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Parkinson's and Depression

Parkinson's and Depression


Johannes HeimannA guest contribution by Dr. med. Johannes Heimann, Nürtingen. Dr. Heimann was a gynecologist and obstetrician during his career and has been diagnosed with Parkinson's for several years. His contributions are to be understood as food for thought and in no way replace advice from a specialist.

WHAT IS DEPRESSION?

When I was still a resident gynecologist, Ms. NN came to the regular check-ups very regularly. She was a happy person, lively, intelligent, had both feet on the ground. The quarter or half hour that she occupied with me was downright relaxing. But suddenly she stopped coming. Unusual! Previously a pattern of reliability. After a break of 2 years, she was suddenly there again and was just the way I knew her: happy, healthy, lively, nice.

But now she was the one with an antidepressant. “Suddenly it was as if someone in me had turned off the light. I didn't get up in the morning. Nothing was my business. I didn't care about anything. I was less sad, more cold, and lifeless. She denied stressful conflicts and emotional injuries in childhood and adolescence. Such is classic depression.

NEUROTRANSMITTER - OVERVIEW

Change of scene. Now we have to do a little theory.

Nerve cells, like every cell, have a cell body and a cell nucleus somewhere. One or more axons emanate from this, most likely to compare electrical cables. These axons can be tenths of a millimeter up to 1,5 meters (!) Long. The individual nerve cells are connected to the other nerve cells via so-called synapses. In the end, nerve fibers do not pass on their excitation directly to the other nerve cell with an electric current, but rather by secreting so-called transmitters (= chemical messenger substances) into the narrow fluid zone between the two nerve cells. The most common of these transmitters are called:

  • Acetylcholine for almost everything
  • Norepinephrine (drive, day-night rhythm).
  • Serotonin (Depression)
  • Dopamine (akinesia, hypokinesia, bradykinesia, rigor, tremor)
  • Glutamate
  • and a few others.

THIS IS THE USUAL PROCEDURE

Parkinson's is mainly characterized by slowed (bradykinesia) or limited (hypokinesis) or nonexistent (akinesia) movements, muscle rigidity (rigidity) and / or tremor. Here the number of dopamine-producing cells in the so-called substantia nigra is reduced. Long before one perceives these symptoms and only then understands what is happening as Parkinson's syndrome, other centers perish:

Stage I:

The Lewy bodies that cause Parkinson's syndrome are probably transmitted via the III. Cranial nerves (n. Olfactorius - "olfactory nerve") and the Xth cranial nerves (n. Vagus - gastrointestinal area) are brought into the brain, so that the first the so-called "nuclei" (areas of gray brain matter), called nucleus olfactorius and nucleus vagus perish.

This causes the early symptoms of loss of smell (III) and tendency to constipation (X). Nobody thinks of Parkinson's.

Stage II:

The next step is an area of ​​gray matter in the area of ​​the so-called "Four Hills" and the so-called Locus coeruleus. These structures control the day-night rhythm and the general mood (neurotransmitters serotonin and norepinephrine). If these centers are disturbed, depression and sleep disorders occur. In particular, the centers that function with serotonin just above the brain stem continue to go under. The result: depression.

Stage III:

Only then is the so-called substantia nigra disturbed. This works with dopamine as a neurotransmitter. If more than 50% of these are broken, classic Parkinson's syndromes occur. And it is only now that Parkinson's syndrome is usually diagnosed.

So let's summarize: Almost every Parkinson's patient probably not only has a dopamine deficiency in the brain, which is treated diligently and faithfully, but also a serotonin deficiency and a less pronounced norepinephrine deficiency.

ENOUGH THEORY FOR TODAY

Years before the diagnosis my life was no longer accompanied by music, and at some point I had an argument with my orchestra conductor: I felt that we had just played the music like dead automatons. In retrospect: That applied to me, I was no longer able to vibrate emotionally.

SO IT WAS WITH ME

My wife didn't notice that very much - she saw me every day and didn't see the changes that way - but my daughters, who came home every now and then: They said that dad has become different.

That's when I started taking antidepressants, which of course means I had them prescribed for me. The success was sudden: I immediately felt better. What are antidepressants?

They have a serotonin effect and thus replace the serotonin that I had no longer produced enough.

The mood was good. But still, sometimes I “didn't get my butt up that much”. I'm a fan of Spain, I've been to the beautiful island of Mallorca, speak fluent Spanish, enjoy mingling with people and chatting away. I stayed in my room for several days and didn't go to the beach or the pubs. Mood good - but drive bad: Norepinephrine deficiency in the brain.

My neurologist implemented: Instead of a pure serotonin active ingredient, I got a mixed serotonin-noradrenaline active ingredient. Now my daughters said: Papa is now back to what it used to be.

I not only take my own mood, but also how my loved ones perceive me as a measure of whether I am correctly adjusted.

From my previous daily practice, I learned that many depression went undiagnosed and unfortunately also remained untreated. In Parkinson's patients, depression is more the rule than the exception. And that is not (only) because the diagnosis lies in the stomach. We had depression or its equivalents before reporting the diagnosis.

For some reason, many feel ashamed to speak of or "admit" to depression. With this we are only harming ourselves.

We all know: The number of years we are in good condition Therapy being able to move well is limited. Ruining this time and the one afterwards with a depression that could in principle be treated would be a “shame”, to say the least.

Perhaps it helps to think that we most likely have a serotonin deficiency in the brain. Not treating it would be the same as if our thyroid no longer supplies enough hormone and we did not swallow the missing amount of hormones that we bought at the pharmacy.

PREJUDICE AGAINST ANTIDEPRESSIVES

  1. Antidepressants make you tired. Wrong: An untreated depression makes you tired.
  2. Antidepressants are addictive. Wrong: Antidepressants are not addictive. Just don't stop abruptly if you've been using them for a long time. Not because of dependency, but because then there is a sharp backlash in the direction of increased depression.
  3. Antidepressants make you fat: We'd like to see that when you feel like living again, whether you then have more sport and exercise or a healthier appetite.
  4. Antidepressants cover up the problems that we should actually solve. Wrong: With too little serotonin in the brain, we have no chance of being happy again even after "working on" a problem, whatever that should be. On the contrary, a drug-balanced serotonin deficiency can only open up the possibility of facing an unpleasant fact.
  5. Antidepressants change personality. Wrong: If you get the right one of the 30 or so antidepressants, at some point your partner or your child will say: You are the same as before.
  6. When and how do I stop taking the antidepressant? For myself, I suspect I will take it by the end of my days. There is no reason to assume that the brain structures that were whole in the past will suddenly become whole again.

There is nothing wrong with starting a treatment attempt over 2 - 3 months and then taking stock of whether it has helped.

PLEASE EVERY NEW SETTING, CHANGEOVER, DOSE CHANGE ONLY IN COOPERATION WITH THE NEUROLOGIST / NEUROPSYCHIATER !!!!!

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