Posted by JohnX2 on February 21, 2002, at 12:36:19
In reply to bad histamine feedback my culprit? Check this out., posted by JohnX2 on February 20, 2002, at 21:14:54
Thanks for all the feedback!
Now what do you think about this. This is
long, so bear with me, but I think a dysfunctional
noradrenaline system from PTSD can explain my atypical
mania/bipolar.Going back to my thoughts about post traumatic
stress disorder. No one in my family has bipolar
symptoms. There is depression, but no bipolar.
I went through about a 3 year period of substantial
durress during a difficult time in my family and
after this I had fairly classical PTSD symptoms
(flashbacks, etc). When I first got an AD response
to St. John's Wort it stuck for 3 days which was
the longest response to date. When it worked I
had an enormous emotional outporing and flashbacks
to memories from my childhood. After 3 days the
medicine did a weird thing and put me into this
emotionally numb state with bad pressure headache
and jaw tension. When i discontinued it I had
panic attacks for 1 week.From what I understand about PTSD there is a lot
of data to show that the noradrenergic alpha-2
receptors become dysfunctional. Their affinity
states (H/L) become skewed towards being high.
That being said they are easily whip-sawed.
There are a lot of thoughts PTSD depression is
very difficult to treat because the feedback
mechanisms involved in the noradrenaline system
are really messed up and difficult to control
with typical medicines. Some people postulate
that better approaches maybe be partial a2a
agonists.There is an interesting coupling between the
noradrenaline system and the serotonin system.
The part of the noradrenaline system that gets
goofed up from stress is the locus coerulus.
Norepinephrine migrates from the locus coerulus
to receptors on the raphe serotonin system
(a target for SSRIs). There are alpha-1 and
alpha-2 noradrenaline receptors on the serotonin
neurons. The alpha-1 receptors increase firing
of the serotonin neuron and the alpha-2 receptors
at the dendrites of the serotonin neurons act
to release serotonin.So its thought that in PTSD that the locus
coeurlus can be hyperactive since the alpha-2
adrenoreceptors can easily become chronically
overly downregulated. Ultimately either more or
less NA would migrate to the serotonin system a2 receptors
and overly downregulate or upregulate them.
This could diminished or hyperactive serotonin
release. You would be "stuck". So I'll shoot
from the hip and guess that somehow I get stuck
because serotonin release is diminished as the
alpha-2 heteroreceptors are downregulated and
the locus coerulus becomes depleted of noradrenaline.Maybe Im firing to much from the hip here. But
in the case of Serzone, you would not get "stuck"
because one of the metabolites is mCPP, a direct
serotonin agonist and hence the medicine may get
around a dysfunctional cross-talk with the
noradrenergic locus coerulus system.Another thing I once tried inadvertly was taking
Manerix while also taking Tizanidine. Tizanidine
is a partial alpha-2 agonist, hence a buffer
for goofy alpha-2 receptors. Normally when I
take Manerix it does not do much, a little anxiety
relief is all. When I took it with Tizanidine I
felt a substantial flushing in my face and it was
very similar to starting up Serzone, plus my
depression improved, weird. So I'm thinking
that the Tizanidine by acting as a noradrenergic
agonist is also braking a dysfunctional loop.Anyways, it has been thought that Clonidine
or Tenex may be useful for PTSD. I got Tizandine
which is a cleaner version of Clonidine, from
a neurologist who thought it would cure my head
pain. The Tizanidine is the only medicine besides
Serzone, Topamax, and Klonopin to help alleviate
my myofacial pain.
-John
poster:JohnX2
thread:94861
URL: http://www.dr-bob.org/babble/20020215/msgs/94937.html