Alumnus e-interview

Robert Marietta, MD (SLU-2000) was a Med-Scholar 1992-1996. He did  several courses from me including this course.

He completed a Navy residency in Psychiatry and served in Okinawa. Now (2012), he is a
practicing psychiatrist in Virginia

This "e-interview" is from 2006



Q:  Prozac and related drugs have revolutionized the treatment of
depression.  From the outset and recently, they have been implicated, by
their detractors, in suicide and homicide.  How do you address these issues?

A:  People with depression have a higher incidence of suicide than
people without depression.  Is suicide caused by depression, caused by
the drug or both?  If you look at the rate of suicide for the entire US
population over time you will see that it dropped around the time
anti-depressants came on the market.  The current consensus in
psychiatry is that anti-depressants are safe, effective and reduce
suicide when used appropriately.  Just as a drug could make someone feel
better it could also make them feel "too good", more agitated or
irritable.  This is especially true in the case of a bipolar patient
presenting in a depressed phase.  An anti-depressant used alone might
flip such a patient into a mania and result in agitation or suicidal
ideation.  The way the clinician addresses this is through the process
of informed consent.  We tell patients the risks and benefits of a drug
and let them decide if they want to take it.  We warn patients to look
out for the potential side-effects and to stop the medication and call
us if they arise.

Q:  Depression, and medication for depression, is now a big issue in
children in teenagers.  What are the appropriate and ethical approaches?

A:  To my knowledge there was only a single study that suggested a small
increase in suicidal IDEATION (not the incidence of completed suicide or
suicide attempts) in children on anti-depressants.  Given the dramatic
and litigious nature of our society, the story was sensationalized and
developed a life of its own.  The study was quickly debunked and
disregarded by child psychiatrists.  The proper approach again is
informed consent.  To provide informed consent the pediatrician or child
psychiatrist has to have a firm understanding of the literature
surrounding issues like this so they can competently talk about the risks.

Children are very dynamic just like the wiring in their brain.  They
tend to have different and more transient symptoms than adults.  For
example, a depressed child might be irritable compared with an adult who
feels sadness and decreased energy.  Many symptoms in children represent
prodomes for disorders that will occur later in life.  The big
difference between the standard of care for treatment of children and
adults is that they require more frequent follow-up.  It might be
appropriate to start and adult on an anti-depressant and wait a month
for follow-up.  However a child patient requires a follow-up after the
first week of starting a medication.

Q:  In the early days of treatment for hyperactivity, it seemed odd that
an amphetamine (dexedrine) should be used. How can it have such
different effects, calming hyperactivity in youth and acting as a
stimulant in adults?

A:  ADHD is divided into 2 main symptom clusters including inattention and hyperactivity.  It is possible to have inattention alone, hyperactivity alone or a mixed presentation.  Approximately half of children with ADHD continue to have the disorder as adults.  It could very well be that these symptom clusters share a similar genetic mechanism of action.  For example, the serotonin transporter gene and dopamine receptor.  Recent neuroimaging studies like the PET scan show that different areas of the brain light up in patients with ADHD vs. normal controls.  There might be separate areas in the brain responsible for attention and impulse control affected by the same genes.  The "genetic load" or number of mutated genes in addition to the severity of the mutations is important to consider.  Regardless of the precise cellular mechanisms one could see how increasing the amount of dopamine or norepinephrine might act on both areas to improve attention because these areas of the brain are stimulated.

Your question is a reminder that for as much as we know about medications including what neurotransmitters they act on, we really don't know the exact mechanism of action for how they alleviate people's symptoms.  For example, we know that norepinephrine and dopamine improve concentration.  At the same time, it might not be accurate to say ADHD is caused by a "deficiency" of these neurotransmitters.  Besides acting directly on neurons, stimulants might increase blood flow to certain areas of the brain.

Q:  Nowadays, Ritalin is widely prescribed and hyperactivity is called ADHD. Tom Cruise, and the Church of Scientology, have been outspoken critics. Answer them on the reality of ADHD and the usefulness of medications.

A:  When neuroimaging studies suggested the possibility of differences between ADHD and control subjects the Church of Scientology claimed that the medications themselves were resulting in brain damage.  A follow-up study was performed that compared neuroimaging studies of patients with ADHD on medication and control subjects with ADHD without medication.  As I recall, the results were the same or better for subjects on medication.  The fact is regardless of the cause of the disorder, stimulants are very effective for ADHD.  There are other non-stimulant medications such as buproprion and atomoxetine that have also been proven effective for the treatment of ADHD.  Neuroimaging, genetic studies and that fact that patient's symptoms improve by drugs affecting specific suggests that our biology plays a significant role in ADHD.  To accept the notion that ADHD doesn't exist and that medications are harmful or ineffective means ignoring all this scientific research.  It is irresponsible and harmful for these parties to make such unsubstantiated claims and I question their motives.  

Q:  Brook Shields was criticized for receiving treatment for her post-partum depression.  Answer this criticism.

A:  There is a clear relationship between hormones and depression.  A disorder called premenstrual dysphoric disorder has been described in the literature where women experience clinically significant depression at a predictable point during their monthly cycle.  Similarly, birth control pills are known to cause depression.  Pregnancy and the post-partum period is a time when hormones are changing rapidly.  There is strong evidence for a biological etiology for post-partum depression.

If someone falls down they are experience pain.  Suppose they were doing something foolish that caused their fall.  Does that make a difference as to whether or not they deserve an effective treatment?  If we suggested withholding medication that would effectively treat the pain that would be unethical and immoral.  The same thing applies to patients with depression.  Even if a patient had a 100% psychological etiology for depression medications could still be considered an effective treatment.  Medications might improve the new mom's mood, energy level and sleeping pattern.  This might benefit the child by improving the mother's ability to bond with her child.

Q: Although it sounds barbaric, electroconvulsive (ECT) shock has played a role in treatment for depression. How useful was it and is it still used?

A: At some point the clinical observation was made that patients with epilepsy
have a lower incidence of psychiatric disorders. Around 1940, someone tried
generating a seizure in a patient with severe psychiatric problems and
reported good outcomes. The problem with a seizure is that it causes
muscular contractions all over the body. In modern ECT, patients are given
a paralytic agent such as succinylcholine prior to the procedure. They are
also given an anesthetic to make them unconscious. The psychiatrist then
connects usually two leads or sometimes one lead ("unipolar") to a machine
and generates a seizure. Unipolar ECT is used with people with dementia and
depression to reduce the chance of memory loss. The leads are connected to
an EEG so that the psychiatrist can make sure an adequate seizure was
generated. ECT is generally administered 1 to 3 times per week for several
weeks and then less frequent for maintenance treatment. ECT is very
effective for mood disorders such as depression and bipolar disorder. It is
unique in that it results in a very rapid improvement of symptoms where
medications act at the cellular level and take weeks to work. I suspect the
mechanism of action has to due with release of neurotransmitters. A
definitive mechnism of action is unknown. ECT has a unique utility for
elderly patients who can't tolerate medications. ECT can result in limited
memory loss and generally has few adverse side-effects.

Q:  Any other thoughts?

A:  One of the biggest areas of research in psychiatry is psychosis
because of the impact on society and costs involved.  The psychotic
disorders especially schizophrenia are considered to be very much a
biological illness.  Probably the number one prognostic factor in this
disorder is compliance with medication.  The neurotransmitter in
psychosis is dopamine.  The medications used for treatment of
schizophrenia block dopamine receptors.  Too much dopamine or overactive
receptors could mean psychotic symptoms like hallucinations.  Cocaine
causes release of dopamine and results in psychotic symptoms sometimes.  
The dopamine receptor subtypes are very important.  Block them all like
the older "typical" anti-psychotic agents and you can get tardive
dyskinesia and a Parkinson like movement disorder.  Block only certain
subtypes with the new "atypical" antipsychotics and you get relief of
symptoms without the movement disorders.  There is a newer class now
that has partial agonist and antagonist effect on dopamine receptors:  
keep them active at a low level but block the rest.

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