit is successfully remediated—then Prozac would never
have gotten off the ground.
In both cases, that of depression and of ADHD, we are facing
a yawning deficit in the understanding of the dynamics and complexity
of neuroregulation. We must go back to a different point of departure
entirely, one that sees regulation as a matter of the dynamic
interaction of a variety of regulatory systems. It is impossible
to intervene unilaterally with such a system. Once that is recognized
we can go beyond overly specific models of deficits and over-constrained
remedies to deal with them.
Dr. Siegfried Othmer
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