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To  Brian Nevin on his introduction to this group
 
First I will be honest, Brian, being in the medical profession does not make
you an expert on diagnosis of your own problems.  It just gives one more
knowledge in alternatives and turns on the spigot of symptoms.  It is kind of
like the car mechanic whose car doesn't run or the plumber with broken water
lines.  They gave up on their own problems.
 
Depression by itself does not seem to be the beginning of PD.  Depression is
found in about 40% of those with PD.  The depression is both reactive and
neurochemical.  Just to give some understanding of the neurochemical side in
PD, I attended a presentation given by Dr. Neal Slatkin of City of Hope
Medical Center in Duarte, CA.  He stated it this way.
 
1.  It seems that two neurochemicals, norepinephrine and serotonin, are found
to be deficient in people with depression. Drugs which reduce the
availability of these neruotransmitters are called "depressants".  On the
other hand drugs that increase the availability of these neruotransmitters
are called antidepressants.
 
2.  The model for norepinephrine is the following:
      Tyrosine x Levodopa ==> ENZ ==> Dopamine --> norepinephrine
 
This says that tyrosine and Levodopa with the help of ENZ  create dopamine
and from dopamine, norepinephrine is created.  If there is a deficiency of
dopamine it would follow that a deficiency of norepinephrine could also
exist.
 
Serotonin is a little more complex.  Serotonin is manufactured in neurons to
form the neruotransmitter.  This process starts with a chemical called
tryptophan and with the help of ENZ makes serotonin.  Now if the process to
make dopamine finds too few neurons, the need for dopamine will cause the
dopamine process to cannibalize the serotonin process for the ENZ.  Thus as
the ability to produce dopamine decreases due to the dying neurons in the
substantia nigra, the dopamine need will cannibalize the serotonin process
ENZ and thus less ENZ will be available for serotonin to be produced.  Now I
am sure this whole process is much more complex than I have stated, but it
does give a basis for neurochemical depression in PD.
 
3. If someone with PD were to go to their physician with any of the following
symptoms
     sad faces
     fatigue
     sleep disturbance
     speech: slow,...
     stooped posture
     constipation
     chronic and recurrent pain
     memory loss
     sexual dysfunction
 
These would be thought to be PD symptoms.  In actuality, they are PD symptoms
but they are also symptoms of depression.  It depends on how you and your
physician will define the cause of the symptoms.  If there has been no
history of depression, these would most likely be treated with PD
medications.  With a history of depression, the treatment becomes complex.
 
4. PD is a movement disorder.  Often you will find PD is one of the diseases
treated by movement disorder specialists, such as neurologists. Not all
neurologists are movement disorder specialists.
 
5. Finally, if you have PD and depression, antidepression drugs can worsen PD
in some cases.  There is a paper from England that talks about SSRI drugs
making PD worse in some patients. There is also the case of "serotonin
syndrome" which may happen if an SSRI and a MAOI are taken together.  This
can also happen if a tricyclic and a MAOI are taken together.  In PD the MAOI
is Eldepryl and your case SSRI is Prozac.  It is possible that the Prozac has
not exited your system before you started Eldepryl and you developed a
reaction.  Check to see how long it takes for Prozac to be out of the system.
 (By the way, I take 5 mg of Eldepryl and 20 mg of Paxil together without
problem.)
 
Now you can apply your medical knowledge and hopefully I have helped.  If I
have not helped I may feel depressed, so be kind in your assessment of my
babbling.
 
Regards,
Alan Bonander
Age 55, Diag 11 yrs, liquid meds, pallidotomy
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