hi all

one of the most difficult aspects of clinical depression [cd]
for me was recognising it in myself:
if my thinking processes are distorted by cd,
how can i evaluate my thinking processes?

i thought this re-post might be timely for anyone
who might be languishing in the seemingly permanent doldrums
of the sea of cd or any situation resembling same

janet


-------------------------------------------------
Date:  08/09/96 21:39
From:  <Janet Paterson >
Subj:  tears, a tale, and a re-run on depression

hello all [including clan-members!]

there has been some discussion recently about 'tear attacks' and pd.

at the risk of destroying any illusions
you all may have about my living in paradise,
[ed. note: the author lived in bermuda from 1981 to 1998]
i thought this little tale of mine might be relevant:

living here necessitates a certain tolerance for the local 'wild life' -
i.e. most new [human] arrivals are dismayed
by the healthy size and abundance
of our cockroaches.

after my initial shock,
i developed a strong hunting instinct, and would stalk them with enthusiasm
[and a large can of bugspray - a practice i have since abandoned -
but that's another tale]

however, one day i surprised myself by reacting completely differently.

bursting into tears at the sight of yet another interloper
was so unlike my normal reaction,
that i had to take a closer look at it.
[my reaction, not the interloper]

since i had learned a bit
about clinical depression from sharing a friend's worries,
i was able to recognise my response as a symptom of a larger problem.

some sessions with a therapist and a prescription for prozac
helped me regain my normal equilibrium.

i don't intend to suggest that
anyone feeling a bit 'teary' is suffering from clinical depression [cd],
but offer this as another viewpoint.

i believe that we pd-ers are more vulnerable than the average population
to our emotions, both mentally and physically.

we are also more likely to suffer with cd,
maybe partly due to our emotional vulnerability
as well as to our brain chemistry.

[the late] alan bonander posted this article about depression last january
and i thought it might be valuable to re-post it. i'm sure he'd approve.


janet

-------------------------------------------------
Date:  Sun, 28 Jan 1996
Subj:  Depression in PD

..... PD is like fighting a war on many fronts and thanks to this list server, each day I learn more about the enemy.  Each time I look at my generals researching the enemy as they see them, I realize the complexity of the problem.  We really need additional funding -- pass the Udall Bill and other bills so the war can really begin.

Here is depression in Parkinson's disease.  Please read slowly.


DEPRESSION IN PARKINSON'S DISEASE

(A Supplement to the Video)
by Alan Bonander

NOTE: This paper is a written supplement to the video of the presentation called 'Depression in Parkinson's Disease' by Neal Slatkin, MD, a presentation made at the state-wide meeting of YPSN of CA on June 10, 1995 in Duarte, CA.  Dr. Slatkin is a neurologist, parkinsonologist and director of the Parkinson Center at the City of Hope Medical Center in Duarte, California.


INTRODUCTION

Our sixteenth president, Abraham Lincoln, stated, "I am now the most miserable man living. If what I feel were equally distributed to the whole human family, there would not be one cheerful face on the earth. Whether I shall ever be better, I cannot tell, I awfully forebode I shall not. To remain as I am is impossible. I must die or be better, it appears to me."

This is one of the best statements on the problems of depression. An eminent psychiatrist once said that more human suffering can be attributed to depression than any other illness affecting mankind.

Approximately 6% of the US population will have a major depression sometime during their life. A major depression is one which significantly limits one's functionality.

In the older population, depression is a very significant problem. There are about 45 million people over the age of 65. It is estimated that between 10% and 20% of these people are having a major depression at any point in time. That means somewhere between 4.5 million and 9 million older people are having a major depression at any point in time.

If we look at a list of all causes of mortality in 1992, suicide is listed between HIV (AIDS) and homicide. Surely if we have an epidemic of HIV (AIDS) and an epidemic of crime in this country, we have an epidemic of suicide. And suicide is only the tip of the iceberg when it comes to depression.

Costs are important in our society today. It is estimated that depression costs $45.3 billion annually. That is composed of $14 billion for direct costs (inpatient, outpatient, drugs), $7.5 billion for death from suicide, $12.1 billion from decreased productivity and $11.7 billion from absenteeism.


DEPRESSION IN PD

Depression is the most common neuro-psychiatric disturbance among PD patients.  It is more common than psychosis, confusion and dementia.

The prevalence in PD, which is about 40%, is higher than for any other chronic illness that is matched for similar degree of functional impairment.

Of those with depression, about 50% are having a major depression.  The other 50% are having a minor or mild depression which only sucks all the joy out of their lives.

In a study performed at Columbia in New York, it was found that the annual incidence, (number of new cases), of depression among Parkinson's patients was 1.90% which was over 10 times the annual incidence of depression in the general population of 0.17%.

Depression seems to appear at anytime.  It is often present at time of diagnosis, after several years and with increasing physical impairments.

Depression can also appear during episodic periods.  About 70% of those experiencing random "ON-OFF" cycles are more depressed when they are "OFF." This change can happen almost instantaneously when they turn "OFF."

It appears that more females have depression (this is questionable) and those with a past history of depression.  Also those experiencing rigidity, bradykinesia and gait problems are more susceptible to depression.

Interestingly, those with PD more on their right side are more likely to have depression.  The patient current age, family history of PD, dementia and tremor seem to not influence depression.

Young onset patients (those getting PD before age 50) are 3 times more likely to have a major depression than those with normal onset (36% vs. 11%).  Mild or minor depression is about the same for any age of onset (16% vs. 14%). Together, Young onset patients are about twice as likely to experience depression than those with normal onset PD (52% vs. 25%).


WHAT IS DEPRESSION

Question:  Is depression merely the exaggeration of a normal mood state (sadness) or is it a qualitatively different mood state?

Temperature and mood can be viewed on a continuous scale.  A temperature of 104 degrees is qualitatively very different than a temperature of 100 degrees.  Similarly, sadness and depression are qualitatively very different.

Question:  Is depression primarily caused by psychological stress and conflict or is it related primarily to a biological abnormality?

There are two different types of depression:  Endogenous which is biological such as neurochemical, and exogenous which is situational coming from the environment.  Normally a depression is composed of some combination of both endogenous and exogenous causes.

Studies have been done on the neurochemical component of depression.  It has been found that the neurochemicals of serotonin and norepinephrine are involved in depression.

Everyone knows that there is a deficiency of dopamine in PD. It turns out that norepinephrine is manufactured from dopamine.

Dopamine is manufactured from tyrosine and levodopa with the help of an enzyme called ENZ.  Thus if there is a deficiency of dopamine there is reason to believe there could be a deficiency of norepinephrine.

Serotonin is manufactured form a substance called tryptophan.  This process uses the same enzyme called ENZ.  As fewer and fewer neurons are available to produce dopamine, there is a cannibalistic effect on the neurons producing serotonin.

The process to create dopamine from levodopa enters the serotonin cells and takes the ENZ, leaving little for the manufacture of serotonin. Thus serotonin levels could fall for that reason.


SYMPTOMS OF DEPRESSION

   Sadness
   Depressed mood (especially in the morning)
   Hopelessness, helplessness and self-blame
   Loss of interest & pleasure in activities
   Loss of energy - fatigue - leading to inactivity
   Decreased concentration - indecisiveness which has led
      some doctors to diagnose dementia incorrectly
   Sleep disturbance
   Preoccupation with negative thoughts - seeing the world through
      maroon colored glasses rather than rose colored.
   Poor appetite and weight loss
   Thoughts of death and suicide and in some cases actually doing it


DIAGNOSING DEPRESSION IN PD

DEPRESSION -->> MOTOR IMPAIRMENTS -->> DEPRESSION

Most people can understand that motor impairments can cause depression. It is more difficult to understand that depression can cause motor impairments.

We have no difficulty believing that the mind can heal the body.  It is more difficult to grasp that the mind can cause physical impairments.

Dr. Slatkin states that when he tells a patient that the mind is causing physical impairment, they do not believe him. He says they are going to be offended and angry with him.

"They think I am telling them that their symptoms are not 'real' and that I feel in some way they are faking it.  This is truly not the case."

Mood state and physical state are interrelated.  Solving only one side of the problem does little.  Both mood state and physical state must be evaluated together.

When there is an rapid deterioration in the physical state of a PD patient keep in mind that adding the Parkinson's medications alone may not help. Dr. Slatkin is convinced, from his many years of working with PD patients, that when a patient is depressed, the medications for PD do not work.

Thus both sides of the equation must be addressed.  Ways of improving mood state are exercise, increased activity, anti-depressants and counseling.

Ways of improving the physical state are with Parkinson's medications.

Clinical Features of Depression
   Sad faces
   Fatigability
   Sleep disturbance
   Speech: slow, ... ,
   Stooped posture
   Constipation
   Diurnal variation
   Low mood
   Motivation loss
   Hopelessness
   Loss of interest
   Feel inadequate
   Suicidal wishes
   Indecisiveness
   Conscious guilt
   Loss of appetite
   Cry in interview

Looking at the clinical features of depression, there is an overlap of clinical features with PD.  The first seven symptoms are common to both depression and PD.

This means that if a PD patient goes in to his/her physician with one or more of the common symptoms, what are the chances that the physician will recognize these as depression and not PD?

There is no objective test of depression.  What doctors rely on are tests such as
the Beck Depression Inventory
[available on the wwweb at:
http://www.newcountry.nu/pd/members/janet/971031.htm],
the Geriatric Depression Scale, SCL-90, MMPI and Hamilton Rating Scale.  These combined with time spent with the patient, good patient history and a proper physical examination help the physician diagnose depression.

The "Mask of Parkinson's" is there to remind us that depression is often masked by physical symptoms.  The symptoms are chronic and recurrent pain, fatigue, memory loss, problems with sleep and sexual dysfunction.

Often no physical cause of these symptoms can be found. What is found is that these are physical symptoms of the underlying depression.

A study was performed that found that 58% of PD patients said, "Fatigue is among my three most disabling symptoms."  Fatigue was highly correlated with depression.

It as also found that 67% were found to have "fatigue with PD was different in quality or severity" than that experienced before the diagnosis. Fatigue was not correlated with disease severity.


TREATMENT OF DEPRESSION

Treatment of depression uses counseling, education, electro-convolsive therapy (ECT), anti-depressants, exercise and stimulants.  Only two will be discussed -- anti-depressants and ECT.  Drugs used are the following:

Anti-depressants Used in Parkinson's Disease
   Tricyclic
        Elavil (amitriptyline)
        Tofranil (lmipramine)
        Pamelor (nortriptyline)
        Norpramiln (desipramine)
        Sinequan (doxepin)
   Selective Serotonin Reuptake Inhibitors (SSRI)
        Prozac (fluoxetine)
        Zoloft (sertraline)
        Paxil (paroxetine)
   Miscellaneous
        Desyrel (treazdone)
        Wellbutrin (buproprion)
        Effexor (ventafaxine)
        Serzone (nofazodone)

The SSRI drugs inhibit the reuptake of serotonin. This allows more serotonin to hang around in the synapse with hope more will cross the synapse to the receptors of the receiving neuron.

One thing that we do not want is dopamine receptor blockade.  The one anti-depressant that is not good for PD patients is Asenden (amoxapine) because of its dopamine receptor blockade function.


REMEMBER: Anti-depressants take time to work

Anti-depressants have both a quick effect and a longer therapeutic effect. Often the synoptic effect and the adverse side effects can show in hours or days.  The therapeutic effect usually takes from three to six weeks.

Thus it is important to stay on these drugs for a few weeks to determine if they can help.  If nothing happens in the first few days, this is correct.

Many of the tricyclic antidepressants are also good pain relievers -- especially for nerve pain syndrome.

There is about a 70% response rate regardless of agent used.  A drug is often selected by looking at the side effects to be avoided.  There are no good biological response markers.

Melancholic and persistent, recurrent depression seem to respond best. The side effects of SSRI drugs are:

Possible Side Effects of SSRI Drugs (Partial listing)
   Nausea
   Diarrhea
   Sexual dysfunction  (delayed ejaculation in men,
      lower libido in both sexes)
   Sleep or near sleep
   General fatigue
   Dry mouth
   Constipation
   Difficulty with urination
   Memory loss (amnesia)
   Dizziness from drop in blood pressure
   Akathisia (need to move)
   Worsening of PD symptoms
   Serotonin Syndrome

Serotonin syndrome [ed note: extremely rare - no cases actually documented] arises when an anti-depressant that inhibits reuptake reacts with a monoamine oxidase inhibitor.

Drugs that increase serotonin activity in the brain are: SSRI (Prozac, Zoloft, Paxil), TCAD (Elavil, Pamelor, Desyrel), Lithium, Tryptophan. The Monoamine oxidase inhibitor is Eldepryl (selegine, deprenyl).

Pharmacists, if they know you are using both Eldepryl and one of the anti-depressants, are required to call your physician to let them know they are prescribing drugs that may be contraindicated. Always discuss the possible interaction with your physician.

Serotonin Syndrome Symptoms
   Motor symptoms
        Jerking of arms and legs
        Increased stiffness and rigidity
        Incoordination
   Mental behavioral symptoms
        Agitation
        Confusion
        Disorientation
        Restlessness
   Miscellaneous
        Fever
        Nausea, Diarrhea
        Shriving, flushing
        Sweating
   Exceptional problems
        High fever
        Seizures
        Coma, Death


ELECTRO-CONVULSIVE THERAPY

Electro-convulsive therapy has a long history of use.  It was observed that when a patient would have a seizure  they would get better.  Various methods were used to cause seizures.  In 1941 the first tests of ECT in the US were done in New York.  Looking in a book on the use of ECT, one finds Parkinson's disease on the list.

ECT can be a very valuable therapy if the patient has had a poor response to anti-depressants or has a poor tolerance or compliance with anti-depressant medications or patients having problems due to manic depressive disorder.


OTHER THERAPIES FOR DEPRESSION

EDITORAL COMMENT: Please note that this paper has discussed therapies involving medications for depression in Parkinson's disease.

These therapies are important; however, the therapies of exercise, increased activity and counseling should also be considered.  Remember to be open with your physician when discussing both mood state and physical state problems


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Archive maintained by Simon Coles.
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-------------------------------------------------

janet paterson - 51 now /41 dx /37 onset - almonte/ontario/canada
<http://www.newcountry.nu/pd/members/janet/index.htm>
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