Tuesday, June 19, 2007

Guest-Blogger Willme on ativan (I)

Willme is my next guest blogger and talks about his experiences with legal drug prescriptions and their impact on his stuttering. Interesting thoughts, and he has a PhD in physics like me. :-)

I started stuttering in early childhood. My first experience with speech therapy occurred when I was 13 years old. The therapy involved voluntary repetitions of the first syllable of each word uttered and the application of this technique in a public context. This approach didn’t work for me. I basically refused to practice this technique in public—perhaps I was too embarrassed, self conscious, etc.
When I started puberty very late at the age of around 17 my fluency substantially improved. I joined the National Forensics Society and on the debate team and engaged in forensic speaking. By the time I entered the 12th grade, my disfluency had returned. Maybe temporary changes in brain chemistry at the start of puberty offered a temporary “cure?
My next speech therapy occurred in my later 20’s after I completed graduate school. It was a group therapy setting with four other males in their late teens and early 20’s. There did not seem to be any particular therapy techniques involved other than making eye contact and the admonition to “just stop it.” Well, strange as it seems, it worked for me. Within two weeks, I became, as far as I could tell, perfectly fluent within that group context. So I called it the “power of positive thinking” (POPT) or the “mind over matter” (MOM) approach. For the next couple of months before I left the group, the POPT/MOM approach did not work for the four other people.
I then started four years of psychotherapy (twice a week) and began teaching in a graduate program at a university. The POPT/MOM approach tided me over but I found that for anxiety inducing situations (speaking before a class or at a conference) I had to expend a huge amount of energy preparing myself, both content-wise and emotionally (psyching myself up?). Also, during psychotherapy, I found that I would be disfluent when discussing emotion laden subjects.
After years of teaching and research, I moved to a career in consulting. Public presentations were fewer than in the teaching career but the POPT/MOM approach still worked (still requiring a huge expenditure of energy). A few years into this period I began to take ativan (Lorazepam) for anxiety and eventually found that at a 2 mg dosage virtually eliminated disfluency. And there was no need for extensive content/mental preparation before presentations. I would merely engage in “normal” preparation, take 2 mg of ativan about a half hour before the presentation (on an empty stomach) and, miraculously, I was perfectly normal.
My last eight years I returned to a career in university teaching and continued with the ativan therapy. I would teach two graduate courses per term and present papers at approximately 4-5 conferences per year. The courses might be scheduled say for Monday and Thursday between 6pm-9pm and the 2 mg of ativan tided me over for the three hours. So my intake of ativan was sporadic rather than regular, which is important because ativan can be addictive, its effect lessens if used regularly, and, hence, you may require larger dosages. I would certainly not recommend the use of ativan to anyone who is an addictive personality.
...to be continued...

NOTE: PLEASE CONSULT WITH A DOCTOR BEFORE TAKING ANY MEDICATION TO TREAT STUTTERING!

23 comments:

manuel said...

hi!

I have a question at the writer of this article,
or people that have experience in taking this kind of drugs.
I would like to know, while you took ativa (or other drugs),
what actually happened inside of your mind?
Didn't you have any (upcoming) Blocks,
or was it just easier to forget/overget
them. How was it while you were speaking ?

Thx for the good post and greetings, manuel :-)

willme said...

In answer to Manuel: Dosing 2mg ativan seems to eliminate ALL disfluency--no blocks (secondary stuttering) and as far as I can tell no primary stuttering (e.g., repetitions, vowel prolongations). The fluency level seems to be at the newscaster level of fluency (<<2%; no hemming and hawing either). Aside from improving fluency the 2mg dosage appears to improve articulateness in that I have greater clarity of thought and can adlib much better. Some ativan trials conducted with dementia patients paradoxically showed that their thought processes improved with small dosages. The theory proposed was that the ativan reduced their "brain noise."

Leo said...

GABA/pagoclone and BG/DS theories are not mutually exclusive. The connection between them may be in the fact of which neurons of the main basal ganglia output nucleus, the pallidum, are GABAergic. That is, the basal ganglia output is mainly GABAergic.

The nervous system contains a toolbox of motor programs in the brainstem and spinal cord - that is, neuronal networks designed to handle the motor repertoire required for speech, locomotion, posture, eye movements, breathing, chewing, swallowing and expression of emotions.

And all these motor programs are just kept under tonic inhibition by GABAergic pallidal neurons (the output cells of the basal ganglia).

Tom Weidig said...

Holger Stenzel wants me to translate this question into English:

"I thought that Pagaclone is not part of the "Benzodiazepinen", and does not lock onto the corresponding rezeptors, but to a subtype of "BZ-Rezeptorfallance" (dont know how to translate) called Omega type."

willme said...

In answer to Holger Stenzel: The original filing by Indevus to the FDA(?) in section 2.2 states: "The cyclopyrrolones have demonsrated high affinity for the benzodiazepine binding site on the GABA-A receptor. Some cyclopyrrolones, e.g., pagoclone have a pharmacological profile consistent with that of a partial agonist at this site." Does this answer your question?

Gustav said...

Wilme, why GABA/pagoclone and BG/DS theories would be mutually exclusive? If what Leo wrote is true, they seems perfectly conformable.

willme said...

While what Leo said may be true, the existence of GABA activity in the basal ganglia area (where dopamine action is also located) does not necessarily imply a relationship between them. Will enhancing one of the neurotransmitters modify or alter the activity of the other? In the reference I cited by P.A. Alm, possible striatal (the striatum is located in the basal ganglia area)synchronization may be initiated by a small number of GABAergic interneurons (see P.A. Alm, section 3.6.3). But no tie-ins are made to the dopamine system.

Ora said...

willme - Thanks for your article.

You might be interested in a recent article by Bothe et al. published in the November 2006 issue of American Journal of Speech-Language Pathology, titled "Stuttering Treatment Research 1970–2005: II. Systematic Review Incorporating Trial Quality
Assessment of Pharmacological Approaches" ?

Let me know if you haven't seen it and I can send you the PDF file. I'm at omccreary (at) nyc (dot) rr (dot) com

They reviewed a lot of articles and studies, including the 1991 Brady article you mention, as well as a 2000 article by the same author mentioning alprazolam (Xanax), which is another one of the benzodiazepines. (Brady, J., & Ali, Z. (2000). Alprazolam, citalopram, and clomipramine for stuttering. Journal of Clinical Psychopharmacology, 20, 287.)

I also have a hardcopy of Gerry Maguire's 2004 article on olanzapine, which he himself has taken for his stuttering for years. (He's the principal researcher for pagoclone.) Here's the abstract: http://www.informaworld.com/smpp/
content~content=a714110971~db=all
I can send you a copy by snailmail if you like.

gustav said...

Willme, the most correct theory would be then BG/GABA/pagoclone?

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