ADD / Social Phobia / MRI Data
Alan J. Robinson
robin073 at maroon.tc.umn.edu
Tue Dec 12 08:37:16 EST 1995
On 9 Dec 1995 12:11:27 -0500,
Sfcom9 <sfcom9 at aol.com > wrote:
>Can you - or anyone you know make sense of the following data found on the
>neuro-physiology of Social Phobia?
>What would you speculate is going on in the brain of a Social Phobic who
>is also diagnosed with ADD?
>Any elucidation, comment or speculation on the following data - especially
>in regards to future treatment directions in a Dual Diagnosis case of ADD
>and Social Phobia - will be immensely appreciated!
>Social Phobic Data:
>* There is some kind of >>Support for a dopaminergic abnormality related
>to social phobia...Recent studies have implicated dopamine and the basal
>ganglia circuits in the pathophysiology of social phobia.<<
>* There seems to be >>growing literature on the processing of information
>among persons with social phobia<<.
>* No evidence of HPA-axis overactivity found
>* Choline and creatine signal-to-noise ratios (SNRs) were significantly
>lower in social phobia than in controls (in Choline and creatine
>subcortical, thalamic, and caudate areas).
>* In the social phobic group, N-acetylaspartate (NAA) SNR was
>significantly lower in cortical and subcortical regions, and ratios of NAA
>to other metabolites were lower in social phobia.
>* Choline, creatine, and N-acetylaspartate NAA SNRs were inversely
>correlated to total social phobia and fear symptoms, in the thalamic and
>noncortical gray areas.
>* In a small number of patients who received clonazepam, posttreatment
>SNRs generally increased relative to baseline.
>* <<an age-related reduction in putamen volumes was revealed in patients
>with social phobia that was greater than that seen in controls.<<
>* MAOI's, Prozac, selective MAOI-A inhibitors and Benzodiazapines have all
>been used effectively to help treat social phobia. Most of the press has
>gone to the traditional MAOI's. Beta blockers have been of dubious value
>and seem least effective.
Much of the data that you mention will one day be part of a comprehensive
picture of the pathophysiology of disorders such as social phobia and
ADD, but right at the moment the picture is too incomplete to be of
much use for such things as treatment planning. In fact, the best
correlations that have been found so far for response to different
medications have been with temperament (personality) and regional
cerebral blood flow.
Many patients do not fit the specific clinical profiles listed in the
DSM, so dual diagnoses tend to be quite common. It is not at all
unusual for patients to have a veritable "smorgasbord" of symptoms,
drawn from a wide variety of DSM and other medical diagnoses. On
the other hand, it is technically possible for someone to have
extensive psychiatric symptomatology, yet not meet the criteria for
any one of the disorders in the DSM.
There is a new class of treatment for psychiatric disorders such
as these which shows great promise, especially when the patient has
not responded to conventional medications. It is a combination of
indirect dopamine and serotonin agonists - one combination is
phentermine and fenfluramine, but other combinations are possible and
are being researched. One of the questions which has not been
addressed yet is how far these combinations could replace the current
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